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Mitochondrial dysfunction occurs in monocytes during obesity and contributes to a low-grade inflammatory state; therefore, maintaining good mitochondrial conditions is a key aspect of maintaining health. Dietary interventions are primary strategies for treating obesity, but little is known about their impact on monocyte bioenergetics. Thus, the aim of this study was to evaluate the effects of calorie restriction (CR), intermittent fasting (IF), a ketogenic diet (KD), and an ad libitum habitual diet (AL) on mitochondrial function in monocytes and its modulation by the gut microbiota. A randomized controlled clinical trial was conducted in which individuals with obesity were assigned to one of the 4 groups for 1 month. Subsequently, the subjects received rifaximin and continued with the assigned diet for another month. The oxygen consumption rate (OCR) was evaluated in isolated monocytes, as was the gut microbiota composition in feces and anthropometric and biochemical parameters. Forty-four subjects completed the study, and those who underwent CR, IF and KD interventions had an increase in the maximal respiration OCR (p = 0.025, n2p = 0.159 [0.05, 0.27] 95% confidence interval) in monocytes compared to that in the AL group. The improvement in mitochondrial function was associated with a decrease in monocyte dependence on glycolysis after the IF and KD interventions. Together, diet and rifaximin increased the gut microbiota diversity in the IF and KD groups (p = 0.0001), enriched the abundance of Phascolarctobacterium faecium (p = 0.019) in the CR group and Ruminococcus bromii (p = 0.020) in the CR and KD groups, and reduced the abundance of lipopolysaccharide (LPS)-producing bacteria after CR, IF and KD interventions compared to the AL group at the end of the study according to ANCOVA with covariate adjustment. Spearman's correlation between the variables measured highlighted LPS as a potential modulator of the observed effects. In line with this findings, serum LPS and intracellular signaling in monocytes decreased with the three interventions (CR, p = 0.002; IF, p = 0.001; and KD, p = 0.001) compared to those in the AL group at the end of the study. We conclude that these dietary interventions positively regulate mitochondrial bioenergetic health and improve the metabolic profile of monocytes in individuals with obesity via modulation of the gut microbiota. Moreover, the evaluation of mitochondrial function in monocytes could be used as an indicator of metabolic and inflammatory status, with potential applications in future clinical trials. This trial was registered with ClinicalTrials.gov (NCT05200468). [Display omitted] [ABSTRACT FROM AUTHOR]

The amino acid profile of young adults is modified by sex, body mass index (BMI) and insulin resistance (IR). However, we do not know if age or the presence of specific polymorphisms in the genes of BCAT2 and BCKDH contribute to changes in the amino acid profile, especially in subjects with obesity. Therefore, we have evaluated the effect of age, the presence of IR and the polymorphisms of BCAT2 rs11548193 and BCKDH rs45500792 on the concentration of amino acids in subjects with obesity. This was a cross-sectional study conducted with 487 subjects with obesity. Participants underwent a physical examination in which their clinical history was obtained and a blood sample was taken for biochemical, hormonal, and DNA analysis. Adults <30 years old with obesity had higher levels of alanine, arginine, aspartate, histidine, leucine, lysine, methionine, phenylalanine, proline, serine and valine than adults ≥30 years old. Interestingly, regardless of age, we found that arginine, aspartate, serine decreased, while proline and tyrosine increased in the presence of IR; tyrosine and sum of branched-chain amino acids (∑BCAA) were the amino acids that increased in the presence of BCAT2 rs11548193 and BCKDH rs45500792 polymorphisms. We found that the amino acid profiles of subjects with obesity are differentially modified by age, the presence of IR, and the presence of the BCAT2 rs11548193 and BCKDH rs45500792 polymorphisms. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) are the leading cause of global death. Hypercholesterolemia is among the main risk factors for developing cardiovascular events, and is highly prevalent in the Mexican population. The primary objective of the present work was to assess the effect of a dietary portfolio (DP) with functional foods containing dehydrated nopal, soy protein, chia seeds, inulin, and oats in LDL-C and TC concentrations of subjects with mild hypercholesterolemia. Also, we explored the changes in the profile of the lipoprotein subclasses measured by nuclear magnetic resonance spectroscopy (NMR). Sixty-two subjects (47 women, 15 men) with mild hypercholesterolemia (LDL-C, ≥130 ≤ 190 mg/dL, TC > 200 mg/dL) completed the randomized, parallel, controlled study. The dietary intervention was given in two stages. First, a dietary standardization stage with a low saturated fat diet (LSFD) which matched the habitual energy intake of the volunteers for 2-weeks, followed by 2.5 months of dietary intervention with a LSFD plus placebo (PL) or DP. Subjects who consumed the LSFD + DP interventions had a significantly higher reduction of LDL-C (−18.05%, P = 0.003) and TC (−17.08%, P = 0.02) compared to volunteers who consumed an LSFD for the same period. Furthermore, the lipoprotein subclass profiling showed that the small low-density-lipoproteins, and the small high-density-lipoproteins significantly decreased (P = 0.04, P < 0.001, respectively), conveying a less atherogenic state. At the end of the study, 78% of the subjects who consumed LSFD + DP reduced their LDL-C below 160 mg/dL, and of these, 47% reduced it below 130 mg/dL. Based on the results obtained from this study, the inclusion of functional foods as part of the lifestyle modifications is recommended to treat mild hypercholesterolemia and reduce cardiovascular risk. Registered under ClinicalTrials.gov Identifier no. NCT04148976. [ABSTRACT FROM AUTHOR]

Background: Dietary intervention (DI) is a primary strategy to attenuate some of the metabolic abnormalities associated with metabolic syndrome (MetS), including low HDL cholesterol. There is no biomarker that can identify individuals who respond to DI by increasing HDL cholesterol.Objective: The aim of this study was to assess the predictive power of a genetic predisposition score (GPS) in Mexican adults with MetS to identify HDL cholesterol responders to DI.Methods: This study followed a prospective cohort design. Sixty-seven Mexican adults aged 20-60 y (21% men) with BMI ≥25 and ≤39.9 kg/m², who had at least 3 of 5 positive criteria for MetS, were included. Participants consumed a low saturated fat diet for 2.5 mo (<7% energy as saturated fat, <200 mg of cholesterol/d) and reduced their usual diet by ∼440 kcal/d, a reduction in total energy intake of about 25%. Anthropometry and serum biochemical markers, including HDL cholesterol, were measured before and after DI. A multilocus GPS was constructed using previously reported genetic variants associated with response to diet in subjects with MetS. GPS values, designed to predict the response of HDL cholesterol to the DI, were computed for each individual as the sum of the number of effect alleles across 14 SNPs.Results: Individuals were dichotomized as high and low GPS according to median GPS (-2.12) and we observed a difference in HDL cholesterol changes on DI of +3 mg/dL (6.3%) in subjects with low GPS, whereas those with high GPS had HDL cholesterol decreases of -3 mg/dL (-7.9%) (P = 0.04).Conclusions: Individuals with low GPS showed greater increases in their HDL cholesterol than those with high GPS. Therefore, the GPS can be useful for predicting the HDL cholesterol response to diet. [ABSTRACT FROM AUTHOR]

