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Background: Decades of intensive genetic selection in the domestic chicken (Gallus gallus domesticus) have enabled the remarkable rapid growth of today's broiler (meat-type) chickens. However, this enhanced growth rate was accompanied by several unfavorable traits (i.e., increased visceral fatness, leg weakness, and disorders of metabolism and reproduction). The present descriptive analysis of the abdominal fat transcriptome aimed to identify functional genes and biological pathways that likely contribute to an extreme difference in visceral fatness of divergently selected broiler chickens. Methods: We used the Del-Mar 14 K Chicken Integrated Systems microarray to take time-course snapshots of global gene transcription in abdominal fat of juvenile [1-11 weeks of age (wk)] chickens divergently selected on bodyweight at two ages (8 and 36 wk). Further, a RNA sequencing analysis was completed on the same abdominal fat samples taken from high-growth (HG) and low-growth (LG) cockerels at 7 wk, the age with the greatest divergence in body weight (3.2-fold) and visceral fatness (19.6-fold). Results: Time-course microarray analysis revealed 312 differentially expressed genes (FDR ≤ 0.05) as the main effect of genotype (HG versus LG), 718 genes in the interaction of age and genotype, and 2918 genes as the main effect of age. The RNA sequencing analysis identified 2410 differentially expressed genes in abdominal fat of HG versus LG chickens at 7 wk. The HG chickens are fatter and over-express numerous genes that support higher rates of visceral adipogenesis and lipogenesis. In abdominal fat of LG chickens, we found higher expression of many genes involved in hemostasis, energy catabolism and endocrine signaling, which likely contribute to their leaner phenotype and slower growth. Many transcription factors and their direct target genes identified in HG and LG chickens could be involved in their divergence in adiposity and growth rate. Conclusions: The present analyses of the visceral fat transcriptome in chickens divergently selected for a large difference in growth rate and abdominal fatness clearly demonstrate that abdominal fat is a very dynamic metabolic and endocrine organ in the chicken. The HG chickens overexpress many transcription factors and their direct target genes, which should enhance in situ lipogenesis and ultimately adiposity. Our observation of enhanced expression of hemostasis and endocrine-signaling genes in diminished abdominal fat of LG cockerels provides insight into genetic mechanisms involved in divergence of abdominal fatness and somatic growth in avian and perhaps mammalian species, including humans. [ABSTRACT FROM AUTHOR]

Glucagon-like peptide-1 (GLP-1) is an incretin hormone released from intestinal L-cells in response to food entering into the gastrointestinal tract. GLP-1-based pharmaceuticals improve blood glucose regulation and reduce feeding. Specific macronutrients, when ingested, may trigger GLP-1 secretion and enhance the effects of systemic sitagliptin, a pharmacological inhibitor of DPP-IV (an enzyme that rapidly degrades GLP-1). In particular, macronutrient constituents found in dairy foods may act as potent secretagogues for GLP-1, and acute preclinical trials show that ingestion of dairy protein may represent a promising adjunct behavioral therapy in combination with sitagliptin. To test this hypothesis further, chow-maintained or high-fat diet (HFD)-induced obese rats received daily IP injections of sitagliptin (6 mg/kg) or saline in combination with a twice-daily 8 ml oral gavage of milk protein concentrate (MPC; 80/20% casein/whey; 0.5 kcal/ml), soy protein (non-dairy control; 0.5 kcal/ml) or 0.9% NaCl for two months. Food intake and body weight were recorded every 24–48 h; blood glucose regulation was examined at baseline and at 3 and 6.5 weeks via a 2 h oral glucose tolerance test (OGTT; 25% glucose; 2 g/kg). MPC and soy protein significantly suppressed cumulative caloric intake in HFD but not chow-maintained rats. AUC analyses for OGTT show suppression in glycemia by sitagliptin with MPC or soy in chow- and HFD-maintained rats, suggesting that chronic ingestion of dairy or soy proteins may augment endogenous GLP-1 signaling and the glycemic- and food intake-suppressive effects of DPP-IV inhibition. [ABSTRACT FROM AUTHOR]

Obesity is considered the second most common health problem in pet cats in developed countries. This study used prospective data from a longitudinal study of pet cats (‘C.L.A.W.S.’, www.bristol.ac.uk/vetscience/claws ) to identify early-life risk factors for feline overweight/obesity occurring at around two years of age. Data were collected via five owner-completed questionnaires (for cats aged two–six months, six months, 12 months, 18 months and two years respectively) completed between May 2011 and April 2015. Owner-reported body condition scores (BCS) of cats at age two years, assessed using images from the 9-point BCS system ( Laflamme, 1997 ), were categorised into a dichotomous variable: overweight/obese (BCS 6–9) and not overweight (BCS 1–5) and used as the dependent variable. Of the 375 cats with owner-reported BCS, 25.3% were overweight or obese at two years of age. Multivariable logistic regression models were built using stepwise forward-selection. To account for potential hierarchical clustering due to multi-cat households two-level random intercept models were considered but clustering had no impact on the analysis. Models were compared using Wald tests. Six factors were significantly associated with overweight/obesity at two years of age: being overweight or obese at one year of age (OR = 10.6, 95%CI 4.4–25.3); owner belief that BCS 7 was the ideal weight (OR = 33.2, 95%CI 8.5–129.4), or that BCS represented overweight cats but they would not be concerned if their cat were classified in this category (OR = 2.7, 95%CI 1.2–6.2), at questionnaire five completion; vets advising owners that the cat should lose weight, or making no comment on their weight, between one and two years of age (OR = 12.1, 95%CI 3.2–44.9 and OR = 3.9, 95%CI 1.5–10.3 respectively); owners giving their cat treats when they “felt happy” with them at 18 months of age (OR = 2.7, 95%CI 1.0 − 7.3); feeding ≥250 g wet food daily between two and six months of age (OR = 2.7, 95%CI 1.2–5.9), and feeding dry food as the only or major part (> 50%) of the diet at two years of age (OR = 2.1, 95%CI 1.0–4.2). These findings have the potential to reduce the current high prevalence of a widespread problem by informing preventive advice, and as such improving the health and welfare of pet cats. [ABSTRACT FROM AUTHOR]

This study tested the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardiac contractile function at rest and in response to adrenergic stimulation in obese swine after myocardial infarction. Obese Ossabaw swine were subjected to gradually developing regional coronary occlusion using an ameroid occluder placed around the left anterior descending coronary artery. Animals received subcutaneous injections of saline or liraglutide (0.005-0.015 mg/kg/day) for 30 days after ameroid placement. Cardiac performance was assessed at rest and in response to sympathomimetic challenge (dobutamine 0.3-10 μg/kg/min) using a left ventricular pressure/volume catheter. Liraglutide increased diastolic relaxation (dP/dt; Tau 1/2; Tau 1/e) during dobutamine stimulation (P < 0.01) despite having no influence on the magnitude of myocardial infarction. The slope of the end-systolic pressure volume relationship (i.e., contractility) increased with dobutamine after liraglutide (P < 0.001) but not saline administration (P = 0.63). Liraglutide enhanced the slope of the relationship between cardiac power and pressure volume area (i.e., cardiac efficiency) with dobutamine (P = 0.017). Hearts from animals treated with liraglutide demonstrated decreased β1-adrenoreceptor expression. These data support that GLP-1 agonism augments cardiac efficiency via attenuation of maladaptive sympathetic signaling in the setting of obesity and myocardial infarction. [ABSTRACT FROM AUTHOR]

The purpose of this study was to analyze the effect of resistance training (RT) in rats with severe obesity. We examined the effects of 4 sessions·wk-1 for 4 wks of RT in Zucker rats with severe obesity. The animals were divided into 4 groups with 4 animals in each: sedentary lean (SEDL), RT lean (RT-L), sedentary obese (SED-O), and RT obese (RTO). The RT attenuated body weight (BW) gain in obese rats (RT-O) compared to the sedentary obese rats (SED-O; P<0.05). The RT-L group increases MS (P<0.05), and there was a difference in gain with respect to RT-O group (P<0.05), which in turn, RT-O did not increase MS (P>0.05). Both SED-O and RT-O groups have a larger deposit of epididymal and brown fat as compared to healthy rats eutrophic (SED-L and RT-L; P<0.05). The muscle weight is lower in obese rats compared to lean rats (P<0.05). The fasting blood glucose was higher in obese rats compared to lean rats (P<0.05), in turn, no difference was observed in cardiovascular parameters between groups (P>0.05). These data show that a short-term RT program attenuated BW gain in Zucker rats with severe obesity, but does not alter the changes generated by severe obesity. [ABSTRACT FROM AUTHOR]

