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Pulmonary rehabilitation (PR) increases exercise capacity, reduces dyspnea, and improves quality of life (QoL) in patients with chronic obstructive pulmonary disease (COPD). Patients requiring PR can present with multiple comorbidities. One of the most common comorbidities is obesity. The prevalence of obesity in patients with COPD is increasing at an alarming rate. To date the efficacy of PR to ameliorate obesity in patients with COPD is unclear. Obesity in patients with COPD is associated with increased morbidity and mortality compared to patients without obesity. However, the benefits of obesity paradox in lower mortality rate health-related QoL and health care utilization remain unclear. This review discusses the challenges of prescribing PR to patients with obesity and COPD. In addition, the definition of and the potential challenges and benefits of the obesity paradox in patients with COPD will be discussed. Treatment strategies that include combining PR with lifestyle management, individually tailored nutritional advice, pharmacotherapy, and surgery need to be tested in prospective, randomized controlled trials. The challenges of providing complex care, prioritizing patient needs, and future directions will also be discussed for patients with obesity and COPD., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Fibroblast growth factor 21 (FGF21) is a metabolic regulator of energy and lipid metabolism. FGF21 is highly expressed in liver while FGF21 receptors (beta-klotho (KLB) and FGFR1c) are highly expressed in white adipose tissues (WATs). Plasma FGF21 has been shown to be increased after 7–10 days of fasting but oppositely plasma FGF21 is also increased in obesity. The aim of this study was to measure the effect of 60 h of fasting on plasma FGF21 levels in obese and lean subjects and to determine the gene expression of KLB and FGFR1c in the subcutaneous WAT before, during and after 60 h of fasting. Eight obese (BMI >30 kg/m2) and seven lean subjects (BMI <25 kg/m2) were fasted for 60 h and blood samples were taken at time 0 and after 12, 36 and 60 h of fasting. A biopsy from the subcutaneous WAT was taken at time 0, 12 and 60 h of fasting. FGF21 was measured in plasma by an ELISA and mRNA expression of KLB and FGFR1c was measured in WAT by quantitative PCR (qPCR). The fast significantly decreased plasma FGF21 in obese subjects while no change in plasma FGF21 was observed in lean subjects. Interestingly, KLB was significantly decreased in WAT in response to fasting in both lean and obese subjects indicating a potential important adaptive regulation of KLB in response to fasting., (2018 Society for Endocrinology)

Obese subjects exhibit lower adipose tissue oxygen consumption in accordance with the lower adipose tissue blood flow. Thereby, compared to lean subjects, obese individuals have almost half lower capillary density and more than half lower vascular endothelial growth factor (VEGF). The VEGF expression together with hypoxia-inducible transcription factor-1 alpha (HIF-1α) activity also requires phosphatidylinositol 3-kinase (PI3K) and mammalian target of rapamycin (mTOR)-mediated signaling. Especially HIF-1α is an important signaling molecule for hypoxia to induce the inflammatory responses. Hypoxia contributes to several biological functions, such as angiogenesis, cell proliferation, apoptosis, inflammation, and insulin resistance (IR). Pathogenesis of obesity-related comorbidities is attributed to intermittent hypoxia (IH), which is mostly observed in visceral obesity. Proinflammatory phenotype of the adipose tissue is a crucial link between IH and the development of IR. Inhibition of adaptive unfolded protein response (UPR) in hypoxia increases β cell death. Moreover, deletion of HIF-1α worsens β cell function. Oxidative stress, as well as the release of proinflammatory cytokines/adipokines in obesity, is proportional to the severity of IH. Reactive oxygen species (ROS) generation at mitochondria is responsible for propagation of the hypoxic signal; however, mitochondrial ROS production is required for hypoxic HIF-1α protein stabilization. Alterations in oxygen availability of adipose tissue directly affect the macrophage polarization and are responsible for the dysregulated adipocytokines production in obesity. Hypoxia both inhibits adipocyte differentiation from preadipocytes and macrophage migration from the hypoxic adipose tissue. Upon reaching a hypertrophic threshold beyond the adipocyte fat loading capacity, excess extracellular matrix (ECM) components are deposited, causing fibrosis. HIF-1α initiates the whole pathological process of fibrosis and inflammation in the obese adipose tissue. In addition to stressed adipocytes, hypoxia contributes to immune cell migration and activation which further aggravates adipose tissue fibrosis. Therefore, targeting HIF-1α might be an efficient way to suppress hypoxia-induced pathological changes in the ECM. The fibrosis score of adipose tissue correlates negatively with the body mass index and metabolic parameters. Inducers of browning/beiging adipocytes and adipokines, as well as modulations of matrix remodeling enzyme inhibitors, and associated gene regulators, are potential pharmacological targets for treating obesity., (© 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.)

Objective: The positive metabolic outcome of Roux-en-Y gastric bypass (RYGB) surgery may involve fibroblast growth factor 21 (FGF21), in both the fasting state and postprandially. We measured the fasting levels of FGF21 before and after bariatric surgery as well as the postprandial FGF21 responses after a glucose load and after a mixed meal., Design: Observational intervention trial., Patients and Measurements: Eight obese, nondiabetic patients underwent RYGB. Plasma FGF21 was measured both before and after surgery on three different days during oral glucose loads (25 g or 50 g glucose) or a mixed meal. Blood samples were taken right before the meal and at 15-min intervals until 90 min and at 150 min and 210 min relative to the start of the meal., Results: Overall, fasting plasma FGF21 did not change significantly before and after surgery (262 ± 71 vs 411 ± 119 pg/ml), but for three subjects, fasting plasma FGF21 increased significantly after surgery. Furthermore, FGF21 levels increased significantly at t = 90 and t = 150 min in response to 50 g glucose, but not after a mixed meal., Conclusions: In conclusion, the observed increase in postprandial plasma FGF21 in response to glucose and the lack of FGF21 response to a mixed meal may have important implications for the physiologic role of FGF21. The increase in postprandial FGF21 in response to glucose in the early postoperative period may contribute to the metabolic improvements observed after gastric bypass., (© 2016 John Wiley & Sons Ltd.)

The cerebral serotonin (5-HT) system shows distinct differences in obesity compared with the lean state. Here, it was investigated whether serotonergic neurotransmission in obesity is a stable trait or changes in association with weight loss induced by Roux-in-Y gastric bypass (RYGB) surgery. In vivo cerebral 5-HT2A receptor and 5-HT transporter binding was determined by positron emission tomography in 21 obese [four men; body mass index (BMI), 40.1 ± 4.1 kg/m(2)] and 10 lean (three men; BMI, 24.6 ± 1.5 kg/m(2)) individuals. Fourteen obese individuals were re-examined after RYGB surgery. First, it was confirmed that obese individuals have higher cerebral 5-HT2A receptor binding than lean individuals. Importantly, we found that higher presurgical 5-HT2A receptor binding predicted greater weight loss after RYGB and that the change in 5-HT2A receptor and 5-HT transporter binding correlated with weight loss after RYGB. The changes in the 5-HT neurotransmission before and after RYGB are in accordance with a model wherein the cerebral extracellular 5-HT level modulates the regulation of body weight. Our findings support that the cerebral 5-HT system contributes both to establish the obese condition and to regulate the body weight in response to RYGB., (Copyright © 2015 the authors 0270-6474/15/355884-06$15.00/0.)

The aim of the present study was to examine gene expression and protein concentrations of beta(1)- and beta(2)-adrenergic receptors in subcutaneous adipose tissue in obese subjects in response to weight loss. Eighteen obese subjects were studied during diet-induced weight loss. Beta-adrenergic receptor mRNA levels were quantified by reverse transcription-PCR-HPLC. Beta-adrenergic receptor protein concentrations were measured by Western blotting using fluorescence laser scanning for detection. Subjects lost 12.8+/-0.8 kg (mean+/-S.E.M.) during diet treatment. There was a 34% decrease in the beta(1)-adrenergic receptor mRNA level (0.92+/-0.09 compared with 0.61+/-0.06 amol/microg of DNA; P<0.002). Beta(2)-adrenergic receptor mRNA did not decrease significantly. Beta(2)-adrenergic receptor protein concentration decreased 37% (25.5+/-7.1 compared with 16.0+/-5.6 arbitrary units/ng of DNA; P=0.008), whereas beta(1)-adrenergic receptor protein concentration did not decrease significantly. The degree of weight loss was correlated with the concentration of beta(1)-adrenergic receptor protein (r=0.65, P<0.003) and changes in receptor protein concentration (r=0.50, P=0.035) during the very-low-calorie diet. In conclusion, the present study demonstrates a relationship between beta(1)-adrenergic receptor protein concentration in adipose tissue and the degree of weight loss. This relationship is not directly related to energy expenditure and deserves further investigation.