A weekly conference series paired with lectures entitled "Microbiome-MX: exploring the Microbiota and Microbiome Research in Mexico" was organized to provide a multidisciplinary overview of the most recent research done in Mexico using high-throughput sequencing. Scientists and postgraduate students from several disciplines such as microbiology, bioinformatics, virology, immunology, nutrition, and medical genomics gathered to discuss state of the art in each of their respective subjects of expertise, as well as advances, applications and new opportunities on microbiota/microbiome research. In particular, high-throughput sequencing is a crucial tool to understand the challenges of a megadiverse developing country as Mexico, and moreover to know the scientific capital and capabilities available for collaboration. The conference series addressed three main topics important for Mexico: i) the complex role of microbiota in health and prevalent diseases such as obesity, diabetes, inflammatory bowel disease, tuberculosis, HIV, autoimmune diseases and gastric cancer; ii) the use of local, traditional and prehispanic products as pre/probiotics to modulate the microbiota and improve human health; and iii) the impact of the microbiota in shaping the biodiversity of economically important terrestrial and marine ecosystems. Herein, we summarize the contributions that Mexican microbiota/microbiome research is making to the global trends, describing the highlights of the conferences and lectures, rather than a review of the state-of-the-art of this research. This meeting report also presents the efforts of a multidisciplinary group of scientist to encourage collaborations and bringing this research field closer for younger generations. [ABSTRACT FROM AUTHOR]

Summary Background & aims Accurate predictive equations of resting energy expenditure (REE) are crucial in devising nutritional strategies to manage overweight/obesity, especially in countries where these are highly prevalent. REE is the most common measurement used to estimate energy requirements in the nutritional context; the most accurate method of measuring REE is indirect calorimetry (IC). However, this method is costly and often rarely feasible in many clinical settings. The objective of the present study was to develop and validate a new equation for predicting REE in adults with overweight and obesity. Methods This was a cross-sectional study including 410 men and women with overweight and obesity (20–60 y). Participants were randomly assigned; the development group included 200 subjects and the validation group 210 subjects. The new predictive equation was derived using stepwise multiple linear regression analysis. The accuracy of the new equation was compared to several existing predictive equations (PEs). The accuracy rate was calculated as the percentage of subjects whose REE-PE was within ±10% of the REE-IC. REE was measured by IC and anthropometric measurements. Results One predictive equation was developed (NEQ) in which weight was the strongest predictor of REE. Compared with others predicted equations already using, the new designed equation showed the less mean bias (Kj/day): NEQ: 25.7, Valencia:129, WHO/FAO/United Nations University: 270, Mifflin-St Jeor: 308, Owen: −808, Carrasco: −1097, Korth: −36.4, Johnstone: −375, Livingstone: −315, De Lorenzo: −28.3, Lazzer: −123, Muller: −145, Huang: −399 and Bernstein: −1335. Conclusions The present equation had the highest predictive accuracy in subjects with overweight or obesity compared with the previous equations derived from different populations. Thus, these new equation can be used to assist the nutritional management of these subjects. [ABSTRACT FROM AUTHOR]

Background: Glutamine is catabolized in the liver by glutaminase 2 (GLS2). Evidence suggests that peroxisome proliferator-activated receptor α (PPARα) represses the expression of several amino acid-catabolizing enzymes, but for Gls2 this is unknown.Objective: The aim of the study was to assess whether PPARα regulates Gls2 expression.Methods: For 8 d, 7-9-wk-old male C57BL/6 wild-type (WT) and Ppara-null mice weighing 23.4 ± 0.5 g were fed diets with different dietary protein:carbohydrate (DP:DCH) ratios (6%:77%, 20%:63%, or 50%:33%). Liver samples were obtained after 16 h of feed deprivation or 3 h of refeeding, and microarrays were performed. Hepatic glutaminase expression was measured by quantitative polymerase chain reaction and Western blotting. Cotransfection analyses in hepatocellular carcinoma cell line (HepG2) cells with PPARα and hepatocyte nuclear factor 4α (HNF4α) expression vectors were performed.Results: The microarray results showed that Gls2 was the only upregulated gene in WT mice, but not in the Ppara-null mice. In the feed-deprived WT mice, the Gls2 mRNA and protein abundances in the 50%:33% group were 2.5- and 1.1-fold greater (P < 0.05), respectively, than those in the 20%:63% group, which were 2.3- and 0.4-fold greater than those in the 6%:77% group (P < 0.01). Gls2 mRNA expression in the 6%:77% group of feed-deprived Ppara-null mice was 33-fold greater than that in the same group of WT mice (P < 0.0001). GLS2 protein abundance in HepG2 cells was 78% greater than that in the controls (P < 0.0001) after HNF4α overexpression, and it was 99% greater after transfection with a short hairpin targeting PPARα.Conclusions: In Ppara-null mice, Gls2 mRNA expression was greater than in WT mice, regardless of the DP:DCH ratio. In HepG2 cells overexpressing HNF4α, Gls2 expression increased, an effect repressed by overexpression of PPARα. This suggests that Gls2 depends on the PPARα/HNF4α counterregulatory transcriptional control. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is a universal problem in modern society. Atherosclerosis is the leading cause of CVD resulting in high rate of mortality in the population. Nutrition science has focused on the role of essential nutrients in preventing deficiencies, at the present time, the nutritional strategies are crucial to promote health and intervene with these global noncommunicable diseases. In many cases, diet is a major driving force, which is much easier to change and follow than other factors. It is important to establish that the first strategy to treat atherosclerosis is to modify lifestyle habits, focusing on the beneficial properties of specific nutrients. In the last decades, epidemiological, clinical and experimental studies have demonstrated that diet plays a central role in the prevention of atherosclerosis. In this review we will focus on the effect of specific foods, nutrients and bioactive compounds, including epidemiological facts, potential mechanisms of action and dietary recommendations to reduce the risk of atherosclerosis. In particular, we include information about fiber, plant sterols and stanols, niacin, taurine, olive oil, omega 3 fatty acids, antioxidants, minerals, methyl nutrients and soy. In addition, we also show that dysbiosis of the intestinal microbiota associated with a consumption of certain animal food sources can generate some metabolites that are involved in the development of atherosclerosis and its consequences on CVD. According to the epidemiological, clinical and experimental studies we suggest a recommendation for some dietary foods, nutrients and bioactive compounds to support the complementary clinical management of patients with atherosclerosis. [ABSTRACT FROM AUTHOR]

The purpose of this study was to characterize the in vitro specific reactive oxygen species (ROS) scavenging activity of nopal extracts and to study the effect of nopal consumption on plasma antioxidant capacity. The in vitro hydrolysis of the extract increased its antioxidant activity and the concentration of total polyphenols. The hydrolyzed extract showed ability to scavenge hydroxyl radical, hydrogen peroxide, peroxynitrite anion, superoxide anion and hypochlorous acid. Quercetin, isorhamnetin and kaempferol were identified in this extract by high-performance liquid chromatography (HPLC)/mass spectrometry and vitamin C by HPLC. The antioxidant activity of nopal was compared with that of different foods and the following order was found: coffee > garlic > nopal > plum > chia seeds. Nopal consumption increased blood and plasma antioxidant activity in healthy subjects. Thus, nopal showed in vitro and in vivo antioxidant activity that may be, at least in part, due to the presence of polyphenols and vitamin C. [ABSTRACT FROM AUTHOR]