Semen quality has certainly declined over the past few decades, possibly owing to modern lifestyle factors. In this sense, the role of overweight and obesity in the development of subfertility in males has generated a considerable amount of interest in recent years. However, there is no consensus on whether overweight or obesity impaired sperm quality. Thus, based on the ongoing debate about risk factors for subfertility associated with overweight and obesity in men, this study was designed to investigate the effect of overweight on sperm quality parameters and fertility success in randomized controlled trial in a rabbit model. Fourteen male rabbits were randomly assigned to a control group in which nutritional requirements were satisfied or a group fed to satiety from 12 to 32 weeks of age. At 24 weeks of age, semen samples were analysed weekly by conventional semen analysis for 8 weeks. In addition, during the trial female rabbits were artificially inseminated by each male to assess the fertility success and the number of offspring. Young males fed to satiety were associated with a significant increase in body weight (13.6% overweight) and perirenal fat thickness (5%). Male overweight presented a significant decrease in sperm concentration. There were no differences in the remaining sperm parameters. However, male overweight showed a clear and significant decrease in fertility success (control group, 64±8.9% versus fed to satiety group, 35±9.2%), but not in the number of offspring. Taken together, our findings provide new evidence on the loss of fertility induced by overweight in males. [ABSTRACT FROM AUTHOR]

We previously reported that maternal overnutrition and obesity (MO) throughout pregnancy and lactation in sheep (MOF0) decreases term fetal pancreatic β-cell numbers and increases perirenal adiposity producing hyperphagia, increased adiposity and insulin resistance in adult female offspring (MOF1) fed ad libitum. Pregnant female MOF1 exhibited increased blood glucose from mid to late gestation vs control F1 (CTRF1) though both groups ate only to NRC recommendations. MOF1 ewes delivered female offspring (F2) who like their MOF1 mothers exhibited increased abdominal adiposity and absent neonatal leptin surge. In the current work, we determined if adult MOF2 exhibited metabolic syndrome components when fed ad libitum. After weaning, MOF2 males (n = 5), MOF2 females (n = 6), CTRF2 males (n = 5), and CTRF2 females (n = 6) were fed to NRC requirements until 19 mo followed by 12-wk ad libitum feeding. Body weight and % fat increased ( P < 0.01) in all F2 during this feeding trial. MOF2 males were heavier ( P < 0.01) than CTRF2 males and females, and MOF2 females throughout the trial. By wk 8, baseline blood glucose concentrations increased ( P < 0.001) in MOF2 females, but not other groups, remaining elevated throughout the trial. Baseline insulin was similar through wk 6, increasing ( P < 0.05) at wk 8 in MOF2 females only. MOF2 female insulin returned to CTRF2 female levels during wk 10 and 12. The progressive increase of plasma glucose on wk 8 in association with increased insulin in MOF2 females but not other groups demonstrated a diet-induced increase ( P < 0.001) in MOF2 female insulin resistance. The subsequent decline in insulin during wk 10 and 12 despite elevated glucose in MOF2 females is consistent with a decrease in glucose-stimulated pancreatic β-cell function. These data indicate that ad libitum feeding exceeds the pancreatic secretory response predisposing MOF2 females to hyperglycemia. Furthermore, there was a sex difference where MOF2 males increased body mass and MOF2 females displayed insulin/glucose dysregulation. [ABSTRACT FROM AUTHOR]

Reduced hepatic glycogenesis is one of the most important causes of metabolic abnormalities in non-alcoholic fatty liver disease. Octreotide, a somatostatin analogue, has been demonstrated to promote weight loss and improve metabolic disorders in mice with high fat diet (HFD)-induced obesity. However, whether octreotide affects hepatic glycogenesis is unknown. The aim of the present study was to verify the effects of octreotide on hepatic glycogenesis in rats with HFD-induced obesity. Male Sprague-Dawley rats were fed a standard diet or a HFD for 24 weeks. Obese rats from the HFD group were further divided into a HFD-control group and an octreotide-administered group. Rats in the latter group were injected with octreotide for 8 days. Glucose and insulin tolerance tests were performed, and the area under the curve (AUC) was calculated. Following sacrifice, their body weights and lengths, fasting plasma glucose (FPG), fasting insulin (FINS), serum triglyceride (TG), total cholesterol (TC), free fatty acid (FFA), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured. In addition, Lee's index and the homeostatic model assessment index were calculated. Hepatic TG, FFA levels and glycogen content were first determined. Hepatic steatosis in the obese rats was assessed based on hematoxylin and eosin and Oil Red O staining. Human hepatoblastoma HepG2 cells were divided into a control group, a palmitate (PA)-treated group and a PA + octreotide-treated group. Establishment of the in vitro fatty liver model using HepG2 cells was confirmed by Oil Red O staining. The expression of phosphorylated Akt and glycogen synthase kinase 3ß (GSK3ß) was detected by western blotting, and glycogen synthase (GS) mRNA levels were detected by reverse transcription-quantitative polymerase chain reaction. Compared with the control group, the body weight, Lee's index, AUC of the intraperitoneal glucose tolerance test and intraperitoneal insulin tolerance test, levels of FPG, FINS, TG, TC, FFA, ALT and AST, and HOMA index values were significantly increased in the obese rats. The body weight, levels of FPG and FINS, and the HOMA index were significantly reduced following octreotide treatment, whereas the decrease in Lee's index, the blood levels of ALT, AST, TC, TG and FFA, and the AUC did not reach statistical significance. Hepatic TG and FFA levels were significantly increased and hepatic glycogen content was significantly decreased in rats with HFD-induced obesity when compared with those in the control group. Octreotide intervention restored these alterations. The expression levels of phosphorylated Akt and GSK3ß protein expression, as well as GS mRNA levels in the HFD group were lower when compared with those in the control group, whereas octreotide treatment reversed these reductions. The in vitro experiments demonstrated that the reduced levels of phosphorylated Akt and GSK3ß protein, and GS mRNA in the PA-treated group were significantly reversed by octreotide treatment. In conclusion, the results indicate that octreotide improved hepatic glycogenesis and decreased FPG concentration in rats with HFD-induced obesity. These mechanisms may be associated with increased GS activity via the promotion of GSK3ß phosphorylation. Therefore, octreotide may be regarded as a novel therapeutic strategy for HFD-induced obesity and obesity-associated metabolic disorders. [ABSTRACT FROM AUTHOR]

Copper-transporting ATPase 2 (ATP7B) is essential for mammalian copper homeostasis. Mutations in ATP7B result in copper accumulation, especially in the liver, and cause Wilson disease (WD). The major role of hepatocytes in WD pathology is firmly established. It is less certain whether the excess Cu in hepatocytes is solely responsible for development of WD. To address this issue, we generated a mouse strain for Cre-mediated deletion of Atp7b and inactivated Atp7b selectively in hepatocytes. Atp7bΔHep mice accumulate copper in the liver, have elevated urinary copper, and lack holoceruloplasmin but show no liver disease for up to 30 wk. Liver inflammation is muted and markedly delayed compared with the age-matched Atp7b-/- null mice, which show a strong type1 inflammatory response. Expression of metallothioneins is higher in Atp7bΔHep livers than in Atp7b-/- mice, suggesting better sequestration of excess copper. Characterization of purified cell populations also revealed that nonparenchymal cells in Atp7bΔHep liver maintain Atp7b expression, have normal copper balance, and remain largely quiescent. The lack of inflammation unmasked metabolic consequences of copper misbalance in hepatocytes. Atp7bΔHep animals weigh more than controls and have higher levels of liver triglycerides and 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase. By 45 wk, all animals develop liver steatosis on a regular diet. Thus copper misbalance in hepatocytes dysregulates lipid metabolism, whereas development of inflammatory response in WD may depend on copper status of nonparenchymal cells. The implications of these findings for the cell-targeting WD therapies are discussed. NEW & NOTEWORTHY Targeted inactivation of copper-transporting ATPase 2 (Atp7b) in hepatocytes causes steatosis in the absence of inflammation. [ABSTRACT FROM AUTHOR]