The aim of the present study was to quantify beta(2)-adrenoceptor protein content in adipose tissue during fasting, and to study the relationships between beta(2)-adrenoceptor protein and mRNA levels and changes in metabolites related to lipolysis. Groups of male subjects with a body mass index of <25 kg/m(2) or >30 kg/m(2) fasted for 60 h. Abdominal subcutaneous fat biopsies were analysed for receptor mRNA levels by reverse transcription-PCR-HPLC. The beta(2)-adrenoceptor protein concentration was measured by Western blotting using fluorescence laser scanning for detection. The beta(2)-adrenoceptor protein concentration per cell (on a DNA basis) was higher in obese subjects ( P <0.03). There were highly significant relationships between beta(2)-adrenoceptor protein concentration and both body mass index and waist/hip ratio ( P <0.001 for both). Furthermore, there was an inverse relationship between the receptor protein concentration and the serum beta-hydroxybutyrate level during fasting ( P <0.005). beta(2)-Adrenoceptor protein levels decreased in both groups during fasting, to a similar degree. Basal beta(2)-adrenoceptor mRNA levels were similar in the two groups, but there was a smaller increase in the obese group during fasting ( P <0.03). The increased beta(2)-adrenoceptor protein level in obese subjects is likely to be related to the greater plasma membrane area of their adipocytes. The decrease during fasting may be due to increased binding of noradrenaline and subsequent internalization and degradation of the receptor. Elevated levels of less responsive beta(2)-adrenoceptor protein in obese subjects may contribute to the development of obesity.

Aim: To evaluate the long-term effect of changes in body composition induced by weight loss on insulin sensitivity (SI), non-insulin mediated glucose disposal, glucose effectiveness (SG)and beta-cell function., Design: Glucose metabolism was evaluated before and after participation in a two-year weight loss trial of Orlistat vs. placebo, combined with an energy and fat restricted diet., Subjects: Twelve obese patients (11 women, 1 man), age 45.8 +/- 10.5 years, body weight (BW) 99.7 +/- 13.3 kg, BMI 35.3 +/- 2.8 kg/m(2)., Measurements: At inclusion and 2 years later an oral glucose tolerance test (OGTT) and a frequently sampled intravenous glucose tolerance test (FSIGT) were performed. Body composition was estimated by a dual-energy X-ray absorptiometry (DXA) whole body scanning., Results: The patients obtained varying changes in BW ranging from a weight loss of 17.8 kg to a weight gain of 6.0 kg. Corresponding changes in fat mass (FM) varied from a 40% reduction to a19% increase. A significant decrease in both fasting (p = 0.038) and 2 h (p = 0.047) blood glucose at OGTT was found. The improvement in insulin sensitivity (SI) estimated by means of Bergmans Minimal Model, was significantly and linearly correlated to change in total FM (r = - 0.83,p = 0.0026). A multiple regression analysis showed that changes in truncal FM was the strongest predictor of change in S(I) explaining 67% of the variation. First phase insulin response (AIRg)remained unchanged whereas insulin disposition index increased significantly (p = 0.044). At inclusion five patients had impaired glucose tolerance of which four, who lost weight, were normalized at the retest 2 years later., Conclusion: In obese subjects long-term minimal or moderate changes in weight were found to be linearly associated with changes in insulin sensitivity. In obese subjects with impaired glucose tolerance even a minor weight loss was able to normalize glucose tolerance.

SUMMARY Aim To evaluate the long-term effect of changes in body composition induced by weight loss on insulin sensitivity (SI ), non-insulin mediated glucose disposal, glucose effectiveness (SG ) and β-cell function. Design Glucose metabolism was evaluated before and after participation in a two-year weight loss trial of Orlistat vs. placebo, combined with an energy and fat restricted diet. Subjects Twelve obese patients (11 women, 1 man), age 45.8 ± 10.5 years, body weight (BW) 99.7 ± 13.3 kg, BMI 35.3 ± 2.8 kg/m2 . Measurements At inclusion and 2 years later an oral glucose tolerance test (OGTT) and a frequently sampled intravenous glucose tolerance test (FSIGT) were performed. Body composition was estimated by a dual-energy X-ray absorptiometry (DXA) whole body scanning. Results The patients obtained varying changes in BW ranging from a weight loss of 17.8 kg to a weight gain of 6.0 kg. Corresponding changes in fat mass (FM) varied from a 40% reduction to a 19% increase. A significant decrease in both fasting (p = 0.038) and 2 h (p = 0.047) blood glucose at OGTT was found. The improvement in insulin sensitivity (SI ) estimated by means of Bergmans Minimal Model, was significantly and linearly correlated to change in total FM (r = - 0.83, p = 0.0026). A multiple regression analysis showed that changes in truncal FM was the strongest predictor of change in SI explaining 67% of the variation. First phase insulin response (AIRg) remained unchanged whereas insulin disposition index increased significantly (p = 0.044). At inclusion five patients had impaired glucose tolerance of which four, who lost weight, were normalized at the retest 2 years later. Conclusion In obese subjects long-term minimal or moderate changes in weight were found to be linearly associated with changes in insulin sensitivity. In obese subjects with impaired glucose tolerance even a minor... [ABSTRACT FROM AUTHOR]

Metabolic and bariatric surgery (MBS) is an effective intervention for patients with severe obesity and metabolic comorbidities, particularly when non-surgical weight loss methods prove insufficient. MBS has shown significant potential for improving quality of life and metabolic health outcomes in individuals with obesity, yet it carries inherent risks. Although these procedures offer a multifaceted approach to obesity treatment and its clinical advantages are well-documented, the limited understanding of its long-term outcomes and the role of multidisciplinary care pose challenges. With an emphasis on quality-of-life enhancements and the handling of postoperative difficulties, the present narrative review seeks to compile the most recent findings on MBS while emphasizing the value of an integrated approach to maximize patient outcomes. Effective MBS and patients' management require a collaborative team approach, involving surgeons, dietitians, psychologists, pharmacists, and other healthcare providers to address not only physiological but also psychosocial patient needs. Comparative studies demonstrate the efficacy of various MBS methods, including Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy that may considerably decrease morbidity and mortality in individuals with obesity. Future studies should target long-term patient treatment, and decision making should be aided by knowledge of obesity, comorbidity recurrence rates, and permanence of benefits. [ABSTRACT FROM AUTHOR]

Simple Summary: Obesity significantly contributes to endometrial cancer (EC) incidence and mortality. Weight loss interventions are pivotal in mitigating endometroid EC risk, showing notable improvements in obesity-related metabolic perturbations, including insulin resistance, dyslipidemia, and inflammation. This review aimed to assess the efficacy of weight loss strategies, including lifestyle modifications, surgical interventions, and pharmacological approaches, on key biological indicators associated with endometroid EC. Findings reveal the assessment of weight loss for reducing inflammatory markers linked to endometroid EC, with bariatric surgery emerging as a prominent intervention. These insights can inform clinical practice, refine therapeutic strategies, and introduce tailored interventions to promote equitable healthcare and enhance outcomes for individuals affected by endometroid EC. Endometrial cancer (EC) includes various histologic types, with estrogen-dependent endometrioid carcinoma being the most common. Obesity significantly increases the risk of developing this type, especially in postmenopausal women, due to elevated estrogen production by adipocytes. This review examines the impact of weight loss from different interventions on reducing obesity-related risk factors for endometrioid EC. A systematic review and meta-analysis were conducted on three weight loss interventions: bariatric surgery, pharmacotherapy, and lifestyle changes. The effects of these interventions on inflammatory biomarkers (CRP, TNF-α, IL-6) and hormones (leptin, estrogen) were analyzed. Data from controlled studies were pooled to assess the significance of weight loss in reducing these biomarkers. Despite heterogeneity, bariatric surgery resulted in an overall 25.8% weight reduction, outperforming lifestyle and pharmacotherapy interventions. Weight loss reduced CRP levels by 33.5% and IL-6 levels by 41.9%. TNF-α levels decreased by 13% with percent weight loss over 7%. Leptin levels also decreased significantly, although the exact weight loss percentage was not statistically significant. Weight loss effectively reduces proinflammatory markers and hormones associated with increased risk of endometrioid EC. The strengths of this review include a comprehensive examination of different weight-loss interventions and a large pool of participants. However, limitations include high heterogeneity among studies and only 43% of the participants being postmenopausal. Limited data on sex hormones and racial disparities underscore the need for further research. [ABSTRACT FROM AUTHOR]