Body nitrogen retention is dependent on the amount of dietary protein consumed, as well as the fat and carbohydrate content in the diet, due to the modulation of amino acid oxidation. PPARα is a transcription factor involved in the upregulation of the expression of enzymes of fatty acid oxidation. However, the role of putative PPARα response elements (PPREs) in the promoter of several amino acid-degrading enzymes (AADEs) is not known. The aim of this work was to study the effect of the synthetic ligand Wy 14643 and the natural ligands palmitate, oleate, and linoleate in rats fed graded concentrations of dietary protein (6, 20, or 50 g/100 g of total diet) on the expression of the AADEs histidase, serine dehydratase, and tyrosine aminotransferase. Thus, we fed male Wistar rats diets containing 6, 20, or 50% casein for 10 d. The results showed that addition of Wy 14643 to the diet significantly reduced the expression of the AADEs. Furthermore, the incubation of hepatocytes with natural ligands of PPARα or feeding rats with diets containing soybean oil, safflower oil, lard, or coconut oil as sources of dietary fat significantly repressed the expression of the AADEs. Gene reporter assays and mobility shift assays demonstrated that the PPRE located at -482 bp of the histidase gene actively bound PPARα in rat hepatocytes. These data indicate that PPARα ligands may reduce amino acid catabolism in rats. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is associated with multiple factors such as obesity, insulin resistance, and oxidative stress. Nopal, a cactus plant widely consumed in the Mexican diet, is considered a functional food because of its antioxidant activity and ability to improve biomarkers of metabolic syndrome. The aim of this study was to assess the effect of nopal consumption on the development of hepatic steatosis and hepatic oxidative stress and on the regulation of genes involved in hepatic lipid metabolism. Obese Zucker [fa/fa) rats were fed a control diet or a diet containing 4% nopal for 7 wk. Rats fed the nopal-containing diet had ～50% lower hepatic TG than the control group as well as a reduction in hepatomegaly and biomarkers of hepatocyte injury such as alanine and aspartate aminotransferases. Attenuation of hepatic steatosis by nopal consumption was accompanied by a higher serum concentration of adiponectin and a greater abundance of mRNA for genes involved in lipid oxidation and lipid export and production of carnitine palmitoyitransferase- 1 and microsomal TG transfer proteins in liver. Hepatic reactive oxygen species and lipid peroxidation biomarkers were significantly lower in rats fed nopal compared with the control rats. Furthermore, rats fed the nopal diet had a lower postprandial serum insulin concentration and a greater liver phosphorylated protein kinase B (pAKT):AKT ratio in the postprandial state. This study suggests that nopal consumption attenuates hepatic steatosis by increasing fatty acid oxidation and VLDL synthesis, decreasing oxidative stress, and improving liver Insulin signaling in obese Zucker (fa/fa) rats. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a health problem throughout the world and is associated with cardiovascular disease and diabetes. Thus, the purpose of the present work was to evaluate the effects of a dietary pattern (DP; soy protein, nopal, chia seed, and oat) on the biochemical variables of MetS, the AUC for glucose and insulin, glucose intolerance (GI), the relationship of the presence of certain polymorphisms related to MetS, and the response to the DP. In this randomized trial, the participants consumed their habitual diet but reduced by 500 kcal for 2 wk. They were then assigned to the placebo (P; n = 35) or DP (n = 32) group and consumed the reduced energy diet plus the P or DP beverage (235 kcal) minus the energy provided by these for 2 mo. All participants had decreases in body weight (BW), BMI, and waist circumference during the 2-mo treatment (P < 0.0001); however, only the DP group had decreases in serum TG, C-reactive protein (CRP), and AUC for insulin and GI after a glucose tolerance test. Interestingly, participants in the DP group with MetS and the ABCA1 R230C variant had a greater decrease in BW and an increase in serum adiponectin concentration after 2 mo of dietary treatment than those with the ABCA1 R230R variant. The results from this study suggest that lifestyle interventions involving specific DP for the treatment of MetS could be more effective if local foods and genetic variations of the population are considered. [ABSTRACT FROM AUTHOR]

Abstract: Obesity is associated with an increase in adipose tissue mass due to an imbalance between high dietary energy intake and low physical activity; however, the type of dietary protein may contribute to its development. The aim of the present work was to study the effect of soy protein versus casein on white adipose tissue genome profiling, and the metabolic functions of adipocytes in rats with diet-induced obesity. The results showed that rats fed a Soy Protein High-Fat (Soy HF) diet gained less weight and had lower serum leptin concentration than rats fed a Casein High-Fat (Cas HF) diet, despite similar energy intake. Histological studies indicated that rats fed the Soy HF diet had significantly smaller adipocytes than those fed the Cas HF diet, and this was associated with a lower triglyceride/DNA content. Fatty acid synthesis in isolated adipocytes was reduced by the amount of fat consumed but not by the type of protein ingested. Expression of genes of fatty acid oxidation increased in adipose tissue of rats fed Soy diets; microarray analysis revealed that Soy protein consumption modified the expression of 90 genes involved in metabolic functions and inflammatory response in adipose tissue. Network analysis showed that the expression of leptin was regulated by the type of dietary protein and it was identified as a central regulator of the expression of lipid metabolism genes in adipose tissue. Thus, soy maintains the size and metabolic functions of adipose tissue through biochemical adaptations, adipokine secretion, and global changes in gene expression. [ABSTRACT FROM AUTHOR]

Obesity is an epidemic condition strongly associated with cardiovascular morbidity and mortality. Heart disease secondary to obesity is associated with myocardial steatosis, leading to ceramide synthesis and cell dysfunction in a process known as lipotoxicity. Soy protein has been demonstrated to reduce lipotoxicity in the liver and pancreas in different rodent models of obesity. Thus, our purpose in the present work was to assess the effect of dietary soy protein on cardiac lipid accumulation and ceramide formation during obesity and to evaluate its effect in the following 2 rodent models of obesity: 1) a diet-induced obesity model in Sprague-Dawley rats was produced by feeding rats a control or a high-fat caseiri or soy protein diet for 180 d; and 2) wild-type and ob/ob mice were fed a casein or soy protein diet for 90 d. Soy protein intake led to lower cholesterol and triglyceride concentrations in the hearts of rats and ob/ob mice in association with a greater PPARa mRNA concentration and a lower level of sterol regulatory element binding protein-1 mIRNA than those fed casein. The ceramide concentration was also lower in hearts of rats and ob/ob mice that were fed soy protein in association with lower serine palmitoyl transferase (SPT)-1 and tumor necrosis factor-α mRNA concentrations. These results indicate that dietary soy protein can reduce the heart ceramide concentration by reducing the expression of SPT-1, a key enzyme in the formation of this sphingolipid in the heart of obese rodents, and by reducing lipid accumulation. Thus, soy protein consumption may be considered as a dietary therapeutic approach for lipotoxic cardiomyopathy prevention. [ABSTRACT FROM AUTHOR]