Background: The etiology of obesity-related cardiac dysfunction (ORCD) is linked to metabolic syndrome in people. Studies have indicated that obese dogs have components of metabolic syndrome, warranting evaluation for ORCD in obese dogs. Objectives: To evaluate cardiac structure and function and metabolic variables in obese dogs compared to ideal weight dogs. Animals: Forty-six healthy, small-breed (<25 pounds), obese dogs (n = 29) compared to ideal weight dogs (n = 17). Methods: A cross-sectional study of cardiac structure and function by standard and strain echocardiographic measurements and quantification of serum metabolic variables (insulin:glucose ratios, lipid analysis, adiponectin, inflammatory markers). Results: Compared to the ideal weight controls, obese dogs had cardiac changes characterized by an increased interventricular septal width in diastole to left ventricular internal dimension in diastole ratio, decreased ratios of peak early to peak late left ventricular inflow velocities, and ratios of peak early to peak late mitral annular tissue velocities, and increased fractional shortening and ejection fraction percentages. The left ventricular posterior wall width in diastole to left ventricular internal dimension in diastole ratios were not significantly different between groups. Systolic blood pressure was not significantly different between groups. Obese dogs had metabolic derangements characterized by increased insulin:glucose ratios, dyslipidemias with increased cholesterol, triglyceride, and high-density lipoprotein concentrations, decreased adiponectin concentrations, and increased concentrations of interleukin 8 and keratinocyte-derived chemokine-like inflammatory cytokines. Conclusions and Clinical Importance: Compared to ideal weight controls, obese dogs have alterations in cardiac structure and function as well as insulin resistance, dyslipidemia, hypoadiponectinemia, and increased concentrations of inflammatory markers. These findings warrant additional studies to investigate inflammation, dyslipidemia, and possibly systemic hypertension as potential contributing factors for altered cardiac function. [ABSTRACT FROM AUTHOR]

Key points α-linolenic acid (ALA) and exercise training both attenuate hyperlipidaemia-related cardiovascular derangements, however, there is a paucity of information pertaining to their mechanisms of action when combined., We investigated both the independent and combined effects of exercise training and ALA consumption in obese Zucker rats, aiming to determine the potential for additive improvements in cardiovascular function., ALA and exercise training independently improved cardiac output, end-diastolic volume, left ventricular fibrosis and mean blood pressure following a 4 week intervention., Combining ALA and endurance exercise yielded greater improvements in these parameters, independent of changes in markers of oxidative stress or endogenous anti-oxidants., We postulate that divergent mechanisms of action may explain these changes: ALA increases peripheral vasodilation, and exercise training stimulates angiogenesis., Abstract Although α-linolenic acid (ALA) and endurance exercise training independently attenuate hyperlipidaemia-related cardiovascular derangements, there is a paucity of information pertaining to their mechanisms of action and efficacy when combined as a preventative therapeutic approach. Therefore, we used obese Zucker rats to investigate the independent and combined effects of these interventions on cardiovascular disease. Specifically, animals were randomly assigned to one of the following groups: control diet-sedentary, ALA supplemented-sedentary, control diet-exercise trained or ALA supplemented-exercise trained. Following a 4 week intervention, although the independent and combined effects of ALA and exercise reduced ( P < 0.05) the serum free/esterified cholesterol ratio, only the ALA supplemented-exercise trained animals displayed a reduction in the content of both serum free and esterified cholesterol. Moreover, although ALA and endurance training individually increased cardiac output, stroke volume and end-diastolic volume, as well as reduced left ventricle fibrosis, mean blood pressure and total peripheral resistance, these responses were all greater following the combined intervention (ALA supplemented-exercise trained). These effects occurred independent of changes in oxidative phosphorylation proteins, markers of oxidative stress or endogenous anti-oxidant capacity. We propose that the beneficial effects of a combined intervention occur as a result of divergent mechanisms of action elicited by ALA and endurance exercise because only exercise training increased the capillary content in the left ventricle and skeletal muscle, and tended to decrease protein carbonylation in the left ventricle ( P = 0.06). Taken together, our data indicate that combining ALA and endurance exercise provides additional improvements in cardiovascular disease risk reduction compared to singular interventions in the obese Zucker rat. [ABSTRACT FROM AUTHOR]

This research provides a cautionary example when evaluating changes in behavioral end points with respect to postulated pharmacologic activity. Various small molecule substrate mimetic protein tyrosine phosphatase 1B (PTP1B) inhibitors were investigated as pharmacologic agents for decreasing food consumption using intranasal (IN) dosing as a means for direct nose-to-brain delivery along the olfactory/trigeminal nerve pathways. Although food consumption was decreased in diet-induced obese (DIO) mice, nasal discharge was observed. Studies were conducted to investigate local effects on the nasal airway and to develop structure–activity relationships. Intranasal administration of PTP1B inhibitors at ≥0.03 mg/d to DIO mice produced dose-dependent injury to various cell types of the nasal epithelia. Protein tyrosine phosphatase 1B inhibitors with calculated log octanol >3.0 were the most toxic. Whereas a pharmacologically inactive analog of a PTP1B inhibitor produced nasal injury, along with decreased food consumption, the marketed IN drug ketorolac produced no lesions at the same dose of 0.3 mg/d and only minor changes at 3 mg/d. Rat skin fibroblast cells were exposed in vitro to PTP1B inhibitors, ketorolac, paraquat, and the detergent sodium dodecylbenzene sulfonate (NDS) followed by measures of cytotoxicity. The most potent PTP1B inhibitors were similar to NDS, whereas ketorolac was the least toxic compound. Cytotoxic potency in vitro was similar to in vivo. In conclusion, PTP1B inhibitors injured nasal epithelium through a mechanism independent of PTP1B inhibition and likely due to nonspecific cytotoxicity such as disruption of the cell membrane. Decreased food consumption in DIO mice was due to toxicity rather than a pharmacologic mode of action. [ABSTRACT FROM AUTHOR]

The C57BL/6J-Daruma mouse is an animal model of obesity derived from the original genetically obese ICR-Daruma mouse by transfer of the phenotype into the C57BL/6J background by backcrossing into the C57BL/6J strain. Although, like the original ICR-Daruma mouse model, both male and female C57BL/6J-Daruma mice develop obesity, the latter strain shows sex differences in several phenotypes. A sex difference in plasma insulin levels was especially notable in C57BL/6J-Daruma mice; only males showed hyperinsulinemia. Orchiectomy suppressed this hyperinsulinemia completely, whereas testosterone supplementation restored it. Glucose administration increased the plasma glucose level in both male and female Daruma mice to a greater extent than in wild-type control mice. Orchiectomy, but not ovariectomy, decreased the plasma glucose level to that seen in wild-type controls. On the other hand, this effect of orchiectomy was abrogated by testosterone supplementation. The expression of mRNAs for several genes related to insulin resistance was significantly changed in white adipose tissue and liver of C57BL/6J-Daruma mice, especially males, as early as 4 weeks of age. The present results suggest that testosterone may be involved in the hyperinsulinemia shown by male C57BL/6J-Daruma mice and that this strain may be an appropriate animal model for examining the relationship between obesity and sex hormones. [ABSTRACT FROM AUTHOR]

Background: The existence of a genetic predisposition to obesity is commonly recognized in humans and rodents. Recently, a link between genetics and overweight was shown in cats. The goal of this study was to identify the effect of diet composition on plasma levels of glucose, insulin, free fatty acids and triglycerides in cats receiving different diets (high-carbohydrate, high-fat and high-protein diets). Results: Insulin and leptin concentrations were significantly correlated with phenotype. Insulin levels were lower, whereas leptin levels were higher in cats predisposed to overweight. The other blood parameters were not correlated with phenotype. Intake of the high-carbohydrate diet resulted in higher insulin concentrations compared with the two other diets. Insulin levels were within the values described for non-obese cats in previous studies. Conclusions: There was no difference in metabolic response between the two groups. As the high-carbohydrate diet led to the highest insulin blood concentrations, it might be useful to avoid such diets in cats predisposed to overweight. In addition, even cats with genetically linked obesity can regain insulin sensitivity after weight loss. [ABSTRACT FROM AUTHOR]

The obesity and its comorbidities, including resistance to leptin, impacts the reproductive function. Testes express leptin receptors in the germ cells and Leydig cells. Then, leptin-deficient animals are obese and infertile. We aimed to evaluate the structure and steroidogenic pathway of the testis of deficient leptin mice. Three months old male C57BL/6 mice (wild-type, WT) and deficient leptin ( ob/ob ) mice had their testes dissected and prepared for analyses. Compared to the WT group, the ob/ob group showed a greater body mass with smaller testes, and alterations in the germinative epithelium: fewer spermatogonia, spermatocytes, and spermatids. The Sertoli cells and the germ cells showed condensed nuclei and nuclear fragmentation indicating cell death, in agreement with a low expression of the proliferating cell nuclear antigen and a high expression of Caspase3. In the ob/ob group, the sperm was absent in the seminiferous tubules, and the steroidogenic pathway was compromised (low 3Beta hydroxysteroid dehydrogenase and steroidogenic acute regulatory protein). Further, all hormone receptors involved in the testicular function were down expressed (androgen, estrogen, follicle-stimulating, luteinizing, aromatase, and nicotinamide adenine dinucleotide phosphate). In conclusion, the findings indicate significant morphological, hormonal and enzymatic changes in the testis of the ob/ob mice. The shifts in the enzymatic steroidogenic pathway and the enzymes related to spermatic activity support the insights about the failures in the fertility of these animals. The study provides new evidence and contributes to the understanding of how the lack of leptin and obesity might negatively modulate the testicular function leading to infertility. [ABSTRACT FROM AUTHOR]