Type 2 diabetes predisposes patients to heart disease, which is the primary cause of death across the globe. Type 2 diabetes often accompanies obesity and is defined by insulin resistance and abnormal glucose handling. Insulin resistance impairs glucose uptake and results in hyperglycemia, which damages tissues such as kidneys, liver, and heart. 2-oxoglutarate (2-OG)- and iron-dependent oxygenases (2-OGDOs), a family of enzymes regulating various aspects of cellular physiology, have been studied for their role in obesity and diet-induced insulin resistance. However, nothing is known of the 2-OGDO family member 2-oxoglutarate and iron-dependent prolyl hydroxylase domain containing protein 1 (OGFOD1) in this setting. OGFOD1 deletion leads to protection in cardiac ischemia-reperfusion injury and cardiac hypertrophy, which are two cardiac events that can lead to heart failure. Considering the remarkable correlation between heart disease and diabetes, the cardioprotection observed in OGFOD1-knockout mice led us to challenge these knockouts with high-fat diet. Wildtype mice fed a high-fat diet developed diet-induced obesity, insulin resistance, and glucose intolerance, but OGFOD1 knockout mice fed this same diet were resistant to diet-induced obesity and insulin resistance. These results support OGFOD1 down-regulation as a strategy for preventing obesity and insulin handling defects. [ABSTRACT FROM AUTHOR]

Obesity is a chronic disease with high prevalence and associated comorbidities, making it a growing global concern. These comorbidities include type 2 diabetes, hypertension, ventilatory dysfunction, arthrosis, venous and lymphatic circulation diseases, depression, and others, which have a negative impact on health and increase morbidity and mortality. GLP-1 agonists, used to treat type 2 diabetes, have been shown to be effective in promoting weight loss in preclinical and clinical studies. This review summarizes numerous studies conducted on the main drugs in the GLP-1 agonists class, outlining the maximum achievable weight loss. Our aim is to emphasize the active role and main outcomes of GLP-1 agonists in promoting weight loss, as well as in improving hyperglycemia, insulin sensitivity, blood pressure, cardio–metabolic, and renal protection. We highlight the pleiotropic effects of these medications, along with their indications, contraindications, and precautions for both diabetic and non-diabetic patients, based on long-term follow-up studies. [ABSTRACT FROM AUTHOR]

Background and Aim: Studies have reported that excessive weight and obesity are common in the early stages of COPD, and malnutrition is common in moderate and severe COPD. COPD is known to show “obesity paradox” i.e., obese and overweight COPD patients have better outcome of disease as compared to underweights. The aim of the study was to assess the BMI of COPD patients, its distribution and relationship with various factors. Material and Methods: Present study was conducted at tertiary care institute of India for the duration of one year. Total 400 COPD patients were selected to assess their body mass index (BMI) using Quetelet’s formula. Study subjects were selected using a systematic random sampling method. Study subjects were categorized as per WHO’s classification of BMI for Asian populations. Results: Out of a total of 400 subjects enrolled in the study, majority (49%) were obese followed by 35% overweights and 7% underweights. Health-related quality of life of undernourished patients was most affected. A statistically significant relation was seen across all the components of SGRQ. Conclusion: Present research established that, the disease related malnutrition is common in COPD patients, therefore, BMI might be a useful indicator to predict the prognosis of disease. This calls for an urgent need by our primary care physicians to provide simultaneous weight management interventions in COPD patients so as to improve their nutritional status, enhance the strength of respiratory muscles and reduce the inflammation which will be effective in long-term management of the disease. [ABSTRACT FROM AUTHOR]

In recent days, the hike in obesity‐mediated epidemics across the globe and the prevalence of obesity‐induced cardiovascular disease has become one of the chief grounds for morbidity and mortality. This epidemic‐driven detrimental events in the cardiac tissues start with the altered distribution and metabolism pattern of high‐density lipoprotein and low‐density lipoprotein (LDL) leading to cholesterol (oxidized LDL) deposition on the arterial wall and atherosclerotic plaque generation, followed by vascular spasms and infarction. Subsequently, obesity‐triggered metabolic malfunctions induce free radical generation which may further trigger pro‐inflammatory signaling and nuclear factor kappa‐light‐chain‐enhancer of activated B cells transcriptional factor, thus inducing interferon‐gamma, tumor necrosis factor‐alpha, and inducible nitric oxide synthase. This terrifying cardiomyopathy can be further aggravated in type 2 diabetes mellitus, thereby making obese diabetic patients prone toward the development of myocardial infarction (MI) or stroke in comparison to their nondiabetic counterparts. The accelerated oxidative stress and pro‐inflammatory response induced cardiomyocyte hypertrophy, followed by apoptosis in obese diabetic individuals, causing progression of athero‐thrombotic vascular disease. Being an efficient antioxidative and anti‐inflammatory indolamine, melatonin effectively inhibits lipid peroxidation, pro‐inflammatory reactions, thereby resolving free radical‐induced myocardial damages along with maintaining antioxidant reservoir to preserve cardiovascular integrity. Prolonged melatonin treatment maintains balanced body weight and serum total cholesterol concentration by inhibiting cholesterol synthesis and promoting cholesterol catabolism. Additionally, melatonin promotes macrophage polarization toward the anti‐inflammatory state, providing a proper shield during the recovery period. Therefore, the protective role of melatonin in maintaining the lipid metabolism homeostasis and blocking the atherosclerotic plaque rupture could be targeted as the possible therapeutic strategy for the management of obesity‐induced acute MI. This review aimed at orchestrating the efficacy of melatonin in ameliorating irrevocable oxidative cardiovascular damage induced by the obesity–diabetes correlation. [ABSTRACT FROM AUTHOR]

Recent studies suggest that circulating fibroblast growth factor 21 (FGF21) may be a marker of metabolic health status. We performed a secondary analysis of a 12-week randomized controlled trial to investigate the effects of two energy restriction (ER) diets on fasting and postprandial plasma FGF21 levels, as well as to explore correlations of plasma FGF21 with metabolic health markers, (macro)nutrient intake and sweet-taste preference. Abdominally obese subjects aged 40–70 years (n = 110) were randomized to one of two 25% ER diets (high-nutrient-quality diet or low-nutrient-quality diet) or a control group. Plasma FGF21 was measured in the fasting state and 120 min after a mixed meal. Both ER diets did not affect fasting or postprandial plasma FGF21 levels despite weight loss and accompanying health improvements. At baseline, the postprandial FGF21 response was inversely correlated to fasting plasma glucose (ρ = −0.24, p = 0.020) and insulin (ρ = −0.32, p = 0.001), HOMA-IR (ρ = −0.34, p = 0.001), visceral adipose tissue (ρ = −0.24, p = 0.046), and the liver enzyme aspartate aminotransferase (ρ = −0.23, p = 0.021). Diet-induced changes in these markers did not correlate to changes in plasma FGF21 levels upon intervention. Baseline higher habitual polysaccharide intake, but not mono- and disaccharide intake or sweet-taste preference, was related to lower fasting plasma FGF21 (p = 0.022). In conclusion, we found no clear evidence that fasting plasma FGF21 is a marker for metabolic health status. Circulating FGF21 dynamics in response to an acute nutritional challenge may reflect metabolic health status better than fasting levels. [ABSTRACT FROM AUTHOR]

