Obese Non-diabetic Males Research Articles

Effect of weight loss on serum osteocalcin and its association with serum adipokines.

Studies have suggested that osteocalcin, a bone formation marker, is related to body metabolism and insulin sensitivity. Whether this relation is mediated through an interaction with adipokines remains unclear. The aim of this study was to assess the effect of weight loss on serum osteocalcin and its relation with three adipokines, adiponectin, chemerin, and resistin. Forty-nine obese nondiabetic males completed a four-month dietary program. Body mass index (BMI) decreased significantly from 39.7 ± 7.6 to 37.8 ± 7.6 (P < 0.001). This was associated with significant reduction in waist circumference, fasting blood glucose, HOMA-IR, total and LDL-cholesterol, bone-specific alkaline phosphatase (BAP), and resistin (P < 0.05). There was significant increase in serum adiponectin and undercarboxylated osteocalcin (uOC) (P < 0.001). The changes in uOC levels were negatively correlated with changes in serum triglycerides (r = −0.51, P < 0.001) and positively correlated with changes in BAP (r = 0.52, P < 0.001). In contrast, the changes in uOC were not correlated with changes in BMI, waist circumference, fasting blood glucose, HOMA-IR, total and LDL-cholesterol, hsCRP, vitamin D, and circulating adipokines. We concluded that the increase in serum uOC following weight loss is not related to the changes in circulating adipokines levels.

Correlation Between Adiponectin, Tumor Necrosis Factor-alpha, Insulin Resistance and Atherogenic Dyslipidemia in Non Diabetic Central Obese Males

BACKGROUND: Obesity raises the risk for atherosclerotic cardiovascular disease (ASCVD) through many risk factors including atherogenic dyslipidemia. Atherogenic dyslipidemia is characterized by high levels of triglyceride, increased small dense low density lipoprotein particles, and reduced levels of high density lipoprotein cholesterol. The exact mechanisms of central obesity and this atherogenic lipoprotein phenotype (ALP) is not clearly understood. Central obesity is characterized by a state of systemic low grade inflammation and insulin resistance. Adipose tissue has recently been shown to secrete a variety of bioactive peptides, called adipocytokines, that can potentially affect glucose and lipid metabolism. The aim of this study was to observe the role of adiponectin, tumor necrosis factor-α (TNF- α) and insulin resistance in atherogenic dyslipidemia in nondiabetic central obese males.METHODS: This was a cross-sectional study on 75 non-diabetic central obese male subjects (waist circumferences &gt; 90 cm). Adiponectin and TNF-α testing were performed by ELISA; insulin resistance was assessed by the Homeostasis Model Assessment (HOMA) index, triglyceride was assessed by GPO-PAP, HDL cholesterol and small dense LDL were measured by homogenous method. Statistical analysis was done by SPSS for Windows v. 11.5 with a significance level at p &lt; 0.05. The Pearson and Spearman’s Rho correlation coefficient was used to assess the correlation between various anthropometric and biochemical parameters.RESULTS: There were 75 patients aged 38.0±6.3 years, Adiponectin concentration was 3.55±1.38 μg/ml, HOMA index was 2.28±1.63, TNF-α was 12.42±11.25 pg/ml, triglyceride was 185.17±109.00, HDL-cholesterol was 44.15±9.23 mg/dL, small dense LDL 23.22±12.26 mg/dL. This study revealed that there were correlations between adiponectin and triglyceride (r=-0.236, p=0.042), adiponectin and HDL cholesterol (r=0.300, p=0.009), adiponectin and atherogenic dyslipidemia (r=-0.256, p=0.027), whereas there was no correlation between insulin resistance and TNF-α with the atherogenic dyslipidemia.CONCLUSION: Adiponectin might contribute to atherogenic dyslipidemia in central obese non-diabetic males. Advancing our understanding of the function and measurement of adiponectin serum concentration will be useful in clinical diagnosis of obesity related atherogenic dyslipidemia.KEYWORDS: obesity, waist circumference, adiponectin, insulin resistance, TNF-α, atherogenic dyslipidemia