α-Linolenic acid (ALA) supplementation or exercise training can independently prevent hepatic lipid accumulation and reduced insulin signaling; however, this may occur through different mechanisms of action. In the current study, obese Zucker rats displayed decreased phospholipid (PL) content in association with hepatic lipid abundance, and therefore, we examined whether ALA and exercise training would prevent these abnormalities differently to reveal additive effects on the liver. To achieve this aim, obese Zucker rats were fed control diet alone or supplemented with ALA and were sedentary or exercise trained for 4 wk (C-Sed, ALA-Sed, C-Ex, and ALA-Ex). ALA-Sed rats had increased microsomal-triglyceride transfer protein (MTTP), a protein required for lipoprotein assembly/secretion, as well as modestly increased PL content in the absence of improvements in mitochondrial content, lipid accumulation, or insulin sensitivity. In contrast, C-Ex rats had increased mitochondrial content and insulin sensitivity; however, this corresponded with minimal improvements in PL content and hepatic lipid accumulation. Importantly, ALA-Ex rats demonstrated additive improvements in PL content and hepatic steatosis, which corresponded with increased mitochondrial content, MTTP and apolipoprotein B100 content, greater serum triacylglyceride, and insulin sensitivity. Overall, these data demonstrate additive effects of ALA and exercise training on hepatic lipid accumulation, as exercise training preferentially increased mitochondrial content, while ALA promoted an environment conducive for lipid secretion. These data highlight the potential for combination therapy to mitigate liver disease progression. [ABSTRACT FROM AUTHOR]

Background Obesity is a global disease, affecting nearly half a billion people. Unfortunately, this trend is mirrored in our canine population. Objectives As obesity is a complex inflammatory disease, there is a need to determine whether routine medical screening tests may indicate, or be influenced by, its presence. The objective of the current study was to determine if significant differences exist between CBC and biochemical profile values from control vs overweight/obese, client-owned dogs considered clinically healthy. Methods Dogs presented for routine health examinations, including minor dental or elective surgical procedures, were retrospectively identified from a hospital population. Animals were allocated to 2 categories based on body condition score (BCS), and data were analyzed by Mann-Whitney nonparametric analysis with statistical significance at a P ≤ .05. Results After exclusions, 116 dogs were assigned to the overweight/obese group (BCS ≥ 7) and 240 dogs to the control group (BCS = 4-6). Overweight/obese dogs had higher total leukocyte counts and higher plasma protein and globulin concentrations. Other differences were attributed to decreased serum water fraction (increased sodium, albumin, calcium, and anion gap) in the overweight/obese group. Interestingly, chloride concentration was decreased (in the face of increased sodium) in the obese group. Conclusions There is CBC and biochemical evidence to support the concern that obesity influences laboratory values, even in dogs considered clinically healthy. Prospective studies aimed at characterizing these changes are needed to provide insight into the connection between obesity and its comorbidities. [ABSTRACT FROM AUTHOR]

Objective: Obesity is a contributing factor to insulin resistance and type 2 diabetes. The aim of this study was to study the therapeutic potential of intestinal electrical stimulation (IES) for obesity and associated glucose intolerance and insulin resistance in diet-induced obesity (DIO) rats.Methods: DIO rats were divided into two groups to receive sham or IES for 8 weeks. Oral glucose tolerance and insulin tolerance tests were performed. Gastric emptying and small bowel transit tests were performed. Blood samples were collected for the analysis of insulin and free fatty acid (FFA).Results: Chronic IES reduced food intake and body weight and decreased the adiposity index in DIO rats. Compared with chow-fed rats, DIO rats had an elevated fasting plasma glucose level, impaired glucose tolerance, and impaired insulin sensitivity, which were improved after chronic IES. FFA was elevated in DIO rats and suppressed with IES. Chronic IES delayed gastric emptying but accelerated small bowel transit.Conclusions: IES reduces food intake and body weight and improves glucose tolerance and insulin resistance in DIO rats. The ameliorating effect on glycemic control may be due to the weight loss and suppression of plasma FFA. Other mechanisms such as the modulation of gastrointestinal transit may also be involved. [ABSTRACT FROM AUTHOR]

The goal of this study is to quantify the impact of the in vivo photochemical treatment of rats with obesity using indocyanine green (ICG) dissolved in saline or dispersed in an encapsulated form at NIR laser irradiation, which was monitored by tissue sampling and histochemistry. The subcutaneous injection of the ICG solution or ICG encapsulated into polyelectrolyte microcapsules, followed by diode laser irradiation (808 nm, 8 W/cm², 1 min), resulted in substantial differences in lipolysis of subcutaneous fat. Most of the morphology alterations occurred in response to the laser irradiation if a free-ICG solution had been injected. In such conditions, membrane disruption, stretching, and even delamination in some cases were observed for a number of cells. The encapsulated ICG aroused similar morphology changes but with weakly expressed adipocyte destruction under the laser irradiation. The Cochran Q test rendered the difference between the treatment alternatives statistically significant. By this means, laser treatment using the encapsulated form of ICG seems more promising and could be used for safe layerwise laser treatment of obesity and cellulite. [ABSTRACT FROM AUTHOR]

The uneven development of adipose tissues reflects a differential occurrence of biological events in vivo while the underlying molecular mechanism remains largely unknown. In the present study, the in vivo inflammatory status of an inbred obese porcine model, Lantang pig, was assessed, aiming to provide evidence for obesity biology. Compared with genetically lean pigs (crossbred, Duroc x Landrace x Large White), Lantang pigs exhibited a larger amount of ultra large adipocytes in subcutaneous adipose tissue accompanied with higher expression of macrophage/monocytes markers and pro-inflammatory genes (TLR4, CD14, CD11β, MCP1, TNFα, IL1β and IL6) and lower expression of cellular antioxidant enzymes (SOD1, 2 and 3). Plasma concentrations of LPS and TNF-α were also higher in Lantang pigs than in lean pigs. Among adipose tissues of Lantang pigs, the subcutaneous tissue had the most abundant expression of inflammation related genes (TLR4, CD14, TNFα and IL6) and the lowest level of cellular antioxidant genes (SOD 1 and 2), while the perirenal adipose tissue had opposite profile. Significant activation of p38 MAPK pathway was indicated by increased phosphorylation of p38 in the subcutaneous adipose tissue of Lantang pigs. Collectively, the bacteria-derived LPS induced inflammation-associated oxidative stress indeed exists in adipose tissues of Lantang pig, and the differential expressions of inflammatory and antioxidant genes, to some extent, account for the uneven development of the adipose tissue within bodies. [ABSTRACT FROM AUTHOR]

Summary This article reviews the biology, prevalence and risks for obesity in people and companion dogs and cats, and explores the links between obesity and diabetes mellitus and cancer across these species. Obesity is a major healthcare problem in both human and veterinary medicine and there is an increasing prevalence of obesity in people and pets. In people and animals, obesity is a complex disorder involving diet, level of physical activity, behavioural factors, socioeconomic factors, environment exposures, genetics, metabolism and the microbiome. Pets and people share a number of obesity-related comorbidities. Obesity is a major risk factor for type 2 diabetes mellitus in people and in cats, but this association is not recognized in dogs. Obesity is a recognized risk factor for a number of human cancers, but there are fewer data available describing this association with canine neoplastic disease. One approach to addressing the problem of obesity is by taking a ‘One Health’ perspective. Comparative clinical research examining shared lifestyle and environmental risk factors and the reasons underlying species differences should provide new perspectives on the fundamental biology of obesity. One Health programmes involving human healthcare professionals and veterinarians could help address obesity with simple interventions at the community level. [ABSTRACT FROM AUTHOR]