Background: Obesity, and in particular extreme obesity, as a global health problem is an important risk factor for many diseases, including atherosclerotic cardiovascular disease (ACVD). Bariatric surgery might stop or slow atherogenesis by decreasing excessive weight in the early stages of atherogenesis, by suppressing low-grade systemic inflammation as well as by inhibiting oxidative stress and endothelial dysfunction. The aim of this meta-analysis was to provide an answer to whether bariatric surgery has a significant effect on intima-media thickness (IMT) which is a surrogate marker of early atherosclerosis and has a good correlation with atherosclerotic coronary heart disease. Methods: A systematic literature search in PubMed, Scopus, Embase, and Web of Science as well as grey literature was performed from inception to 1 July 2022. The meta-analysis was performed using Comprehensive Meta-Analysis (CMA) V3 software. Overall, the estimate of effect size was measured by a random effects meta-analysis. To account for the heterogeneity of studies regarding study design, characteristics of the populations, and treatment duration, a random-effects model (using the DerSimonian–Laird method) and the generic inverse variance weighting approach were used. To assess the existence of publication bias in the meta-analysis, the funnel plot, Begg's rank correlation, and Egger's weighted regression tests were used. Results: The meta-analysis of 30 trials, including 1488 subjects, demonstrated a significant decrease in IMT after bariatric surgery. The reduction in IMT was also robust in the leave-one-out sensitivity analysis. It must be stressed that the results of the random-effects meta-regression did not suggest any relationship between the changes in IMT and delta body mass index (BMI) or duration of follow-up after the bariatric surgery. However, the subgroup analyses showed a better IMT reduction after laparoscopic sleeve gastrectomy (LSG) when compared to Roux-en-Y gastric bypass (RYGB). Within a year, the IMT follow-up values showed a further improvement. Conclusions: Bariatric surgery significantly reduced IMT. Significant associations were found between the surgery type and IMT changes, as well as a significant effect of follow-up duration on the changes of IMT after bariatric surgery. [ABSTRACT FROM AUTHOR]

Fibroblast growth factor 21 (FGF21) is a hormone that is involved in the regulation of lipid, glucose, and energy metabolism. Pharmacological FGF21 administration promotes weight loss and improves insulin sensitivity in rodents, non-human primates, and humans. However, pharmacologic effects of FGF21 likely differ from its physiological effects. Endogenous FGF21 is produced by many cell types, including hepatocytes, white and brown adipocytes, skeletal and cardiac myocytes, and pancreatic beta cells, and acts on a diverse array of effector tissues such as the brain, white and brown adipose tissue, heart, and skeletal muscle. Different receptor expression patterns dictate FGF21 function in these target tissues, with the primary effect to coordinate responses to nutritional stress. Moreover, different nutritional stimuli tend to promote FGF21 expression from different tissues; i.e., fasting induces hepatic-derived FGF21, while feeding promotes white adipocyte-derived FGF21. Target tissue effects of FGF21 also depend on its capacity to enter the systemic circulation, which varies widely from known FGF21 tissue sources in response to various stimuli. Due to its association with obesity and non-alcoholic fatty liver disease, the metabolic effects of endogenously produced FGF21 during the pathogenesis of these conditions are not well known. In this review, we will highlight what is known about endogenous tissue-specific FGF21 expression and organ cross-talk that dictate its diverse physiological functions, with particular attention given to FGF21 responses to nutritional stress. The importance of the particular experimental design, cellular and animal models, and nutritional status in deciphering the diverse metabolic functions of endogenous FGF21 cannot be overstated. [ABSTRACT FROM AUTHOR]

Background: Little is known about how long-term weight gain affects the health perception of COPD patients.Objectives: The aim is to evaluate the long-term association of BMI change and health-related quality of life (HRQoL) in obese COPD patients.Methods: Claims and survey data from a COPD disease management program were used to match two groups of COPD patients with BMI ≥ 30 who have differing weight trajectories over a 5-year timespan via propensity score and genetic matching. EQ-5D-5L, including visual analog scale (VAS) and COPD Assessment Test (CAT), were used as outcomes of interest. Sociodemographic and disease-based variables were matched.Results: Out of 1202 obese COPD patients, 126 with a weight increase of four or more BMI points were matched separately with 252 (propensity score matching) and 197 (genetic matching) control subjects who had relatively stable BMI. For the EQ-5D-5L, patients with BMI increase reported significantly worse health perception for VAS and all descriptive dimensions except pain/discomfort. For the CAT, especially the perception of ability to complete daily activities and overall energy results were significantly worse. VAS differences reach the range of minimal important differences. Stopping smoking and already being in obesity class II were the most influential risk factors for BMI increase.Conclusion: Obese COPD patients who gain four or more BMI points over 5 years report significantly lower results in different dimensions of generic and disease-specific HRQoL than their peers with stable BMI. To improve real-world outcomes, tracking and preventing specific BMI trajectories could constitute a clinically relevant aspect of managing COPD patients. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a common disease with an increasing prevalence, characterised by persistent respiratory symptoms and airflow limitation. Apart from cigarette smoking, certain occupational and environmental exposures, low socioeconomic status and genetic factors may contribute to the pathogenesis of COPD. Comorbidities, e. g. diabetes mellitus (DM), can negatively affect quality of life, COPD outcomes and cardiovascular risk. The present narrative review considers the potential links between COPD and DM, such as systemic inflammation, oxidative stress, hypoxaemia and hyperglycaemia. The effects of antidiabetic drugs on lung function and COPD outcomes, as well as the possibility of common therapeutic modalities are also briefly considered. Further research is needed in this field to elucidate these relationships as well as their potential clinical implications in daily practice. [ABSTRACT FROM AUTHOR]

Summary: Some studies indicate potential beneficial effects of metformin on body composition and bone. This trial compared metformin + insulin vs placebo + insulin. Metformin treatment had a small but positive effect on bone quality in the peripheral skeleton, reduced weight gain, and resulted in a more beneficial body composition compared with placebo in insulin-treated patients with type 2 diabetes. Introduction: Glucose-lowering medications affect body composition. We assessed the long-term effects of metformin compared with placebo on whole body bone and body composition measures in patients with type 2 diabetes mellitus. Methods: This was a sub-study of the Copenhagen Insulin and Metformin Therapy trial, which was a double-blinded randomized placebo-controlled trial assessing 18-month treatment with metformin compared with placebo, in combination with different insulin regimens in patients with type 2 diabetes mellitus (T2DM). The sub-study evaluates the effects on bone mineral content (BMC), density (BMD), and body composition from whole body dual-energy X-ray absorptiometry (DXA) scans which were assessed at baseline and after 18 months. Results: Metformin had a small, but positive, (p < 0.05) effect on subtotal, appendicular, and legs BMC and BMD compared with placebo. After adjustment for sex, age, vitamin D, smoking, BMI, T2DM duration, HbA1c, and insulin dose, the effects on appendicular BMC and BMD persisted (p < 0.05 for both). The changes in appendicular BMC and BMD corresponded approximately to a 0.7% and 0.5% increase in the metformin group and 0.4% and 0.4% decrease in the placebo group, respectively. These effects were mostly driven by an increase in BMC and BMD in the legs and a loss of BMC and BMD in the arms. During 18 months, all participants increased in weight, fat mass (FM), FM%, and lean mass (LM), but decreased in LM%. The metformin group increased less in weight (subtotal weight (weight-head) − 2.4 [− 3.5, − 1.4] kg, p value < 0.001) and FM (− 1.5 [− 2.3, − 0.8] kg, p value < 0.001) and decreased less in LM% (0.6 [0.2, 1.1] %, p value < 0.001) compared with the placebo group. Conclusion: Metformin treatment had a small positive effect on BMC and BMD in the peripheral skeleton and reduced weight gain compared with placebo in insulin-treated patients with T2DM. [ABSTRACT FROM AUTHOR]