Abstract: Several studies have evaluated the effect of soy protein or soluble fiber on serum cholesterol in hypercholesterolemic subjects, with different results. We hypothesized that this response is associated with the presence of polymorphisms in genes encoding proteins involved in lipoprotein metabolism or reverse cholesterol transport. Thus, the aims of the present work were to study the effectiveness of a dietary portfolio consisting of a combination of soy protein and soluble fiber integrated in a low saturated fat (LSF) diet on blood lipids in a Mexican group with hyperlipidemia and to determine the association between responsiveness to the diet and the frequency of apolipoprotein (Apo) E and ApoA1 and ABCG5/8 polymorphisms. Forty-three hyperlipidemic subjects (20 men and 23 women) were given an LSF diet for 1 month, followed by an LSF diet that included 25 g of soy protein and 15 g of soluble fiber daily for 2 months. After the 3-month dietary intervention, serum total cholesterol (TC) significantly decreased by 20.6%, and serum triglycerides (TGs) decreased by 40.4%. Fifty-one percent of the subjects had a reduction more than 20% in serum TC, and 77% of the subjects had a reduction more than 20% in serum TG (hyperresponders). Approximately 14% of the hypercholesterolemic subjects had the ABCG8 (52 G/C) polymorphism, 65% had the ABCG5 (1950 C/G and G/G) polymorphism, 53.5% had the ApoA1 (−75 G/A and A/A) polymorphism, and 23.3% had the ApoE (3/4) polymorphism. Independently of genotype, the combination of cholesterol-lowering foods in an LSF diet significantly reduced serum TC and TG in Mexican hypercholesterolemic subjects. [Copyright &y& Elsevier]

Abstract: During lactation, the mammary gland increases the needs for nutrients to fulfill the milk production requirements. Among these nutrients, amino acids play an important role for the synthesis of milk proteins. Amino acids are supplied to the mammary gland through amino acid transporters, although some are synthesized in situ. The purpose of this study was to establish the pattern of changes in messenger RNA abundance of the amino acid transporters ASC, system L, EAAC1, GLAST, CAT-1, and Tau in the mammary gland of the rat during different stages of pregnancy and lactation. Rats were fed during pregnancy and lactation a 20% casein diet. Food intake increased significantly during the lactation period. Amino acid transporter ASC expression increased during the first days of pregnancy about 2-fold, and it was increased in a lesser extent again during the peak of lactation. The expression of system L (LAT-1) and CAT-1 transporters was increased only during the lactation period. On the other hand, the expression of the transporters for anionic amino acids EAAC1 and GLAST was low during both stages. Finally, taurine transporter expression decreased during pregnancy; and it was significantly lower during lactation. These results showed that amino acid transporters were not expressed similarly in the mammary gland during pregnancy and lactation, indicating that the expression of these transporters did not respond only to the metabolic needs of the gland but depended on the dietary protein supply and possibly the specific hormonal changes that occur during pregnancy and lactation. [Copyright &y& Elsevier]

Due to the public health problem represented by obesity, the study of adipose tissue, particularly of the adipocyte, is central to the understanding of metabolic abnormalities associated with the development of obesity. The concept of adipocyte as endocrine and functional cell is not totally understood and can be currently defined as the capacity of the adipocyte to sense, manage, and send signals to maintain energy equilibrium in the body. Adipocyte functionality is lost during obesity and has been related to adipocyte hypertrophy, disequilibrium between lipogenesis and lipolysis, impaired transcriptional regulation of the key factors that control adipogenesis, and lack of sensitivity to external signals, as well as a failure in the signal transduction process. Thus, dysfunctional adipocytes contribute to abnormal utilization of fatty acids causing lipotoxicity in non-adipose tissue such as liver, pancreas and heart, among others. To understand the metabolism of the adipocyte it is necessary to have an overview of the developmental process of new adipocytes, regulation of adipogenesis, lipogenesis and lipolysis, endocrine function of adipocytes and metabolic consequences of its dysfunction. Finally, the key role of adipose tissue is shown by studies in transgenic animals or in animal models of diet-induced obesity that indicate the contribution of adipose tissue during the development of metabolic syndrome. Thus, understanding of the molecular process that occurs in the adipocyte will provide new tools for the treatment of metabolic abnormalities during obesity. [Copyright &y& Elsevier]

Chronic consumption of high-fat or -carbohydrate diets is associated with the development of obesity; however, it is not well established whether dietary protein plays a role in the development of abnormalities of lipid metabolism that occur during obesity. To determine the effect of different types of protein during diet-induced obesity on hepatic and adipocyte lipid metabolism, rats were fed casein (CAS) or soy (SOY) protein diets with 5% fat or high-fat diets with 25% fat (HF-CAS and HF-SOY) for 180 d. Rats fed soy diets had lower hepatic sterol regulatory element binding protein-1 (SREBP-1) expression and higher SREBP-2 expression than those fed casein diets, leading to less hepatic lipid deposition. On the other hand, long-term HF-SOY consumption prevented hyperleptinemia in comparison with rats fed HF-CAS. Rats fed soy protein diet showed higher adipocyte perilipin mRNA expression and smaller adipocyte area than those fed casein diets, which was associated with a lower body fat content. Furthermore, the lipid droplet area in brown adipose tissue was significantly lower in rats fed soy diets than in those fed casein diets and it was associated with higher uncoupling protein-1 (UCP-1) expression. As a result, rats fed the soy diets gained less weight than those fed the casein diets, in part due to an increase in the thermogenic capacity mediated by UCP-1. These results suggest that the type of protein consumed and the presence of fat in the diet modulate lipid metabolism in adipose tissue and liver. [ABSTRACT FROM AUTHOR]

Abstract: Soybeans have a high-quality protein that has been consumed for approximately 5000 years in Oriental countries. The awareness that soy products are healthy has increased their consumption in Western countries. Substantial data from epidemiological surveys and nutritional interventions in humans and animals indicate that soy protein reduces serum total and low-density lipoprotein (LDL) cholesterol and triglycerides as well as hepatic cholesterol and triglycerides. This review examines the evidence on the possible mechanisms for which soy protein has beneficial effects in diabetes, obesity and some forms of chronic renal disease. Consumption of soy protein due to low methionine content reduces serum homocysteine concentration, decreasing the risk of acquiring a cardiovascular disease. On the other hand, soy protein reduces the insulin/glucagon ratio, which in turn down-regulates the expression of the hepatic transcription factor sterol regulatory element binding protein (SREBP)-1. The reduction of this factor decreases the expression of several lipogenic enzymes, decreasing in this way serum and hepatic triglycerides as well as LDL cholesterol and very LDL triglycerides in diabetes and obesity, reducing lipotoxicity in the liver. Soy protein intake also reduces hepatic lipotoxicity by maintaining the number of functional adipocytes, preventing the transfer of fatty acids to extra adipose tissues. Furthermore, soy protein isoflavones stimulate the transcription factor SREBP-2, increasing serum cholesterol clearance. The reduction of serum cholesterol and triglyceride concentrations by soy protein intake produces beneficial effects in the kidney preventing the inflammatory response, increasing the renal flow by releasing endothelial nitric oxide (NO) synthase from the caveolae, facilitating the synthesis of NO. Thus, soy protein consumption may reduce the clinical and biochemical abnormalities in diseases mediated by lipid disorders. [Copyright &y& Elsevier]