Summary Despite the high prevalence of overweight and obesity in the human and companion animal populations, and the global trends for increasing numbers of affected people and pets, there are few successful interventions that are proven to combat this complex multifactorial problem. One key strategy involves effective communication between human and veterinary healthcare professionals with patients and clients about obesity. In human healthcare, the focus of communication should be on physical activity as part of overall health and wellbeing, rather than assessment of the body mass index; clinical examination of patients should record levels of physical activity as a key ‘vital sign’ as part of their assessment. Successful weight loss programmes for companion animals also involves strategic communication with the entire healthcare team leading clients through the ‘stages of change’. There is great potential in employing a ‘One Health’ framework to provide novel solutions for the prevention and treatment of this condition in people and their pets. Comparative clinical research into the biology of obesity and its comorbidities in dogs and cats is likely to lead to knowledge relevant to the equivalent human conditions. The advantages of companion animal clinical research over traditional rodent models include the outbred genetic background and relatively long lifespan of pets and the fact that they share the human domestic environment. The human–companion animal bond can be leveraged to create successful programmes that promote physical activity in people and their pets with obesity. Dog walking is a proven motivator for human physical activity, with health benefits to both the owner and the dog. Realizing the potential of a One Health approach will require the efforts and leadership of a committed group of like-minded individuals representing a range of scientific and medical disciplines. Interested parties will need the means and opportunities to communicate and to collaborate, including having the resources and funding for research. One Health proponents must have a role in forming public policy related to the prevention and management of overweight and obesity. [ABSTRACT FROM AUTHOR]

Summary People who are overweight or have obesity are estimated to comprise 30% of the global population and up to 59% of companion dogs and cats are estimated to be above their optimal body weight. The prevalence of human and companion obesity is increasing. The direct and indirect costs of obesity and associated comorbidities are significant for human and veterinary healthcare. There are numerous similarities between obesity in people and companion animals, likely related to the shared environmental and lifestyle elements of this multifactorial disease. While the study of human obesity is relatively robust, research conducted in pets is generally limited to small studies, studies with cross-sectional designs or reports that have yet to be replicated. Greater understanding of human obesity may elucidate some of the factors driving the more recent rise in pet obesity. In particular, there are overlapping features of obesity in children and pets that are, in part, related to dependency on their ‘parents’ for care and feeding. When feeding is used in a coercive and controlling fashion, it may lead to undesirable feeding behaviour and increase the risk for obesity. A ‘responsive parenting’ intervention teaches parents to respond appropriately to hunger–satiety cues and to recognize and respond to others' distress. Such interventions may impact on childhood overweight and obesity and have the potential to be adapted for use with companion animals. Social behaviour towards people with obesity or owners of pets with obesity is often driven by beliefs about the cause of the obesity. Educating healthcare professionals and the public about the multifactorial nature of this complex disease process is a fundamental step in reducing the bias and stigma associated with obesity. Children living in low-income households have particularly high rates of obesity and as household income falls, rates of obesity also rise in pets and their owners. There are risk regulators (i.e. dynamic components of interconnected systems that influence obesity-related behaviours) and internal factors (i.e. biological determinants of obesity) that may influence the development of both childhood and pet obesity, and poverty may intersect with these variables to exacerbate obesity in low-income environments. This review discusses the costs, behaviours and psychology related to obesity in people and pets, and also proposes potential techniques that can be considered for prevention and treatment of this disease in pets. A ‘One Health’ approach to obesity suggests that an understanding of human obesity may elucidate some of the factors driving the more recent rise in pet obesity. [ABSTRACT FROM AUTHOR]

Background: The risks during early growth on becoming overweight in adulthood are widely studied in humans. However, early-life predictive factors for canine adult overweight and obesity have not yet been studied. To identify factors that may help explain the development of overweight and obesity at adulthood in dogs, a longitudinal study of 2 years was conducted in 24 female Beagle dogs of the same age, sexual status, and raised under identical environmental conditions. By means of a hierarchical classification on principal components with the following quantitative values: fat-free mass (FFM), percentage fat mass and pelvic circumference at 2 years of age, three groups of dogs were established and were nominally named: ideal weight (IW, n = 9), slightly overweight (OW1, n = 6) and overweight (OW2, n = 9). With the aim of identifying predictive factors of development of obesity at adulthood parental characteristics, growth pattern, energy balance and plasma factors were analysed by logistic regression analysis. Results: At 24 months, the group compositions were in line with the body condition scores (BCS 1-9) values of the IW (5 or 6/9), the OW1 (6/9) and the OW2 (7 or 8/9) groups. Logistic regression analysis permitted the identification of neonatal growth rate during the first 2 weeks of life (GR2W) and BCS at 7 months as predictors for the development of obesity at adulthood. Seventy percent of dogs with either GR2W >125% or with BCS > 6/9 at 7 months belonged to the OW2 group. Results from energy intake and expenditure, corrected for FFM, showed that there was a greater positive energy imbalance between 7 and 10 months for the OW2, compared to the IW group. Conclusion: This study expands the understanding of previously reported risk factors for being overweight or obese in dogs, establishing that (i) 15 out of 24 of the studied dogs became overweight and (ii) GR2W and BCS at 7 months of age could be used as predictive factors as overweight adult dogs in the OW2 group had higher values compared the other groups of dogs. [ABSTRACT FROM AUTHOR]

Eared grebes Podiceps nigricollis, like shorebirds and other long-distance migrants, lay down large amounts of fat to power their journeys. To investigate the pattern of how fat and soft tissue might be mobilized, we used grebes killed in migration and applied computed tomography to reconstruct how stores in the chest, thorax, and abdomen were reduced as body weight decreased. Fat and soft tissue were each mobilized at a constant rate through the entire migration. Fat stores in birds embarking on migration were greater in the abdomen than thorax than chest. In contrast to previous studies indicating that abdominal fat was mobilized first, we found that fat from all areas was mobilized concurrently, but that abdominal fat was catabolized at a greater rate. We suggest why this pattern might be advantageous, consider whether inter-depot differences in fat composition might be involved, and note possible energetic consequences. Whether our findings pertain to other obese or long distance migrants remains to be determined. [ABSTRACT FROM AUTHOR]

The objective of this study was to develop a proof of concept for using off-the-shelf Red Green Blue-Depth (RGB-D) Microsoft Kinect cameras to objectively assess P8 rump fat (P8 fat; mm) and muscle score (MS) traits in Angus cows and steers. Data from low and high muscled cattle (156 cows and 79 steers) were collected at multiple locations and time points. The following steps were required for the 3-dimensional (3D) image data and subsequent machine learning techniques to learn the traits: 1) reduce the high dimensionality of the point cloud data by extracting features from the input signals to produce a compact and representative feature vector, 2) perform global optimization of the signatures using machine learning algorithms and a parallel genetic algorithm, and 3) train a sensor model using regression-supervised learning techniques on the ultrasound P8 fat and the classified learning techniques for the assessed MS for each animal in the data set. The correlation of estimating hip height (cm) between visually measured and assessed 3D data from RGB-D cameras on cows and steers was 0.75 and 0.90, respectively. The supervised machine learning and global optimization approach correctly classified MS (mean [SD]) 80 (4.7) and 83% [6.6%] for cows and steers, respectively. Kappa tests of MS were 0.74 and 0.79 in cows and steers, respectively, indicating substantial agreement between visual assessment and the learning approaches of RGB-D camera images. A stratified 10-fold cross-validation for P8 fat did not find any differences in the mean bias (P = 0.62 and P = 0.42 for cows and steers, respectively). The root mean square error of P8 fat was 1.54 and 1.00 mm for cows and steers, respectively. Additional data is required to strengthen the capacity of machine learning to estimate measured P8 fat and assessed MS. Data sets for Bos indicus and continental cattle are also required to broaden the use of 3D cameras to assess cattle. The results demonstrate the importance of capturing curvature as a form of representing body shape. A data-driven model from shape to trait has established a proof of concept using optimized machine learning techniques to assess P8 fat and MS in Angus cows and steers. [ABSTRACT FROM AUTHOR]