Diet-induced gastrointestinal distension is known to evoke satiation and suppress postprandial hyperglycemia; however, the underlying mechanisms remain poorly understood. This study explored how gastrointestinal distension regulates energy homeostasis by using inflating stomach formulation (ISF), the carbonated solution containing pectin that forms stable gel bubbles under acidic condition in the stomach. Here we show that, in mice, oral administration of ISF induced distension of stomach and proximal intestine temporarily, stimulated intestinal glucagon-like peptide-1 (GLP-1) secretion, and activated vagal afferents and brainstem. ISF suppressed food intake and improved glucose tolerance via enhancing insulin sensitivity. The anorexigenic effect was partially inhibited, and the beneficial glycemic effect was blunted by pharmacological GLP-1 receptor blockade and chemical denervation of capsaicin-sensitive sensory nerves. In HFD-fed obese mice showing arrhythmic feeding and obesity, subchronic ISF treatment at the light period (LP) onset for 10 days attenuated LP hyperphagia and visceral fat accumulation. These results demonstrate that gastrointestinal distension by ISF stimulates GLP-1 secretion and the vagal afferent signaling to the brain, thereby regulating feeding behavior and glucose tolerance. Furthermore, subchronic ISF treatment ameliorates HFD-induced visceral obesity. We propose the diet that induces gastrointestinal distension as a novel treatment of hyperphagic obesity and diabetes. [ABSTRACT FROM AUTHOR]

Background: Cut offs for fat-free mass index (FFMI) and appendicular skeletal muscle mass index (ASMI) are available for diagnosing low muscle mass in patients with COPD. This study aimed to investigate: (1) the frequency of low muscle mass (FFMI and ASMI) applying different cut-offs and (2) the functional translation (clinical impact) of low muscle mass, in patients with COPD stratified into BMI categories.Methods: Patients with COPD were assessed regarding body composition, exercise capacity, quadriceps muscle strength, symptoms of anxiety and depression, dyspnea and quality of life upon referral to pulmonary rehabilitation. The proportion of patients with low muscle mass was compared among BMI categories. Clinical outcomes between patients with normal and low muscle mass within each BMI category were compared.Results: 469 patients with COPD were included for analyses. The frequency of patients classified as low FFMI varied significantly according to the choice of cut-off (32 to 54%; P < 0.05), whereas the frequency of patients with low ASMI was 62%. When applying age-gender-BMI-specific cut-offs, 254 patients (54%) were classified as low FFMI. The choice of the cut-off affected the frequency of patients with low muscle mass in all BMI categories. Overweight and obese patients with low muscle mass were more frequently males and presented worse pulmonary function, exercise capacity and muscle strength compared with overweight and obese patients with normal muscle mass.Conclusions: Approximately half of the overweight and obese patients with COPD have low muscle mass when applying age-gender-BMI-specific cut-offs. Low muscle mass is associated with worse functional outcomes in overweight and obese COPD patients. [ABSTRACT FROM AUTHOR]

Physical activity is an evidence-based, effective treatment for type 2 diabetes mellitus (T2D), yet insufficient numbers of adults achieve recommended daily levels, particularly amongst higher weight classes. This cross-sectional study assessed whether the Information-Motivation-Behavioural Skills (IMB) Model explained physical activity levels in adults with T2D across different body mass index (BMI) levels (N = 381). Measures included the American Adults Knowledge of Exercise Recommendations (AAKER), Behavioural Regulation in Exercise Questionnaire (BREQ-2), Barriers Specific Self-Efficacy Scale (BARSE) and the outcome measure, International Physical Activity Questionnaire (IPAQ-short form). Analyses included structural equation modelling (SEM) and ordinal logistic regression models. SEM demonstrated a good fit of the IMB Model to the data, accounting for 44% of variance in physical activity levels. Both motivation and self-efficacy had a direct effect, and motivation indirectly predicted physical activity through self-efficacy. Further analyses found the effect of the IMB predictors did not vary according to BMI status. This study supports the application of the IMB Model in explaining physical activity behavior in adults with T2D. In particular, the contribution of motivation and self-efficacy as substantive and modifiable predictors of physical activity will facilitate the development of targeted and evidence-based interventions for individuals of all BMI classes. [ABSTRACT FROM AUTHOR]

Human fibroblast growth factor 21 (FGF21) is primarily produced and secreted by the liver as a hepatokine. This hormone circulates to its target tissues (e. g., brain, adipose tissue), which requires two components, one of the preferred FGF receptor isoforms (FGFR1c and FGFR3c) and the co-factor beta-Klotho (KLB) to trigger downstream signaling pathways. Although targeting FGF21 signaling in humans by analogues and receptor agonists results in beneficial effects, e. g., improvements in plasma lipids and decreased body weight, it failed to recapitulate the improvements in glucose handling shown for many mouse models. FGF21's role and metabolic effects in mice and its therapeutic potential have extensively been reviewed elsewhere. In this review we focus on circulating FGF21 levels in humans and their associations with disease and clinical parameters, focusing primarily on obesity and obesity-associated diseases such as type-2 diabetes. We provide a comprehensive overview on human circulating FGF21 levels under normal physiology and metabolic disease. We discuss the emerging field of inactivating FGF21 in human blood by fibroblast activation protein (FAP) and its potential clinical implications. [ABSTRACT FROM AUTHOR]

Inflammation is central to pathogenic processes in diabetes mellitus and the metabolic syndrome and particularly implicates innate immunity in the development of complications. Inflammation is a primary event in Type 1 diabetes where infectious (viral) and/or autoimmune processes initiate disease; in contrast, chronic inflammation is typical in Type 2 diabetes and is considered a sequel to increasing insulin resistance and disturbed glucose metabolism. Diabetic retinopathy (DR) is perceived as a vascular and neurodegenerative disease which occurs after some years of poorly controlled diabetes. However, many of the clinical features of DR are late events and reflect the nature of the retinal architecture and its cellular composition. Retinal microvascular disease is, in fact, an early event pathogenetically, induced by low grade, persistent leukocyte activation which causes repeated episodes of capillary occlusion and, progressive, attritional retinal ischemia. The later, overt clinical signs of DR are a consequence of the retinal ischemia. Metabolic dysregulation involving both lipid and glucose metabolism may lead to leukocyte activation. On a molecular level, we have shown that macrophage-restricted protein tyrosine phosphatase 1B (PTP1B) is a key regulator of inflammation in the metabolic syndrome involving insulin resistance and it is possible that PTP1B dysregulation may underlie retinal microvascular disease. We have also shown that adherent CCR5+CD11b+ monocyte macrophages appear to be selectively involved in retinal microvascular occlusion. In this review, we discuss the relationship between early leukocyte activation and the later features of DR, common pathogenetic processes between diabetic microvascular disease and other vascular retinopathies, the mechanisms whereby leukocyte activation is induced in hyperglycemia and dyslipidemia, the signaling mechanisms involved in diabetic microvascular disease, and possible interventions which may prevent these retinopathies. We also address a possible role for adaptive immunity in DR. Although significant improvements in treatment of DR have been made with intravitreal anti-VEGF therapy, a sizeable proportion of patients, particularly with sight-threatening macular edema, fail to respond. Alternative therapies targeting inflammatory processes may offer an advantage. [ABSTRACT FROM AUTHOR]

Survival in chronic obstructive pulmonary disease (COPD) is enhanced in obese patients, which is called the obesity paradox. Despite some theories, the precise mechanism remains unclear. Since COPD exacerbations play a major role in COPD survival, this study aimed to stratify patients into BMI classes and investigate exacerbation frequency, time to readmission and survival in patients hospitalized with a COPD exacerbation. Therefore, patients hospitalized with an exacerbation of COPD were categorized into BMI groups using cut-offs <18.5, 25, 30 and ≥35 kg/m2 for underweight, normal, overweight, moderately obese and severely obese groups and followed for five years. A total of 604 COPD patients was included. In comparison to normal weight patients, the 5-year exacerbation frequency was significantly decreased by 34–40% in obese patients depending on the BMI group (1.83 ± 1.60 per year in the normal weight group; overweight 1.60 ± 1.41; moderately obese 1.20 ± 1.18; severely obese 1.09 ± 1.13 per year; and 1.59 ± 1.30 in the underweight group). The time to readmission was up to 1.7 times longer for moderately obese patients compared to normal weight patients (954 ± 734 versus 564 ± 660 days). The data were supported by enhanced survival in obese patients and a regression analysis showing that both time to readmission and survival were associated with BMI independent of other possible confounders. In conclusion, this study shows a 'dose dependent' reduced exacerbation frequency and an increased time to readmission in obese patients admitted to the hospital with an exacerbation of COPD. [ABSTRACT FROM AUTHOR]