Dyslipidaemia in hypertensive obese type 2 diabetic patients in Jamaica

IntroductionHypertension and obesity are common problems among diabetic patients accelerating progression of vascular diabetic complications.Materials and methodsA two-stage stratified random sampling design was used, and individuals aged 15 years and over were interviewed. This cross-sectional study evaluated lipid abnormalities of 117 obese type 2 diabetic patients (28 males and 89 females), and 56 hypertensive obese type 2 diabetic patients (22 males and 34 females). Total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C) and high-density lipoprotein cholesterol (HDL-C) concentrations were assayed using standard biochemical methods.ResultsHypertensive obese type 2 diabetic females had significantly higher mean serum concentrations of TC (p = 0.043), TG (p = 0.046), LDL-C (p= 0.040), TC/HDL-C ratio (p = 0.001) and LDL-C/HDL-C ratio (p = 0.003) compared with hypertensive obese non-diabetic females. Similar results were found in hypertensive obese type 2 diabetic males compared with hypertensive obese non-diabetic males. Hypertensive obese type 2 diabetic females had significantly higher serum TC, TG and TC/HDL-C ratio (p < 0.05) than hypertensive obese type 2 diabetic males. Hypertensive obese type 2 diabetic females had significantly higher mean serum concentrations of TG (p = 0.03) and TC (p = 0.01) than obese type 2 diabetic females. There was a significant association between blood glucose and LDL-C concentrations in type 2 diabetic subjects (r = 0.36; p< 0.05).ConclusionObese hypertensive type 2 diabetic females are exposed more profoundly to risk factors including atherogenic dyslipidaemia compared with males.

Fibroblast Growth Factor 21 (FGF21), Free Fatty Acid (FFA), High Sensitivity C-reactive Protein (hsCRP) and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) Among Indonesian Obese Non-Diabetic Males

BACKGROUND: Fibroblast growth factor-21 (FGF21) is known as an important endocrine and paracrine regulator of metabolic homeostasis. Recent studies have shown that FGF21 attenuates lipolysis in human adipocytes, which is suggested as a FGF21's mechanism as anti-hyperlipidemia, anti-hyperglycemia and anti-obesity. The aim of this study was to measure the correlation between FGF21, FFA, hsCRP and HOMA-IR among Indonesian obese non diabetic males.METHOD: The study was observational with cross sectional design. The analysis was done in 137 subjects aged 30-60 years with non diabetic abdominal obesity. We measured the biochemical markers FGF21, FFA, hsCRP, fasting insulin and fasting glucose. We also measured weight, height, waist circumrefence (WC), creatinine, serum glutamin oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT), systolic blood pressure (SBP) and diastolic blood pressure (DBP). Correlation between markers was measured using Pearson and Spearman's analysis. RESULT: There were significant positive correlations between FGF21-HOMA-IR (r=0.314, p=0.000); FGF21-WC (r=0.173, p=0.043); FFA=hsCRP (r=0.270, p=0.001); and WC-HOMA-IR (r=0.279, p=0.001). There was significant negative correlation between FGF21-FFA (r=-0.038, p=0.657) and FGF21-hsCRP (r=-0.061, p=0.482). CONCLUSION: In this study we found that although there was no significant correlation, FGF21 might act as an anti-lipolytic and anti-inflammation agent among Indonesian obese non-diabetic males. Our findings agree with results of previous studies that the positive correlation between FGF21-WC and FGF21-HOMA-IR moght occur as a compensatory mechanism or resistance to FGF21 in obesity.KEYWORDS: Obesity, FGF21, FFA, hsCRP, HOMA-IR

Fibrinogen kinetics and protein turnover in obese non‐diabetic males: effects of insulin