The consumption of soy protein was shown to reduce blood lipids in humans and other animal species. Furthermore, it was shown that the ingestion of soy protein maintains normal insulinemia. Thus, the purpose of the present study was to determine whether soy protein affects the synthesis of lipids in the liver through sterol-regulatory element binding protein-1 (SREBP-1) due to modulation of insulin levels. We first conducted a short-term study in which rats were fed a diet containing 18 g/100 g soy protein or casein for 10 d. Rats fed soy protein had significantly lower serum insulin concentrations than rats fed casein, and this response was accompanied by an elevation in hepatic SREBP-1 mRNA that was 53% lower than that in rats fed casein at d 10. The increase in SREBP-1 mRNA occurred 30 min after consumption of the casein mean, and increased steadily for the next 2 h. We then conducted a second study to assess the long-term effect of soy protein consumption for 150 d on hepatic SREBP-1 expression. Long-term consumption of soy protein maintained normal insulin concentrations compared with rats fed casein, which were hyperinsulinemic. Thus, rats fed the soy protein diet had significantly lower expression of SREBP-1 mRNA than rats fed the casein diet. Soy protein intake also reduced the expression of fatty acid synthase (FAS) and malic enzyme, leading to low hepatic lipid depots of triglycerides and cholesterol, whereas rats fed the casein diet developed fatty liver. These data suggest that soy protein regulates SREBP-1 expression by modulating serum insulin concentration, thus preventing the development of fatty liver. [ABSTRACT FROM AUTHOR]

: ObjectiveThe purpose of the present work was to determine the fasting plasma total homocysteine (tHcy) levels and the time-course response of tHcy concentrations after the consumption of urban and rural Mexican model diets in two groups of Mexican women from urban and rural areas.: MethodsThirty-three adult women (age range = 18–49 y) were studied. Fifteen women were from a rural community in the state of Mexico. The other 18 were from cities and consumed diets that regularly included an important amount of animal foods. The study was designed as a two-period crossover study in which subjects consumed the model urban or rural diet in a 2-wk interval. Seven milliliters of venous blood was drawn before ingestion of experimental diets (basal) to measure total cholesterol, high-density lipoprotein cholesterol, triacylglycerol, tHcy, folate, vitamin B12, and methionine. Blood samples were then obtained 30, 60, 90, 180, and 240 min after the beginning of meal consumption.: ResultsThe rural and urban groups showed similar concentrations of tHcy 4 h after meal consumption and after fasting. However, the urban and rural groups had higher methionine plasma concentrations after the urban diet than after the rural diet. In contrast, there was no significant difference in methionine plasma levels between the rural and urban groups with each diet. Those women with low tHcy concentrations maintained those values over the study period, and those with high tHcy concentrations maintained those values. There was no significant difference in tHcy concentrations due to consumption of the two diets (P = 0.31) or the interaction between population and diet (P = 0.84). However, there was a significant difference in the concentration of tHcy between the rural (8.73 ± 0.17 μM/L) and the urban (9.27 ± 0.13 μM/L) populations (P = 0.01). In both groups, average tHcy concentration was in the normal range. In both populations, the nutrition status for folate and vitamin B12 was adequate, although plasma folate concentration was significantly lower in the rural population than in the urban population (P < 0.01). Plasma vitamin B12 concentrations were similar in both groups. No subject had low plasma vitamin B12.: ConclusionsPlasma tHcy concentrations in rural and urban Mexican women were within the range considered adequate; however, urban women showed significant higher concentrations than did rural women independently of the consumed diet and the plasma methionine concentration. These results indicated that there is no short-term variation in plasma tHcy due to the consumption of rural or urban diets. [Copyright &y& Elsevier]

Nephrotic syndrome (NS) is characterized by the presence of proteinuria and hyperlipidemia. However, ingestion of soy protein has a hypolipidemic effect. The present study was designed to determine whether the ingestion of a 20% soy protein diet regulates the expression of hepatic sterol regulatory element binding protein (SREBP)-1, fatty acid synthase (FAS), malic enzyme, beta-hydroxy-beta-methylglutaryl-CoA (HMG-CoA) reductase (r) and synthase (s), and LDL receptor (r), and to assess whether soy protein improves lipid and renal abnormalities in rats with chronic NS. Male Wistar rats were injected with vehicle or with puromycin aminonucleoside to induce NS and were fed either 20% casein or soy protein diets for 64 d. NS rats fed 20% soy protein had improved creatinine clearance and reduced proteinuria, hypercholesterolemia, hypertriglyceridemia, as well as VLDL-triglycerides and LDL cholesterol compared with NS rats fed the 20% casein diet. In addition, the soy protein diet decreased the incidence of glomerular sclerosis, and proinflammatory cytokines in kidney. Ingestion of the soy protein diet by control rats reduced the gene expression of SREBP-1, malic enzyme, FAS and increased HMG-CoAr, HMG-CoAs and LDLr. However, NS rats fed either casein or soy protein diets had low insulin concentrations with reductions in SREBP-1, FAS and malic enzyme expression compared with control rats fed the casein diet. NS rats fed the soy diet also had lower HMG-CoAr and LDLr mRNA levels than NS rats fed casein. In conclusion, the beneficial effects of soy protein on lipid metabolism are modulated in part by SREBP-1. However, in NS rats, the benefit may be through a direct effect of this protein on kidney rather than mediated by changes in expression of hepatic lipid metabolism genes. [ABSTRACT FROM AUTHOR]

A high protein concentration in the diet induces the gene expression of several amino acid degrading enzymes such as histidase (Hal) in rats. It is important to understand whether the amino acid pattern of the dietary protein affects the gene expression of these enzymes. The purpose of the present work was to study the effect of a histidine-imbalanced diet on the activity and mRNA concentration of rat hepatic histidase. Seven groups of six rats were fed one of the following diets: 1) 6% casein (basal), 2) 20% casein, 3) 35% casein, 4) an imbalance diet containing 6% casein plus a mixture of indispensable amino acids (IAA) equivalent to a 20% casein diet without histidine (I-20), 5) 6% casein plus a mixture of IAA equivalent to a 35% casein diet without histidine (I-35), 6) a corrected diet containing 6% casein plus IAA including histidine equivalent to a 20% casein diet, 7) a corrected diet containing 6% casein plus IAA including histidine equivalent to a 35% casein diet. Serum histidine concentration was inversely proportional to the protein content of the diet, and it was significantly higher in rats fed the corrected diets compared to their respective imbalanced diet groups. Hal activity increased as the protein content of the diet increased. Greater histidine imbalance resulted in lower food intake and higher Hal activity. Rats fed histidine-corrected diets had lower activity than their respective imbalanced groups. Differences in Hal activity were associated with differences in the concentration of Hal mRNA. These results indicate that rats fed a histidine-imbalanced diet exhibit reduced food intake and weight gain and increased Hal gene expression as a consequence of an increased amino acid catabolism. [ABSTRACT FROM AUTHOR]

Provides information on a study that examines the effect of the protein content of the diet in well-nourished and protein-undernourished rats. Information on branched-chain amino acids (BCAA); Materials and methods used in the study; Results of the study.