An obesity paradox in chronic obstructive pulmonary disease (COPD), whereby overweight/obese individuals have improved survival, has been well-described. These studies have generally included smokers. It is unknown whether the paradox exists in individuals with COPD arising from factors other than smoking. Nonsmoking COPD is understudied yet represents some 25%–45% of the disease worldwide. To determine whether the obesity paradox differs between ever- and never-smokers with COPD, 1,723 adult participants with this condition were examined from 2 iterations of the National Health and Nutrition Examination Survey (1988–1994, 2007–2010), with mortality outcomes followed through December 2011. Using Cox proportional hazards models, adjusted for sociodemographic factors, lung function, and survey cycle, ever/never-smoking was found to modify the association between body mass index and hazard of death. Compared with normal-weight participants, overweight/obese participants had lower hazard of death among ever-smokers (for overweight, adjusted hazard ratio (aHR) = 0.56, 95% confidence interval (CI): 0.43, 0.74; for obesity, aHR = 0.66, 95% CI: 0.48, 0.92), but never-smokers did not (overweight, aHR = 1.41, 95% CI: 0.66, 3.03; obesity, aHR = 1.29, 95% CI: 0.48, 3.48). An obesity paradox appeared to be absent among never-smokers with COPD. This, to our knowledge, novel finding might be explained by pathophysiological differences between smoking-related and nonsmoking COPD or by smoking-associated methodological biases. [ABSTRACT FROM AUTHOR]

Smoking and obesity are important factors related to the etiology and clinical features of chronic obstructive pulmonary disease (COPD). The aim of this study was to carry out deeper analyses of the links between smoking status and body mass index as well as of the links between individual dimensions of health-related quality of life (QoL) and acceptance of life with disease in patients with COPD. Information about BMI, smoking status, clinical features of COPD, a COPD assessment test, and airflow obstruction indicators were obtained from 105 outpatients attending a pulmonary clinic. Analysis of covariance demonstrated that the subgroups of patients distinguished based on smoking status and BMI differed significantly in severity of Cough, Dyspnea, Limitation of daily activities, Lack of self-confidence, and Quality of sleep, independently of sociodemographic factors and clinical features of COPD. The results of our study suggest a certain path of the potential effects of obesity and smoking status on QoL. Risky health behaviors, such as smoking and at-risk body mass, only affect some aspects of health-related QoL. [ABSTRACT FROM AUTHOR]

Malnutrition is one of the most important factors that lead to lower quality of life in patients suffering from chronic obstructive pulmonary disease (COPD). There are several methods for assessing malnutrition including anthropometric indexes. The aim of this study was to determine the association of anthropometric indexes with disease severity in male patients with COPD in Qazvin, Iran. This cross-sectional study was conducted on 72 male patients with COPD in Qazvin, Iran, from May to December 2014. Spirometry was performed for all participants. Disease severity was determined using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline. Body mass index (BMI), mid-arm muscle circumference (MAMC), and triceps skinfold thickness (TSF) were measured. MAMC and TSF were categorized into three subgroups as <25th P, between 25th P and 75th P, and >75th P (Where P is the abbreviation for percentile.). Data were analyzed using ANOVA and logistic regression analysis. Mean age was 60.23 ± 11.39 years. Mean BMI was 23.23 ± 4.42 Kg/m2, mean MAMC was 28.34 ± 3.72 cm2, and mean TSF was 10.15 ± 6.03 mm. Mean BMI and MAMC in the GOLD stage IV were significantly lower than other stages. Of 72, 18.1% were underweight while 6.9% were obese. The GOLD stage IV was associated with 16 times increased risk of underweight and nine times increased risk of MAMC < 25th P. Disease severity was associated with BMI and MAMC as indexes of malnutrition in patients with COPD in the present study. The GOLD stage IV was associated with increased risk of underweight and low MAMC. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes is associated with substantial cardiovascular morbidity and mortality arising from the high prevalence of cardiovascular risk factors such as hypertension, dyslipidaemia, obesity, poor glycaemic control and albuminuria. Adequacy of control of these risk factors determines the frequency and outcome of cardiovascular events in the patients. Current clinical practice guidelines emphasize primary prevention of cardiovascular disease in type 2 diabetes. There is scarce data from the developing countries, Kenya included, on clinical care of patients with type 2 diabetes in the regions that are far away from tertiary health facilities. So we determined the adequacy of control of the modifiable risk factors: glycaemic control, hypertension, dyslipidemia, obesity and albuminuria in the study patients from rural and peri-urban dwelling. Methods: This was a cross-sectional study on 385 randomly selected ambulatory patients with type 2 diabetes without overt complications. They were on follow up for at least 6 months at the Out-patient diabetes clinic of Nyeri County Hospital, a public health facility located in the central region of Kenya. Results: Females were 65.5%. The study subjects had a mean duration of diabetes of 9.4 years, IQR of 3.0-14 years. Their mean age was 63.3 years, IQR of 56-71 years. Only 20.3% of our subjects had simultaneous optimal control of the three (3) main cardiovascular risk factors of hypertension, high LDL-C and hyperglycaemia at the time of the study. The prevalence of cardiovascular risk factors were as follows: HbA1c above 7% was 60.5% (95% CI, 55.6-65.5), hypertension, 49.6% of whom 76.6% (95% CI, 72.5-80.8) were poorly controlled. High LDL-Cholesterol above 2.0 mmol/L was found in 77.1% (95% CI 73.0-81.3) and Albuminuria occurred in 32.7% (95% CI 27.8-37.4). The prevalence of the other habits with cardiovascular disease risk were: excess alcohol intake at 26.5% (95% CI 27.8-37.4) and cigarette-smoking at 23.6%. A modest 23.4% of the treated patients with hypertension attained target blood pressure of <140/90 mmHg. Out of a paltry 12.5% of the statin-treated patients and others not actively treated, only 22.9% had LDL-Cholesterol of target <2.0 mmol/L. There were no obvious socio-demographic and clinical determinants of poor glycaemic control. However, old age above 50 yrs., longer duration with diabetes above 5 yrs. and advanced stages of CKD were significantly associated with hypertension. Female gender and age, statin non-use and socio-economic factor of employment were the significant determinants of high levels of serum LDL-cholesterol. Conclusion: The majority of the study patients attending this government-funded health facility had high prevalence of cardiovascular risk factors that were inadequately controlled. Therefore patients with type 2 diabetes should be risk-stratified by their age, duration of diabetes and cardiovascular risk factor loading. Consequently, composite risk factor reduction strategies are needed in management of these patients to achieve the desired targets safely. This would be achieved through innovative care systems and modes of delivery which would translate into maximum benefit of primary cardiovascular disease prevention in those at high risk. It is a desirable quality objective to have a higher proportion of the patients who access care benefiting maximally more than the numbers we are achieving now. [ABSTRACT FROM AUTHOR]

Besides the role in energy storing and body health isolating, adipose tissue produces proteins, the so-called adipokines, with pro-inflammatory or anti-inflammatory actions that contribute to metabolic control and to appetite and energy expenditure regulation. The marked adipose tissue loss following bariatric surgery corresponds to a rearrangement of serum adipokine pattern, with increase of anti-inflammatory and decrease of pro-inflammatory agents. This might play a relevant role in the postoperative improvement of metabolic conditions. However, after surgically induced weight loss, other investigations failed to evidence significant modifications of serum concentration of some adipokines. This review speculates that the composition of adipose tissue lost could influence postoperative changes in some adipokine concentration and that an adequate adipokine pattern plays a pivotal role for the long-term metabolic outcome. [ABSTRACT FROM AUTHOR]