Many organisms exhibit compensatory growth ( CG), an accelerated growth rate during recovery from periods of low nutrient resources. Despite numerous studies, many aspects of CG, particularly fine-scale temporal effects early in life, remain poorly understood. We manipulated early-life feeding regimens in threespine stickleback ( Gasterosteus aculeatus) to study compensatory responses in growth rate and lipid storage during the first growing season. Laboratory-reared stickleback, including ancestral oceanic and derived freshwater populations, were divided into three age-specific dietary treatment groups - DPR1, DPR2 and DPR3 - which were exposed to a half-ration nutrient deprivation for 30 days at the onset of 2, 3 and 4 months of age, respectively. We hypothesised that these month-long periods of nutrient deprivation would result in strong, yet variable CG responses across stickleback populations and dietary treatments following a return to optimal ration levels. The youngest two age classes of fish ( DPR1 &and DPR2) exhibited strong CG responses, matching growth rates and lipid generation levels seen in control fish fed an ad libitum diet. The oldest nutrient-deprived group ( DPR3) showed a reduced CG response, with body growth recovering only partially, and lipid levels exhibiting even less recovery. Our results demonstrate that compensatory growth responses in juvenile stickleback depend on the timing of deprivation during the first growing season and further that responses to late-season deprivation have favoured development of a larger body frame entering the overwintering season over lipid regeneration. [ABSTRACT FROM AUTHOR]

Background: Obese individuals differ in their risk of developing metabolic and cardiovascular complications depending on fat distribution (subcutaneous versus visceral) and adipose tissue (AT) phenotype (hyperplasic versus hypertrophic). However, the exact mechanisms which determine whether an obese individual is metabolically healthy or unhealthy are not clear, and analyses of the underlying pathomechanisms are limited by the lack of suitable in vivo models in which metabolically healthy versus metabolically unhealthy AT accumulation can be specifically induced. In the current study, we aimed to establish a protocol for the use of zebrafish as a model for obesity-related metabolically healthy versus metabolically unhealthy AT accumulation. Methods: We overfed adult male zebrafish of the AB strain with normal fat diet (NFD) or high fat diet (HFD) for 8 weeks and compared parameters related to obesity, i.e. body weight, body mass index, condition index and body fat percentage, to control zebrafish fed under physiological conditions. In addition, we investigated the presence of early obesity-related metabolic alterations by quantifying blood glucose levels, plasma triglyceride and cholesterol levels, and by assessing ectopic lipid accumulation in the liver of zebrafish. Finally, we determined gene expression levels of marker genes related to lipid metabolism, inflammation and fibrosis in visceral AT and liver. Results: We show that 8-weeks overfeeding with either NFD or HFD leads to a significant increase in body weight and AT mass compared to controls. In contrast to NFD-overfed zebrafish, HFD-overfed zebrafish additionally present metabolic alterations, e.g. hyperglycemia and ectopic lipid accumulation in the liver, and a metabolically unhealthy AT phenotype with adipocyte hypertrophy especially in the visceral AT depot, which is accompanied by changes in the expression of marker genes for lipid metabolism, inflammation and fibrosis. Conclusions: In summary, we have established a method for the specific induction of metabolically distinct obesity phenotypes in zebrafish. Our results indicate that zebrafish represents an attractive model to study regulatory mechanisms involved in the determination of AT phenotype during development of metabolically healthy versus metabolically unhealthy obesity. [ABSTRACT FROM AUTHOR]

Background Diabetes mellitus (DM) in dogs is a common endocrinopathy with a complex genetic architecture. Disease susceptibility in several breeds is associated with polymorphisms in immune response genes, but in the Labrador retriever breed, no genetic associations with DM have been identified. A deletion in the pro-opiomelanocortin ( POMC) gene in Labrador retrievers is associated with increased appetite and risk of obesity. Hypothesis/Objectives To characterize the POMC deletion in Labrador retrievers, to develop a simple genetic test for this mutation, and to test the hypothesis that the POMC gene deletion is associated with an increased risk of DM in this breed. Animals Sixty-one non-diabetic Labrador retrievers aged >6 years and 57 Labrador retrievers with DM. Methods Case-control genotyping study to compare the frequency of the POMC deletion in dogs with and without DM. After polymerase chain reaction (PCR) and sequencing to characterize the mutation, a PCR-based test was developed and validated using 2 different restriction fragment length polymorphism assays. Results A 14-base-pair deletion was confirmed and localized to exon 3 of the canine POMC gene. A PCR-based test for the deletion was successfully developed. There was no association between the presence of the POMC deletion mutation and DM in this population of Labrador retriever dogs ( P = .31). Conclusions and Clinical Importance This study adds to the existing scientific literature indicating that there is little evidence for a direct link between obesity and DM in dogs. [ABSTRACT FROM AUTHOR]

Despite the increasing interest in insect-based bioactive products, the biological activities of these products are rarely studied adequately. Larvae of Tenebrio molitor, the yellow mealworm, have been eaten as a traditional food and provide many health benefits. Therefore, we hypothesized that T. molitor larvae might influence adipogenesis and obesity-related disorders. In the present study, we investigated the anti-adipogenic and antiobesity effects of T. molitor larvae in vitro and in vivo. The lipid accumulation and triglyceride content in mature adipocytes was reduced significantly (up to 90%) upon exposure to an ethanol extract of T. molitor larvae, without a reduction in cell viability. Exposure also resulted in key adipogenic and lipogenic transcription factors. Additionally, in adipogenic differentiation medium the extract induced phosphorylation of adenosine monophosphate (AMP)-activated protein kinase and mitogen-activated protein kinases. Daily oral administration of T. molitor larvae powder to obese mice fed high-fat diet attenuated body weight gain. We also found that the powder efficiently reduced hepatic steatosis as well as aspartate and alanine transaminase enzyme levels in mice fed a high-fat diet. Our results suggest that T. molitor larvae extract has an antiobesity effect when administered as a food supplement and has potential as a therapeutic agent for obesity. [ABSTRACT FROM AUTHOR]

Key points Maternal high-fat diet impairs brown adipocyte function and correlates with obesity in offspring., Maternal resveratrol administration recovers metabolic activity of offspring brown adipose tissue., Maternal resveratrol promotes beige adipocyte development in offspring white adipose tissue., Maternal resveratrol intervention protects offspring against high-fat diet-induced obesity., Abstract Promoting beige/brite adipogenesis and thermogenic activity is considered as a promising therapeutic approach to reduce obesity and metabolic syndrome. Maternal obesity impairs offspring brown adipocyte function and correlates with obesity in offspring. We previously found that dietary resveratrol (RES) induces beige adipocyte formation in adult mice. Here, we evaluated further the effect of resveratrol supplementation of pregnant mice on offspring thermogenesis and energy expenditure. Female C57BL/6 J mice were fed a control diet (CON) or a high-fat diet (HFD) with or without 0.2% (w/w) RES during pregnancy and lactation. Male offspring were weaned onto a HFD and maintained on this diet for 11 weeks. The offspring thermogenesis and related regulatory factors in adipose tissue were evaluated. At weaning, HFD offspring had lower thermogenesis in brown and white adipose tissues compared with CON offspring, which was recovered by maternal RES supplementation, along with the appearance of multilocular brown/beige adipocytes and elevated thermogenic gene expression. Adult offspring of RES-treated mothers showed increased energy expenditure and insulin sensitivity when on an obesogenic diet compared with HFD offspring. The elevated metabolic activity was correlated with enhanced brown adipose function and white adipose tissue browning in HFD+RES compared with HFD offspring. In conclusion, RES supplementation of HFD-fed dams during pregnancy and lactation promoted white adipose browning and thermogenesis in offspring at weaning accompanied by persistent beneficial effects in protecting against HFD-induced obesity and metabolic disorders. [ABSTRACT FROM AUTHOR]

Obesity is one of the most prevalent metabolic diseases in the Western world and correlates directly with insulin resistance, which may ultimately culminate in type 2 diabetes (T2D). We sought to ascertain whether the human metalloproteinase A Disintegrin and Metalloproteinase 19 (ADAM19) correlates with parameters of the metabolic syndrome in humans and mice. To determine the potential novel role of ADAM19 in the metabolic syndrome, we first conducted microarray studies on peripheral blood mononuclear cells from a well-characterised human cohort. Secondly, we examined the expression of ADAM19 in liver and gonadal white adipose tissue using an in vivo diet induced obesity mouse model. Finally, we investigated the effect of neutralising ADAM19 on diet induced weight gain, insulin resistance in vivo, and liver TNF-α levels. Significantly, we show that, in humans, ADAM19 strongly correlates with parameters of the metabolic syndrome, particularly BMI, relative fat, HOMA-IR, and triglycerides. Furthermore, we identified that ADAM19 expression was markedly increased in the liver and gonadal white adipose tissue of obese and T2D mice. Excitingly, we demonstrate in our diet induced obesity mouse model that neutralising ADAM19 therapy results in weight loss, improves insulin sensitivity, and reduces liver TNF-α levels. Our novel data suggest that ADAM19 is pro-obesogenic and enhances insulin resistance. Therefore, neutralisation of ADAM19 may be a potential therapeutic approach to treat obesity and T2D. [ABSTRACT FROM AUTHOR]