There is evidence that during lactation, uptake of the essential branched-chain amino acids (BCAA) by mammary glands exceeds their output in milk protein. In this study, we have measured the potential of lactating rats to catabolize BCAA. The activity, relative protein and specific mRNA levels of the first two enzymes in the BCAA catabolic pathway, branched-chain aminotransferase (BCAT) and branched-chain alpha-keto acid dehydrogenase (BCKD), were measured in mammary gland, liver and skeletal muscle obtained from rat dams at peak lactation (12 d), from rat dams 24 h after weaning at peak lactation and from age-matched virgin controls. Western analysis showed that the mitochondrial BCATm isoenzyme was found in mammary gland. Comparison of lactating and control rats revealed that tissue BCATm activity, protein and mRNA were at least 10-fold higher in mammary tissue during lactation. Values were 1.3- to 1. 9-fold higher after 24 h of weaning. In mammary gland of lactating rats, the BCKD complex was fully active. In virgin controls and weaning dams, only about 20% of the complex was in the active state. Hypertrophy of the liver and mammary gland during lactation resulted in a 73% increase in total oxidative capacity in lactating rats. The results are consistent with increased expression of the BCATm gene in the mammary gland during lactation, whereas oxidation appears to be regulated primarily by changes in activity state (phosphorylation state) of BCKD. [ABSTRACT FROM AUTHOR]

Presents a study which examines the effect of dietary protein on the expression of histidase (Hal) and studies the mechanism of induction of histidase by a high protein diet. Materials and methods used in the study; Effect of diet on weight gain; Effect of dietary protein on Hal concentration.

Determines the effects of concentrations of leucine on the transport, transamination and oxidation of valine and on incorporation of valine into the heart proteins. Neutral amino acids for transport into heart occurring at physiological concentrations of amino acids in plasma; Effects of inhibition of valine uptake by leucine; Depletion of tissue valine concentration.

The preservation of body proteins is essential to guarantee their functions in organisms. Therefore, the utilization of amino acids as energy substrates is regulated by a precise fine-tuned mechanism. Recent evidence suggests that the transcription factors peroxisome proliferator-activated receptor alpha (PPARα) and hepatocyte nuclear factor 4 alpha (HNF4α) are involved in this regulatory mechanism. Thus, the aim of this study was to determine how these transcription factors interact to regulate the expression of amino acid catabolism genes. In vivo studies using PPARα-knockout mice (Pparα-null) fed different amounts of dietary protein showed that in the absence of PPARα, there was a significant increase in HNF4α abundance in the liver, which corresponded with an increase in amino acid catabolizing enzyme (AACE) expression and the generation of increased amounts of postprandial urea. Moreover, this effect was proportional to the increase in dietary protein consumed. Chromatin immunoprecipitation assays showed that HNF4α can bind to the promoter of AACE serine dehydratase (SDS), an effect that was potentiated by dietary protein in the Pparα-null mice. The mechanistic studies revealed that the presence of retinoid X receptor alpha (RXRα) is essential to repress HNF4α activity in the presence of PPARα, and this interaction accelerates HNF4α degradation via the proteasome pathway. These results showed that PPARα can downregulate liver amino acid catabolism in the presence of RXRα by inhibiting HNF4α activity. Unlabelled Image • PPARα deletion increases HNF4α and the expression of amino acid catabolism genes in the liver. • Increase in dietary protein intake and PPARα deletion promotes HNF4α binding to the Sds promoter. • Upon activation, PPARα interacts with HNF4α and this interaction requires the presence of RXRα. • PPARα and RXRα repress HNF4α transcriptional activity by inducing its proteasomal degradation. [ABSTRACT FROM AUTHOR]

Angiotensin-(1-7) [Ang-(1-7)], a component of the renin angiotensin system, is a vasodilator that exerts its effects primarily through the Mas receptor. The discovery of the Mas receptor in white adipose tissue (WAT) suggests an additional role for this peptide. The aim of the present study was to assess whether Ang-(1-7) can induce the expression of thermogenic genes in white adipose tissue and increase mitochondrial respiration in adipocytes. Stromal Vascular fraction (SVF)-derived from mice adipose tissue was stimulated for one week with Ang-(1-7), then expression of beige markers and mitochondrial respiration were assessed. Mas+/+ and Mas−/− mice fed a control diet or a high fat-sucrose diet (HFSD) were exposed to a short or long term infusion of Ang-(1-7) and body weight, body fat, energy expenditure, cold resistance and expression of beige markers were assessed. Also, transgenic rats overexpressing Ang-(1-7) were fed with a control diet or a high fat-sucrose diet and the same parameters were assessed. Ang-(1-7) circulating levels from human subjects with different body mass index (BMI) or age were measured. Incubation of adipocytes derived from SVF with Ang-(1-7) increased the expression of beige markers. Infusion of Ang-(1-7) into lean and obese Mas+/+mice also induced the expression of Ucp1 and some beige markers, an effect not observed in Mas−/− mice. Mas−/− mice had increased body weight gain and decreased cold resistance, whereas rats overexpressing Ang-(1-7) showed the opposite effects. Overexpressing rats exposed to cold developed new thermogenic WAT in the anterior interscapular area. Finally, in human subjects the higher the BMI, low circulating concentration of Ang-(1-7) levels were detected. Similarly, the circulating levels of Ang-(1-7) peptide were reduced with age. These data indicate that Ang-(1-7) stimulates beige markers and thermogenesis via the Mas receptor, and this evidence suggests a potential therapeutic use to induce thermogenesis of WAT, particularly in obese subjects that have reduced circulating concentration of Ang-(1-7). Unlabelled Image • Ang-(1-7) induces the expression of beige markers in white adipose tissue. • Ang-(1-7) stimulates energy expenditure and increases mitochondrial respiration. • Thermogenesis is activated by Ang-(1-7) via Mas receptor. • Overexpression of Ang-(1-7) induces resistance to obesity. • Obese humans show low levels of circulating Ang-(1-7). [ABSTRACT FROM AUTHOR]

In recent years, the gut microbiota has been of great interest due to its role in maintaining health and its association with the development of different diseases such as obesity and diabetes. The objective of the present review is to show the main functions of the gut microbiota, the role in the degradation of complex carbohydrates particularly soluble fiber, resistant starches and bioactive compounds particularly polyphenols. In addition, the review will focus on the nutrient-gut microbiota interaction and its role on the development of dysbiosis (imbalance) and low-grade inflammation during the obesity and type 2 diabetes. Finally, several strategies using prebiotics will be discussed to reduce the gut microbiota dysbiosis, and to improve some biochemical abnormalities during obesity and type 2 diabetes. [ABSTRACT FROM AUTHOR]