In COPD, body composition studies have focused primarily on low BMI. We examined obesity (BMI ≥ 30 kg/m2) as a risk factor for poor function and longitudinal functional decline. Data from a longitudinal cohort of adults with COPD (n = 1096) and an age- and sex-matched comparison group collected in two in-person visits ∼49 months apart were analyzed. Two measures of functioning were examined: six-minute walk distance (6MWD) and Short Physical Performance Battery (SPPB). Multivariate regression analyses examined relationships of obesity with functioning. Secondary analyses stratified by GOLD classification (GOLD-0/1, GOLD-2, GOLD-3/4). Obesity (53% of COPD cohort) was associated cross-sectionally with 6MWD and SPPB in COPD, and only with 6MWD in the comparison group. Obesity predicted significant functional decline in 6MWD for individuals with COPD (odds ratio (OR) for decline [95% CI] 1.8 [1.1, 2.9]), but not the comparison group. Secondary analyses revealed that the risk of decline was significant only in those with more severe COPD (GOLD 3/4, OR = 2.3 [1.0, 5.4]). Obesity was highly prevalent and was associated with poor function concurrently and with subsequent decline in 6MWD in COPD. Obesity in COPD should be considered a risk not only for more co-morbidities and greater health care use, but also for functional decline. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial function declines with age; however, the relationship between adiposity and mitochondrial function among older adults is unclear. This study examined relationships between skeletal muscle mitochondrial content and electron transport chain complex 2 driven respiration with whole body and thigh composition, body fat distribution, and insulin sensitivity in older adults. Methods: 25 healthy, sedentary, weight-stable men (N = 13) and women (N = 12) >65 years of age, with a BMI range of 18-35 kg/m², participated in this study. Vastus lateralis biopsies were analyzed for citrate synthase (CS) activity and succinate mediated respiration of isolated mitochondria. Whole body and thigh composition were measured by DXA and CT. HOMA-IR was calculated using fasting glucose and insulin as an estimate of insulin sensitivity. Results: Similar to reports in middle-aged adults, skeletal muscle CS activity was negatively correlated with BMI (R = -0.43) in our cohort of older adults. Higher total and thigh adiposity were correlated with lower CS activity independent of BMI (R = -0.50 and -0.71 respectively). Maximal complex 2 driven mitochondrial respiration was negatively correlated with lower body adiposity in males (R = -0.66). In this cohort of non-diabetic older adults, both HOMA-IR and insulin were positively correlated with CS activity when controlling for BMI (R = 0.57 and 0.66 respectively). Conclusions: Adiposity and body composition are correlated with skeletal muscle mitochondrial content and electron transport chain function in healthy, sedentary, community dwelling, older adults. Specific relationships of mitochondrial bioenergetics with gender and insulin sensitivity are also apparent. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency of risk factors of coronary artery disease (CAD) in apparently healthy soldiers of Pakistan Armed Forces. Study Design: Cross sectional descriptive study. Place and Duration of Study: Department of medicine, CMH Okara from July 2012 to Dec 2012. Patients and Methods: The study included 2215 male currently serving soldiers in age range of 18 to 52 years by consecutive sampling. Relevant history, body mass index (BMI), waist circumference (WC) and blood pressure (BP) of each subject were recorded. BMI > 25 kg/m² and WC > 90 cm was considered obesity and abdominal obesity respectively. BP > 140/90 mmHg was defined as hypertension. All the participants of study underwent blood glucose fasting, blood glucose random, ECG recording, personality assessment and lipid profile. Risk estimation was done using Eric Brittain scoring system. Results: In our study group 95.5% patients were having at least 1 risk factor of CAD, 54 % were having 2 to 4 risk factors while 3.93% had > 4 risk factors. Risk estimation of CAD using Eric Brittain scoring system showed that a large proportion of study group had high probability of developing ischemic heart disease in next 6 years. Conclusion: A large proportion of our soldiers are harboring risk of CAD due to increase in frequency of 8 conventional CAD risk factors especially obesity. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency of risk factors of coronary artery disease (CAD) in apparently healthy soldiers of Pakistan Armed Forces. Study Design: Cross sectional descriptive study. Place and Duration of Study: Department of medicine, CMH Okara from July 2012 to Dec 2012. Patients and Methods: The study included 2215 male currently serving soldiers in age range of 18 to 52 years by consecutive sampling. Relevant history, body mass index (BMI), waist circumference (WC) and blood pressure (BP) of each subject were recorded. BMI > 25 kg/m2 and WC > 90 cm was considered obesity and abdominal obesity respectively. BP > 140/90 mmHg was defined as hypertension. All the participants of study underwent blood glucose fasting, blood glucose random, ECG recording, personality assessment and lipid profile. Risk estimation was done using Eric Brittain scoring system. Results: In our study group 95.5% patients were having at least 1 risk factor of CAD, 54 % were having 2 to 4 risk factors while 3.93% had > 4 risk factors. Risk estimation of CAD using Eric Brittain scoring system showed that a large proportion of study group had high probability of developing ischemic heart disease in next 6 years. Conclusion: A large proportion of our soldiers are harboring risk of CAD due to increase in frequency of 8 conventional CAD risk factors especially obesity. [ABSTRACT FROM AUTHOR]

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Low adiposity has been linked to elevated mortality from several causes including respiratory disease. However, this could arise from confounding or reverse causality. We explore the association between two measures of adiposity (BMI and WHR) with COPD in the British Women’s Heart and Health Study including a detailed assessment of the potential for confounding and reverse causality for each adiposity measure. Low BMI was found to be associated with increased COPD risk while low WHR was not (OR = 2.2; 95% CI 1.3 – 3.1 versus OR = 1.2; 95% CI 0.7 – 1.6). Potential confounding variables (e.g. smoking) and markers of ill-health (e.g. unintentional weight loss) were found to be higher in low BMI but not in low WHR. Women with low BMI have a detrimental profile across a broad range of health markers compared to women with low WHR, and women with low WHR do not appear to have an elevated COPD risk, lending support to the hypothesis that WHR is a less confounded measure of adiposity than BMI. Low adiposity does not in itself appear to increase the risk of respiratory disease, and the apparent adverse consequences of low BMI may be due to reverse causation and confounding. [ABSTRACT FROM AUTHOR]

The role of obesity and its influence on mortality in the general population has been well established. However, over the last decade, there has been substantial focus on the paradox that exists among the obese with various chronic diseases, where overweight and at least mild-moderately obese with these chronic diseases appear to have a better prognosis than do their leaner counterparts. Among them, congestive heart failure and coronary heart disease have received considerable attention. However, the influence of the obesity paradox on outcomes among patients with chronic obstructive pulmonary disease (COPD), including those requiring long-term oxygen therapy, has not been elucidated. This paper highlights the current research in this area and brings to light the lacunae that exists with regard to this paradox in COPD. [ABSTRACT FROM AUTHOR]

Obesity is characterized by hypertrophy of adipose tissue and chronic obstructive pulmonary disease (COPD) by lung damage; both diseases are associated with systemic low-grade inflammation. There are no animal models combining obesity and COPD; therefore, these diseases were induced simultaneously in rats to analyze their effects on the expression of inflammatory mediators and enzymes involved in lung tissue remodeling. Obesity was induced with sucrose (30%) for 4 months concomitant with tobacco smoke exposure (20 cigarettes/day, 5 days/wk) for the last 2 months. Were evaluated: body weight, abdominal fat, dyslipidemia, glucose tolerance test (GTT), histology, inflammatory mediators with qPCR and enzyme-linked immunosorbent assay, matrix metalloproteinases (MMP-2), MMP-9, MMP-12, TIMP-1 and TIMP-2 through qRT-PCR, and MMP-2 and MMP-9 by gelatin zymography. The rats on a sucrose diet exhibited increased body weight, abdominal fat, triglycerides, GTT, and plasma levels of insulin, adiponectin, leptin, resistin, IL-6, IL-1β, tumor necrosis factor-α (TNF-α) and IFN-γ, upregulated lung IL-6, IL-1β, TNF-α and IFN-γ, showing hyperplastic bronchial and alveolar epithelium. The animals exposed to sucrose and tobacco smoke exhibited decreased body weight, abdominal fat and plasma levels of leptin, resistin, IL-1β and IFN-γ, reducing inflammation but showing emphysematous lesions. Expression of gelatinases and MMP-12 augmented in the rats exposed to tobacco smoke alone or combined with sucrose. Zymography showed prominent gelatinases activity in all the experimental groups. These results suggest that simultaneous exposure to sucrose and tobacco smoke decreases inflammation but results in emphysematous lesions similar to those observed with tobacco smoke exposure, suggesting that obesity does not confer any protective effect against lung damage. [ABSTRACT FROM AUTHOR]