Feeding behavior shows a rhythmic daily pattern, which in nocturnal rodents is observed mainly during the dark period. This rhythmicity is under the influence of the hypothalamic suprachiasmatic nucleus (SCN), the main biological clock. Nevertheless, various studies have shown that in rodent models of obesity, using high-energy diets, the general locomotor activity and feeding rhythms can be disrupted. Here, we review the data on the effects of diet-induced obesity (DIO) on locomotor activity and feeding patterns, as well as the effect on the brain sites within the neural circuitry involved in metabolic and rewarding feeding behavior. In general, DIO may alter locomotor activity by decreasing total activity. On the other hand, DIO largely alters eating patterns, producing increased overall ingestion and number of eating bouts that can extend to the resting period. Furthermore, within the hypothalamic areas, little effect has been reported on the molecular circadian mechanism in DIO animals with ad libitum hypercaloric diets and little or no data exist so far on its effects on the reward system areas. We further discuss the possibility of an uncoupling of metabolic and reward systems in DIO and highlight a gap of circadian and metabolic research that may help to better understand the implications of obesity. [ABSTRACT FROM AUTHOR]

It has been clearly demonstrated that the maternal nutritional status during pregnancy and lactation has long-term effects on offspring health. In mammals, milk represents the first maternal support provided to the newborns so that its composition may play a major role in long-term programming. We therefore assessed the effects of maternal high-fat/ high-sugar obesogenic (OD) or control (CD) diets on offspring growth and adiposity in the rabbit. Between 7 and 20 wk of age, the BW gain of OD milk-fed rabbits was higher than that of CD milk-fed rabbits (P < 0.05). Body fat mass measurements at 21 wk of age revealed a significant increase in body adiposity as a function of milk ingested during the neonatal period, in both female and male offspring (P < 0.05). A marked weight gain difference was observed according to the milk in both female and male offspring. Moreover, we investigated the composition in major proteins and leptin levels in milk from OD or CD diet-fed dams. Liquid chromatography-mass spectrometry analysis of individual CD skimmed milk samples enabled identification and quantification of the rabbit main milk proteins and of their main phosphorylated isoforms at 2 different stages of lactation (3 and 10 d). Here we show that the OD diet induced a reduction in the whey acidic protein content concomitantly with both an increase in serum albumin and lactoferrin contents and in the phosphorylated isoforms of the main milk proteins. Furthermore, a sharp rise in leptin levels was observed in the milk of OD diet-fed dams on Day 10 of lactation when compared with CD diet animals (P < 0.05). Taken together, these findings provide evidence that lactation is a critical window of development during which exposure to a deleterious diet is highly detrimental to long-term outcomes. Moreover, these insights suggest that it may be possible to prevent at least some of the adverse effects of inadequate maternal nutrition on the long-term metabolic outcomes of the offspring through nutritional interventions applied during the lactation period. [ABSTRACT FROM AUTHOR]

Background: Obesity is one of the most prevalent health problems in the canine population. While haemostatic parameters and markers of endothelial function have been evaluated in various disease conditions in dogs, there are no studies of these markers in canine obesity. This study was designed to evaluate the effect of naturally gained weight excess and obesity on inflammatory, hemostatic and endothelial biomarkers in dogs. A total of 37 overweight and obese dogs were compared with 28 normal weight dogs. Results: Overweight and obese dogs had significantly elevated concentrations of serum interleukin-6 (IL-6) and C-reactive protein (hsCRP). Number of platelets, activity of factor X and factor VII were significantly higher, while activated partial thromboplastine time (aPTT) and soluble plasminogen activator receptor (suPAR) were significantly decreased. Statistical analysis of high mobility group box - 1 protein (HMGB-1), soluble intercellular adhesive molecule -1 (sICAM-1) and plasminogen activator inhibitor type 1 (PAI-1) concentrations did not show significant differences between the total overweight and obese group and the normal weight group of dogs. Conclusions: Analytical changes in the dogs in our study reflects that weight excess in dogs can be associated with a chronic low degree of inflammation and a hypercoagulable state, where primary and secondary hemostasis are both affected. However obesity is not associated with impairment of endothelial function in dogs. [ABSTRACT FROM AUTHOR]

Some of the most common nutritional disorders are overweight and obesity, a proportion of approximately 59% of dogs and cats being affected. A permanent challenge for vets is weight management, including the prevention and treatment of overweight and obesity. Corporeal score and body-weight loss in dogs and cats have been monitored by feeding various diets. The study was conducted on a total of 10 animals (6 dogs and 4 cats), monitoring the effect of three types of food for dogs and two types for cats suffering from overweight and obesity. Cooked food, dry food diet and premium dry food were investigated. We determined the quality and gross chemical composition of food and we measured corporeal score, weekly weight loss percentage and the number of calories consumed daily. We also appreciated the quality of life and activity level of the animals at the beginning and at the end of the trial. Nutritional management of investigated diets for overweight and obesity in dogs and cats revealed that through the smallest caloric restriction, dry food diet presented the highest efficiency, dogs and cats loosing weight steadily without losing muscle mass. Although the satiety effect occurs when the animals reach their ideal weight, the Rebound effect was not present. [ABSTRACT FROM AUTHOR]

Epidemiologic studies and studies in rodents point to potential risks from developmental exposure to BPA on cardiometabolic diseases. Furthermore, it is becoming increasingly evident that the manifestation and severity of adverse outcomes is the result of interaction between developmental insults and the prevailing environment. Consistent with this premise, recent studies in sheep found prenatal BPA treatment prevented the adverse effects of postnatal obesity in inducing hypertension. The gene networks underlying these complex interactions are not known. mRNA-seq of myocardium was performed on four groups of four female sheep to assess the effects of prenatal BPA exposure, postnatal overfeeding and their interaction on gene transcription, pathway perturbations and functional effects. The effects of prenatal exposure to BPA, postnatal overfeeding, and prenatal BPA with postnatal overfeeding all resulted in transcriptional changes (85-141 significant differentially expressed genes). Although the effects of prenatal BPA and postnatal overfeeding did not involve dysregulation of many of the same genes, they affected a remarkably similar set of biological pathways. Furthermore, an additive or synergistic effect was not found in the combined treatment group, but rather prenatal BPA treatment led to a partial reversal of the effects of overfeeding alone. Many genes previously known to be affected by BPA and involved in obesity, hypertension, or heart disease were altered following these treatments, and AP-1, EGR1, and EGFR were key hubs affected by BPA and/or overfeeding. Environ. Mol. Mutagen. 58:4-18, 2017. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background: Obesity in dogs and cats is usually managed by dietary energy restriction using a purpose-formulated weight loss diet, but signs of hunger and begging commonly occur causing poor owner compliance. Altering diet characteristics so as to reduce voluntary food intake (VFI) can improve the likelihood of success, although this should not be at the expense of palatability. The aim of the current study was to compare the VFI and palatibility of novel commercially available canine and feline weight loss diets. Methods: The relative performance of two canine (C1 and C2) and two feline (F1 and F2) diets was assessed in groups of healthy adult dogs and cats, respectively. Diets varied in energy, protein, fibre, and fat content. To assess canine VFI, 12 (study 1) and 10 (study 2) dogs were offered food in 4 meals, for 15 min on each occasion, with hourly intervals between the meals. For feline VFI, 12 cats were offered food ad libitum for a period of 18 h per day over 5 consecutive days. The palatability studies used separate panels of 37 dogs and 30 cats, with the two diets being served, side-by-side, in identical bowls. Results: In dogs, VFI was significantly less for diet C1 than diet C2 when assessed on energy intake (study 1, 42% less, P = 0.032; study 2, 28% less, P = 0.019), but there was no difference in gram weight intake (study 1: P = 0.964; study 2: P = 0.255). In cats, VFI was 17% less for diet F1 than diet F2 when assessed by energy intake (P < 0.001), but there was again no difference in gram weight (P = 0.207). There was no difference in palatability between the two canine diets (P = 0.490), whilst the panel of cats diet preferred F1 to F2 (P < 0.001). Conclusion: Foods with different characteristics can decrease VFI without affecting palatability in both dogs and cats. The effects seen could be due to decreased energy content, decreased fat content, increased fibre content, different fibre source, and increased protein content. Further studies are now needed to determine whether similar findings occur in obese dogs and cats on controlled weight loss programmes. [ABSTRACT FROM AUTHOR]