A prolonged and elevated postprandial glucose response (PPGR) is now considered a main factor contributing for the development of metabolic syndrome and type 2 diabetes, which could be prevented by dietary interventions. However, dietary recommendations to prevent alterations in PPGR have not always been successful. New evidence has supported that PPGR is not only dependent of dietary factors like the content of carbohydrates, or the glycemic index of the foods, but is also dependent on genetics, body composition, gut microbiota, among others. In recent years, continuous glucose monitoring has made it possible to establish predictions on the effect of different dietary foods on PPGRs through machine learning methods, which use algorithms that integrate genetic, biochemical, physiological and gut microbiota variables for identifying associations between them and clinical variables with aim of personalize dietary recommendations. This has allowed to improve the concept of personalized nutrition, since it is now possible to recommend through these predictions specific dietary foods to prevent elevated PPGRs that are highly variable among individuals. Additional components that can enrich the predictive algorithms are findings of nutrigenomics, nutrigenetics and metabolomics. Thus, this review aims to summarize the evidence of the components that integrate personalized nutrition focused on the prevention of PPGRs, and to show the future of personalized nutrition by laying the groundwork for the development of individualized dietary management and its impact on the improvement of metabolic diseases. [ABSTRACT FROM AUTHOR]

• Diabetes is a metabolic disorder characterized by inadequate insulin secretion, which generates deterioration in the individual, and is a significant global health problem. • Intestinal microbiota plays a crucial role in the regulation of metabolism, and its diversity is an indicator of health. • Current diabetes drugs have serious side effects, so finding agents with fewer adverse effects is a priority. • Streptozotocin administration in mice is considered a model of diabetes that permits the analysis of natural nutritional components. • Molecular iodine supplements can reduce tissue oxidative damage and restore the diversity of intestinal microbiota generated by the presence of Streptozotocin. Diabetes mellitus (DM) is a multifactorial condition that involves oxidative alterations and dysbiosis of the gut microbiota associated with an imbalance in glucose metabolism. Therefore, the need to develop integrative therapies that are both effective and have fewer side effects has become evident in recent years. Molecular iodine (I 2) has antioxidant effects in preclinical hyperglycemic models. The present work analyzes the preventive and therapeutic effects of oral I 2 supplementation in a DM model induced by low doses of streptozotocin (STZ). Male CD1 mice (12 weeks old) were divided into the following groups: control, STZ (20 mg/kg/day, i.p., for 5 days), I 2 (0.2 mg/Kg in drinking water), preventive (STZ + I 2), and therapeutic (I 2 supplementation from day 35 to day 90; STZ + I 2(Ther)). The supplementation with I 2 prevented and normalized hyperglycemia, hypercholesterolemia, and hypertriglyceridemia associated with STZ, preserving pancreatic, liver, muscle, and adipose tissue morphology and normalizing inflammatory gene induction (TLR2, TLR4, NFkβ, TNFα) in several tissues. Furthermore, compared to the STZ group, the presence of I 2 favored a more significant abundance of beneficial bacteria that support the integrity of the intestinal epithelial barrier and higher α-diversity. In conclusion, the I 2 supplement has preventive and therapeutic effects, reducing oxidative damage and reestablishing microbiota diversity following STZ exposure. [ABSTRACT FROM AUTHOR]

Background and Aims: Maternal nutrition during gestation is critical for mammary gland cell proliferation and differentiation and development of optimal delta-6 (Δ6D) and delta-5 (Δ5D) desaturase and elongase 2 and 5 (Elovl 2 and 5) activity for synthesis of the long chain polyunsaturated fatty acids (LC-PUFAs), arachidonic (AA), eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, important for normal fetal and neonatal brain development. We hypothesized that maternal low protein diet (LPD) impairs mammary gland preparation for lactation and PUFA synthesis. The aim of the study was to evaluate consequences of maternal LPD on mammary gland structure and development and expression of enzymes responsible for LC-PUFA production. Methods: Pregnant rats were assigned to control or protein restricted, isocaloric diet (R). At 19 days gestation, mammary gland tissue was removed for histological analysis and lipid, AA, EPA and DHA determination by gas chromatography. Gene transcription was quantified by RT–PCR and protein by Western blot. Results: In R mothers, mammary gland lobuloalveolar development was decreased and showed fat cell infiltration. Δ6D, Δ5D, and Elovl 5 mRNA were lower in R, whereas protein levels measured by Western blot were unchanged. This is the first report that detects mammary gland desaturase and elongase protein. Although Elovl 2 mRNA was not detectable by RT–PCR, Elovl 2 protein was not different between groups. AA and DHA were lower and EPA undetectable in the mammary gland of R mothers. Conclusions: Maternal LPD decreased late gestation mammary gland lobuloalveolar development and LC–PUFAs. Protein restriction negatively impacts maternal mammary gland development prior to lactation. [Copyright &y& Elsevier]

White adipose tissue (WAT) can differentiate into beige adipose tissue by the browning process. Some polyphenols, including isoflavones, particularly genistein, are suggested to increase the expression of browning markers. There is evidence that consumption of genistein can attenuate body weight gain and improve glucose tolerance and blood lipid levels. The aim of the present study was to investigate the potential mechanisms of stimulation by which genistein activates the browning of WAT. We studied the stimulation of the expression of browning markers in the following models: mice fed genistein; preadipocytes from 3 T3-L1 cells; and the stromal vascular fraction (SVF) from the inguinal adipose tissue of mice. The results indicated that genistein can stimulate the browning process by at least two mechanisms. An indirect mechanism was involved in the induction of PGC-1α/FNDC5 in skeletal muscle leading to an increase in the myokine irisin. In preadipocytes, irisin was able to increase the expression of Ucp1 and Tmem26, markers of browning, to increase energy expenditure. Interestingly, genistein was also able to activate browning by a direct mechanism. Incubation of preadipocytes with genistein increased UCP1 expression as well as some biomarkers of browning in a concentration-dependent manner, possibly via phosphorylation of AMPK. The effect of genistein was accompanied by an increase in the number of mitochondria as well as in the maximum respiration rate of the adipocytes. In conclusion, this study indicated that genistein can increase energy expenditure by stimulating the browning process directly in preadipocytes and indirectly by increasing the circulating levels of irisin. [ABSTRACT FROM AUTHOR]

Metabolic profiling studies have highlighted increases in the plasma free fatty acid (FFA) and branched-chain amino acid (BCAA) concentrations, which are hallmarks of the obese and insulin-resistant phenotype. However, little is known about how the increase of the BCAA concentration modifies the metabolic fate of FFA, and vice versa, in adipocytes. Therefore, we incubated differentiated 3T3-L1 adipocytes or primary adipocytes from rats fed a control or a high-fat diet with: (1) 0, 250, 500 and 1000 μM of leucine and determined the oxidation and incorporation of [1-14C]-palmitate into lipids or proteins or (2) 0, 250, 500 or 1000 μM of palmitate and evaluated the oxidation and incorporation of [U-14C]-leucine into lipids or proteins. Leucine decreased palmitate oxidation and increased its incorporation into the lipid fraction in adipocytes; the latter was reduced in adipocytes from obese rats. However, palmitate increased leucine oxidation in adipocytes as well as reduced leucine incorporation into the protein and lipid fractions in adipocytes from obese rats. These results demonstrate that leucine modifies the metabolic fate of palmitate, and vice versa, in adipocytes and that the metabolic interaction between leucine and palmitate catabolism is altered in adipocytes from obese rats. [ABSTRACT FROM AUTHOR]