In the general population, the lowest mortality risk is considered to be for the body mass index (BMI) range of 20-24.9 kg/m. In chronic diseases (chronic kidney disease, chronic heart failure or chronic obstructive pulmonary disease) the best survival is observed in overweight or obese patients. Recently above-mentioned phenomenon, called obesity paradox, has been described in patients with coronary artery disease. Our aim was to analyze the relationship between BMI and total mortality in patients after acute coronary syndrome (ACS) in the context of obesity paradox. We searched scientific databases for studies describing relation in body mass index with mortality in patients with ACS. The study selection process was performed according to PRISMA statement. Crude mortality rates, odds ratio or risk ratio for all-cause mortality were extracted from articles and included into meta-analysis. 26 studies and 218,532 patients with ACS were included into meta-analysis. The highest risk of mortality was found in Low BMI patients-RR 1.47 (95 % CI 1.24-1.74). Overweight, obese and severely obese patients had lower mortality compared with those with normal BMI-RR 0.70 (95 % CI 0.64-0.76), RR 0.60, (95 % CI 0.53-0.68) and RR 0.70 (95 % CI 0.58-0.86), respectively. The obesity paradox in patients with ACS has been confirmed. Although it seems to be clear and quite obvious, outcomes should be interpreted with caution. It is remarkable that obese patients had more often diabetes mellitus and/or hypertension, but they were younger and had less bleeding complications, which could have influence on their survival. [ABSTRACT FROM AUTHOR]

Background: Many epidemiologic studies have shown that women with type 2 diabetes have an increased risk of developing cardiovascular disease compared with men with diabetes. The aim of this study is to elucidate whether disparities of adiposity, age and insulin resistance (IR) at the time of diabetes diagnosis exist between women and men in the adult Korean population. Methods: Data from The Korea National Health and Nutrition Examination Survey, performed in Korea from 2007 to 2010, were used. In the survey, anthropometric data and blood samples were obtained during a fasting state. IR and β-cell function were calculated using the homeostasis model assessment (HOMA-IR and HOMA-β, respectvely). Results: The mean age of diabetes diagnosis was 58.5 years in women and was 55.1 years in men (P=0.015). The mean body mass index (BMI) of newly diagnosed diabetes subjects was 26.1 kg/m2 in women and 25.0 kg/m2 in men (P=0.001). The BMI was inversely related to age in both genders, and the higher BMI in women than men was consistent throughout all age groups divided by decade. The HOMA-IR in women with diabetes is higher than in men with diabetes (7.25±0.77 vs. 5.20±0.32; P=0.012). Conclusion: Korean adult women are diagnosed with type 2 diabetes at higher BMI and older age than men and are more insulin-resistant at the time of diabetes diagnosis. This may help explain why women with diabetes have an increased risk of developing cardiovascular disease after the diagnosis of diabetes, compared to men. [ABSTRACT FROM AUTHOR]

In the present study, the effect of long-term fructose feeding on skeletal muscle mitochondrial energetics was investigated. Measurements in isolated tissue were coupled with the determination of whole-body energy expenditure and insulin sensitivity. A significant increase in plasma NEFA, as well as in skeletal muscle TAG and ceramide, was found in fructose-fed rats compared with the controls, together with a significantly higher plasma insulin response to a glucose load, while no significant variation in plasma glucose levels was found. Significantly lower RMR values were found in fructose-fed rats starting from week 4 of the dietary treatment. Skeletal muscle mitochondrial mass and degree of coupling were found to be significantly higher in fructose-fed rats compared with the controls. Significantly higher lipid peroxidation was found in fructose-fed rats, together with a significant decrease in superoxide dismutase activity. Phosphorylated Akt levels normalised to plasma insulin levels were significantly lower in fructose-fed rats compared with the controls. In conclusion, a fructose-rich diet has a deep impact on a metabolically relevant tissue such as skeletal muscle. In this tissue, the consequences of high fructose feeding are altered glucose tolerance, elevated mitochondrial biogenesis and increased mitochondrial coupling. This latter modification could have a detrimental metabolic effect by causing oxidative stress and energy sparing that contribute to the high metabolic efficiency of fructose-fed rats. [ABSTRACT FROM PUBLISHER]

Understanding the metabolic factors that contribute to obesity development and weight loss success are critical for combating obesity and obesity-related disorders. This review provides an overview of energy metabolism with a particular focus on mitochondrial function in health and in obesity. Mitochondrial proton leak contributes significantly to whole body energy expenditure and the potential role of energy uncoupling in weight loss success is discussed. We provide evidence to support the hypothesis that differences in energy efficiency are important regulators of body weight and weight loss success. [ABSTRACT FROM AUTHOR]

Objective The existence of an 'obesity paradox' in asymptomatic patients with preclinical heart failure (HF) has not been investigated. The prognostic value of BMI in a cohort of hypertensive and diabetic patients with stage A/B HF enrolled in the PROBE-HF study was explored. Design and Methods BMI was measured in 1003 asymptomatic subjects (age 66.4 ± 7.8 years, 48% males) with hypertension and/or type 2 diabetes and no clinical evidence of HF. Predefined endpoints were all-cause mortality and a composite of death and hospitalization for cardiac causes. Results During a follow-up of 38.5 ± 4.1 months, 33 deaths were observed. Mortality in the normal BMI group (1.6 deaths per 100 patient-years) did not differ to that in the overweight group (1.1 per 100 patient-years, p = 0.31), but was higher than that in the obese group (0.4 per 100 patient-years, p = 0.0089). In multivariable analysis, obesity (hazard ratio [HR] 0.27 [0.09-0.85], p = 0.025) but not overweight (HR 0.68 [0.32-1.45], p = 0.32) was associated with lower risk of death. Obesity was also independently associated with reduced risk of the composite endpoint (HR 0.54 [0.28-0.99], p = 0.047). Conclusion In asymptomatic hypertensive and diabetic patients with preclinical HF, obesity is associated with better survival and reduced risk of events. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes mellitus (T2DM) is a disease with high prevalence, associated with severe co-morbidities as well as being a huge burden on public health. It is known that glycemic control decreases long-term morbidity and mortality. The current standard therapy for T2DM is medical treatment. Several randomized controlled trials (RCTs) performed in obese patients showed remission of T2DM after bariatric surgery. Recent RCTs have shown bariatric procedures to produce a similar effect in non-morbidly and non-severely obese, insulin-dependent T2DM patients suggesting procedures currently used in bariatric surgery as new therapeutical approach in patients with T2DM. This study aims at investigating whether Roux-en-Y gastric bypass (RYGB) is an efficient treatment for non-severely obese T2DM patients in terms of preventing long-term complications and mortality.Methods: The DiaSurg 2 trial is a multicenter, open randomized controlled trial comparing RYGB including standardized medical treatment if needed to exclusive standardized medical treatment of T2DM (control group). The primary endpoint is a composite time-to-event endpoint (cardiovascular death, myocardial infarction, coronary bypass, percutaneous coronary intervention, non-fatal stroke, amputation, surgery for peripheral atherosclerotic artery disease), with a follow-up period of 8 years. Insulin-dependent T2DM patients aged between 30 and 65 years will be included and randomly assigned to one of the two groups. The experimental group will receive RYGB and, if needed, standardized medical care, whereas the control group will receive exclusive standardized medical care, both according to the national treatment guidelines for T2DM. Statistical analysis is based on Cox proportional hazards regression for the intention-to-treat population. Assuming a loss to follow-up rate of 20%, 200 patients will be randomly allocated to the comparison groups. A total sample size of n=400 is sufficient to ensure 80% power in a two-tailed significance test at alpha=5%.Discussion: The DiaSurg2 trial will yield long-term data (8 years) on diabetes-associated morbidity and mortality in patients with insulin-dependent T2DM receiving either RYGB or standardized medical care.Trial Registration: The trial protocol has been registered in the German Clinical Trials Register DRKS00004550. [ABSTRACT FROM AUTHOR]