Lack of activities for dogs, that is, decreased body motion and lack of opportunities to exercise, can cause dogs to become overweight. Swimming is one of the best physical exercises for a dog that has been approved by a veterinary doctor, and it provides a form of supported exercise. Almost all the muscles are required for the movement that involves improving strength, working the cardiovascular and respiratory system, and increasing the metabolic rate withoutimpact on joints. One interesting aspect of swimming is its ability for weight and serum lipid control. The effect of frequency-controlled swimming activity on a dog's weight and its effect on the serum lipid profile level have been well examined and recorded in this study. The dogs were randomly categorized into four groups that swam every day, four times a week, two times a week, and once a week, respectively. The dogs exercised twice a day for 20 minutes each time. The swimming program was continued for a period of four months. Swimming every day significantly reduced the dogs' weight and cholesterol level after one month, while swimming four days per week significantly reduced weight and cholesterol level after four months. After just one month of swimming four days per week, serum triglyceride level was found to be significantly reduced compared with the other groups. HDL level decreased steadily until the third month in the group that swam every day. However, in all the groups, no significant changes were found in the levels of LDL and VLDL in dog serum after 4 months of swimming. In conclusion, higher frequency of swimming per week yields better results than lower frequency for weight and serum lipid control. [ABSTRACT FROM AUTHOR]

Testosterone deficiency causes fat deposition, particularly in visceral fat, and its replacement might reverse fat accumulation, however, the underlying mechanisms of such processes under diet-induced adiposity are largely unknown. To gain insights into the genome-wide role of androgen on visceral adipose tissue (VAT), RNA-Seq was used to investigate testosterone deficiency induced changes of VAT in miniature pigs fed a high-fat and high-cholesterol (HFC) diet among intact male pigs (IM), castrated male pigs (CM), and castrated male pigs with testosterone replacement (CMT) treatments. The results showed that testosterone deficiency significantly increased VAT deposition and serum leptin concentrations. Moreover, a total of 1732 differentially expressed genes (DEGs) were identified between any two groups. Compared with gene expression profiles in IM and CMT pigs, upregulated genes in CM pigs, i.e., LOC100520753 (CD68), LCN2, EMR1, S100A9, NCF1 (p47phox), and LEP, were mainly involved in inflammatory response, oxidation-reduction process, and lipid metabolic process, while downregulated genes in CM pigs, i.e., ABHD5, SPP1, and GAS6, were focused on cell differentiation and cell adhesion. Taken together, our study demonstrates that testosterone deficiency alters the expression of numerous genes involved in key biological processes of VAT accumulation under HFC diet and provides a novel genome-wide view on the role of androgen on VAT deposition under HFC diet, thus improving our understanding of the molecular mechanisms involved in VAT changes induced by testosterone deficiency. [ABSTRACT FROM AUTHOR]

The article presents a study which explores the common disorders and demography of Pugs under veterinary care in England which shows that the most prevalent disorders include obesity/overweight, corneal disorder and otitis externa.

Among the health disorders caused by obesity in dogs stand out hyperglycemia and hyperlipidemia. Glycemic responses are directly related to the amount and type of starch. Thus, this study aimed to evaluate the effect of different sources of starch on glycemic and lipid levels in obese dogs. These dogs were distributed in a completely randomized design in a factorial 3x2x2 (three sources starchy - corn (60%), sorghum (60%) and corn: sorghum (30:30%), two breeds - Beagle and Dachshund and males and females. After 28 days of experiment, dogs fed with corn had higher amounts of glucose (93.79A mg dL-1) (P<0.05) compared with diets containing sorghum (88.00Bmg dL-1) and corn: sorghum (88.75B mg dL-1) (P>0.05). Thus, dogs that consumed corn had a higher glycemic peak in a shorter time compared with dogs that ingested sorghum. Furthermore, the dogs fed with diet containing sorghum showed lower levels of fructosamine that dogs that ingested corn diet (P<0.05) demonstrating that the diet containing sorghum maintained blood glucose over a longer time period that reduces the fluctuation of glucose in dogs. At 56 and 112 days of the experiment, a positive correlation between glucose levels and body weight (P<0.05) was also observed. At 28, 56, 84 and 112 days, Beagle dogs showed higher serum concentrations of total cholesterol compared with Dachshund dogs (P<0.05). It was concluded that the starchy source and breed can interfere with metabolic rates of obese dogs. [ABSTRACT FROM AUTHOR]

This mini-review deals with the neuropeptide 26RFa (or QRFP) which is a member of the RFamide peptide family discovered simultaneously by three groups in 2003. 26RFa (or its N-extended form 43RFa) was subsequently shown to be the endogenous ligand of the human orphan receptor GPR103. In the brain, 26RFa and GPR103mRNA are primarily expressed in hypothalamic nuclei involved in the control of feeding behavior, and at the periphery, the neuropeptide and its receptor are present in abundance in the gut and the pancreatic islets, suggesting that 26RFa is involved in the regulation of energy metabolism. Indeed, 26RFa stimulates food intake when injected centrally, and its orexigenic effect is even more pronounced in obese animals. The expression of 26RFa is up-regulated in the hypothalamus of obese animals, supporting that the 26RFa/GPR103 system may play a role in the development and/or maintenance of the obese status. Recent data indicate that 26RFa is also involved in the regulation of glucose homeostasis. 26RFa reduces glucose-induced hyperglycemia, increases insulin sensitivity and insulinemia. Furthermore, an oral ingestion of glucose strongly stimulates 26RFa release by the gut, indicating that 26RFa is a novel incretin. Finally, 26RFa is able to prevent pancreatic β cell death and apoptosis. This brief overview reveals that 26RFa is a key neuropeptide in the regulation of energy metabolism. Further fields of research are suggested including the pathophysiological implication of the 26RFa/GPR103 system. [ABSTRACT FROM AUTHOR]

Objective To determine the prevalence of obesity within a population of pleasure horses and ponies in Victoria, Australia, and to compare owners' perceptions of their animals' body condition with researchers' assessments. Design An observational study plus owner questionnaire. Methods Ten Pony Club rallies in different regions of Victoria were attended. Information regarding 229 horses and ponies were obtained from owner questionnaires, and owners' perceptions of the current body condition of their animals were assessed using a visual analogue scale. Body condition score ( BCS) was assessed by the researchers using the modified Henneke method. Results The prevalence of researcher-assessed obesity ( BCS ≥7/9) in the total surveyed population was 23.1%. A higher prevalence of obesity was identified in Shetland ponies (71.5%) and other pony types (32.0%) compared with horse breeds (9.3%). Owners perceived their animals to be in significantly lower body condition compared with the researchers' assessments (P < 0.001). Conclusion Although the overall prevalence of obesity within Australian pleasure horses and ponies was 24.5%, a considerably higher proportion of pony breeds fell into this category. Owners frequently underestimated their own animal's body condition. Knowing the prevalence of obesity in this population and understanding how owners perceive the body condition of their animals may help with targeting education around preventative health care, with the aim of reducing the risk of conditions such as insulin dysregulation and laminitis. [ABSTRACT FROM AUTHOR]

We investigated the physiological regulation of adiponectin exocytosis in health and metabolic disease by a combination of membrane capacitance patch-clamp recordings and biochemical measurements of short-term (30-min incubations) adiponectin secretion. Epinephrine or the β3-adrenergic receptor (AR) agonist CL 316,243 (CL) stimulated adiponectin exocytosis/secretion in cultured 3T3-L1 and in primary subcutaneous mouse adipocytes, and the stimulation was inhibited by the Epac (Exchange Protein directly Activated by cAMP) antagonist ESI-09. The β3AR was highly expressed in cultured and primary adipocytes, whereas other ARs were detected at lower levels. 3T3-L1 and primary adipocytes expressed Epac1, whereas Epac2 was undetectable. Adiponectin secretion could not be stimulated by epinephrine or CL in adipocytes isolated from obese/type 2 diabetic mice, whereas the basal (unstimulated) adiponectin release level was elevated twofold. Gene expression of β3AR and Epac1 was reduced in adipocytes from obese animals, and corresponded to a respective ∼35% and ∼30% reduction at the protein level. Small interfering RNA–mediated knockdown of β3AR (∼60%) and Epac1 (∼50%) was associated with abrogated catecholamine-stimulated adiponectin secretion. We propose that adiponectin exocytosis is stimulated via adrenergic signaling pathways mainly involving β3ARs. We further suggest that adrenergically stimulated adiponectin secretion is disturbed in obesity/type 2 diabetes as a result of the reduced expression of β3ARs and Epac1 in a state we define as “catecholamine resistance.” [ABSTRACT FROM AUTHOR]