Obesity is characterized by an excess of white adipose tissue (WAT). Recent evidence has demonstrated that WAT can change its phenotype to a brown-like adipose tissue known as beige/brite adipose tissue. This transition is characterized by an increase in thermogenic capacity mediated by uncoupling protein 1 (UCP1). This browning process is a potential new target for treating obesity. The aim of this review is to integrate the different mechanisms by which beige/brite adipocytes are formed and to describe the physiological, pharmacological and nutritional inducers that can promote browning. An additional aim is to show evidence of how some of these inducers can be used as potential therapeutic agents against obesity and its comorbidities. This review shows the importance of brown and beige/brite adipose tissue and the mechanisms of their formation. Particularly, the two theories of beige/brite adipocyte origin are discussed: de novo differentiation and transdifferentiation. The gene markers that identify these types of adipocytes and the involvement of microRNAs in the epigenetic regulation of the browning process is also discussed. Additionally, we describe the transcriptional control of UCP1 expression by some of the inducers of browning. Furthermore, we describe in detail how some bioactive dietary compounds can induce browning and their subsequent beneficial health effects. The evidence suggests that browning is a new potential strategy for the treatment of obesity and obesity-associated metabolic disorders. [ABSTRACT FROM AUTHOR]

Nopal is a plant used in traditional Mexican medicine to treat diabetes. However, there is insufficient scientific evidence to demonstrate whether nopal can regulate postprandial glucose. The purpose for conducting this study was to evaluate the glycemic index, insulinemic index, glucose-dependent insulinotropic peptide (GIP) index, and the glucagon-like peptide 1 (GLP-1) index, and the effect of nopal on patients with type 2 diabetes after consumption of a high-carbohydrate breakfast (HCB) or high-soy-protein breakfast (HSPB) on the postprandial response of glucose, insulin, GIP, GLP-1, and antioxidant activity. In study 1, the glycemic index, insulinemic index, GIP index, and GLP-1 index were calculated for seven healthy participants who consumed 50 g of available carbohydrates from glucose or dehydrated nopal. In study 2, 14 patients with type 2 diabetes consumed nopal in HCB or HSPB with or without 300 g steamed nopal. The glycemic index of nopal was 32.5±4, insulinemic index was 36.1±6, GIP index was 6.5±3.0, and GLP-1 index was 25.9±18. For those patients with type 2 diabetes who consumed the HCB+nopal, there was significantly lower area under the curve for glucose (287±30) than for those who consumed the HCB only (443±49), and lower incremental area under the curve for insulin (5,952±833 vs 7,313±1,090), and those patients with type 2 diabetes who consumed the HSPB avoided postprandial blood glucose peaks. Consumption of the HSPB+nopal significantly reduced the postprandial peaks of GIP concentration at 30 and 45 minutes and increased the antioxidant activity after 2 hours measured by the 2,2-diphenyl-1-picrilhidracyl method. These findings suggest that nopal could reduce postprandial blood glucose, serum insulin, and plasma GIP peaks, as well as increase antioxidant activity in healthy people and patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Abstract: Background: Although dietary treatments can successfully reduce blood lipids in hypercholesterolemic subjects, individual variation in that response has on occasion been linked to allelic differences. SNP rs12449157 has shown association with HDL-C concentrations in GWAS and falls in the glucose-fructose oxidoreductase domain containing 2 (GFOD2) locus. Of interest, previous data suggest that this SNP may be under environmentally driven selection. Thus, the aim of this study was to assess if rs12449157 may mediate the response of lipid traits to a dietary supplementation (DS) with soy protein and soluble fiber in a Mexican population with hypercholesterolemia. Methods: Forty-one subjects with hypercholesterolemia were given a low saturated fat diet (LSFD) for 1month, followed by a LSFD+DS that included 25g of soy protein and 15g of soluble fiber (S/SF) daily for 2months. Anthropometric, clinical, biochemical and dietary variables were determined. We analyzed the gene–diet interaction between the GFOD2 genotype, with the minor allele frequency of 0.24, and the DS on total cholesterol (TC) and LDL-C concentrations. Results: Hypercholesterolemic subjects with GFOD2 rs12449157 G allele had higher serum TC and LDL-C at the baseline and showed a greater response to the LSCD+S/SF (−83.9 and −57.5mg/dl, respectively) than those with GFOD2 AA genotype (−40.1 and −21.8mg/dl, respectively) (P =0.006 for TC, 0.025 for LDL-C, respectively). Conclusion: The observed differences in allele-driven, diet-induced changes in blood lipids may be the result of a recent environmentally driven selection on the rs12449157 minor allele. Variation in the GFOD2 gene contributes to the genetic basis for a differential response to a cholesterol- or lipid-lowering diet. [Copyright &y& Elsevier]

Abstract: Recent evidence indicates that several metabolic abnormalities developed during obesity are associated with the presence of dysfunctional adipose tissue. Diet is a key factor that modulates several functions of adipose tissue; however, each nutrient in the diet produces specific changes. Thus, the aim of this work was to study the effect of the interaction of the type (coconut or soybean oil) and amount (5% or 10%) of fat with the type of dietary protein (casein or soy protein) on the functionality of white adipose tissue of Zucker (fa/fa) rats. The results showed that soybean oil reduced adipocyte size and decreased esterified saturated fatty acids in white adipose tissue. Excess dietary fat also modified the composition of esterified fatty acids in white adipose tissue, increased the secretion of saturated fatty acids to serum from white adipose tissue and reduced the process of fatty acids re-esterification. On the other hand, soy protein sensitized the activation of the hormone-sensitive lipase by increasing the phosphorylation of this enzyme (Ser 563) despite rats fed soy protein were normoglucagonemic, in contrast with rats fed casein that showed hyperglucagonemia but reduced hormone-sensitive lipase phosphorylation. Finally, in white adipose tissue, the interaction between the tested dietary components modulated the transcription/translation process of lipid and carbohydrate metabolism genes via the activity of the PERK–endoplasmic reticulum stress response. Therefore, our results showed that the type of protein and the type and amount of dietary fat selectively modify the activity of white adipose tissue, even in a genetic model of obesity. [Copyright &y& Elsevier]

Background and Aims: Dietary fat plays a central role in the development of obesity. However, the metabolic consequences of dietary fat can vary depending on their fatty acid composition. Therefore, the aim of the present work was to study the effect of the type and amount of dietary fat on the expression of genes controlling lipogenesis and fatty acid oxidation in the liver or adipose tissue of rats. Methods: The expression of hepatic or adipose tissue lipid metabolic genes from Sprague Dawley or Zucker fa/fa rats, respectively, was measured after chronic consumption of diets containing different types/amounts of dietary fats or after rats were adapted for 2 months to a high-fat Western diet and then fed different types and amounts of fats. Results: Each fat or oil in the diet regulated differentially the expression of transcription factors involved in lipogenesis and fatty acid oxidation as well as some of its target genes in liver. The expression of these genes after a chronic consumption of a high-fat Western diet was reestablished in the presence of less dietary fat and was dependent on the type of fat. In obese Zucker fa/fa rats, consumption of a high-fat diet repressed the expression of lipogenic, fatty acid oxidation and thermogenic genes in adipose tissue. Conclusions: Type of fat influences the expression of genes that are involved in lipid metabolism in liver and adipose tissue, but this response is repressed when the amount of dietary fat is excessive, diminishing the differences between each type of fat. [Copyright &y& Elsevier]