Although hyperfibrinogenemia and insulin resistance are common in obesity and diabetes mellitus, the impact of obesity per se on fibrinogen turnover and the insulin effects on fibrinogen and protein kinetics is unknown. We measured fibrinogen and albumin fractional (FSR) and absolute (ASR) synthesis rates, as well as protein turnover, in non-diabetic, obese and in control male subjects both before and following an euglycemic, euaminoacidemic, hyperinsulinemic clamp, using L-[(2)H(3)]-Leucine isotope infusion. In the obese, basal fibrinogen concentrations was approximately 25% greater (p < 0.035), and fibrinogen pool approximately 45% greater (p < 0.005), than in controls. Both FSR and ASR of fibrinogen were similar to control values. With hyperinsulinemia, although fibrinogen FSR and ASR were not significantly modified with respect to baseline in either group, fibrinogen ASR resulted to be approximately 50% greater in the obese than in controls (p < 0.015). Hyperinsulinemia equally stimulated albumin synthesis and suppressed leucine appearance from endogenous proteolysis in both groups. Amino acid clearance was also similar. In the obese, the insulin-mediated glucose disposal was approximately 50% lower (p < 0.03) than in controls, and it was inversely correlated with fibrinogen ASR during the clamp in both groups (r = - 0.58). In obese, non-diabetic males, post absorptive fibrinogen production is normal. Whole-body amino acid disposal, basal and insulin-responsive protein degradation, and albumin synthesis are also normal. However, the greater fibrinogen ASR in the obese with hyperinsulinemia, and the inverse relationship between insulin sensitivity and clamp fibrinogen production, suggest a role for hyperinsulinemia and/or insulin resistance on fibrinogen production in obesity.

Association of Free Fatty Acid (FFA), Fatty Acid Binding Protein (FABP) and Adiponectin with Tumor Necrosis Factor-alpha (TNF-alpha) and Interleukin-6 (IL-6) Among Obese Non Diabetic Males

BACKGROUND: The prevalence of obesity has increased dramatically in recent years. It is commonly associated with type 2 diabetes, coronary artery disease, and hypertension. White adipose tissue (WAT) is a major site of energy storage and is important for energy homeostasis. WAT has been increasingly recognized as an important endocrine organ that secretes a number of biologically active “adipokines”. The resultant higher FFA, FABP4, FABP5 concentration; and lower concentration of adiponectin is known to be correlated with inflammation. The aim of this study was to observe the correlation between FFA, FABP4, FABP5 and adiponectin with TNF-α and Interleukin-6 as markers of inflammation.METHOD: The study was observational with a cross sectional design. The analysis was done on 69 male subjects aged 30-60 years with non diabetic abdominal obesity which is characterized by waist circumference (WC) 98.7±6.5 cm and fasting blood glucose 87.1±9.7 mg/dL. FFA testing was performed by enzymatic colorimetric assay; whereas FABP4, FABP5, TNF-α, adiponectin and IL-6 were performed by ELISA. All statistical calculations were performed with the SPSS 11.5 statistical software package. We used the Pearson or Spearman’s rho correlation coefficient to assess the correlation between various anthropometric and biochemical measures. We also used path analysis Lisrel 8.30 for Windows.RESULT: This study revealed that there was no correlation between FFA, FABP4 and adiponectin with TNF-α and Interleukin-6, whereas there was correlation between FABP5 with TNF- and Interleukin-6. This study also showed there were correlations between WC and hsCRP (r=0.314, p=0.000), WC and IL-6 (r=0.276, p=0.022), FFA and FABP4 (r=0.263, p=0.029), FABP4 and WC (r=0.249, p =0.039), FABP4 and BMI (r=0.311, p=0.009), FABP5 and TNF- (r=0.408, p=0.000), FABP5 and FABP4 (r=0.296, p=0.014), FABP5 and Interleukin-6 (r=0.248, p=0.04), Adiponectin and HDL-Cholesterol (r=0.301, p=0.012).CONCLUSION: Abdominal obesity might contribute to inflammation in obese nondiabetic males. This study indicated that in abdominal obesity, FFA may induce inflammation through FABP4 and FABP5. Advancing our understanding of the function and measurement of FABP4 and FABP5 serum concentration will give insight into the clinical diagnosis of obesity-related metabolic disorders.KEYWORDS: Obesity, Waist Circumference, Free Fatty Acid (FFA), Fatty Acid Binding Protein (FABP), Adiponectin, TNF-α, Interleukin-6, Inflammation

Gender-Specific Leptinemia and Its Relationship with Some Components of the Metabolic Syndrome in Moroccans

The levels of the liporegulatory hormone leptin are increased in obesity, which contributes to the metabolic syndrome; the latter is associated with elevated cardiovascular risk and morbidity. Leptin may play a role in the metabolic syndrome since correlations have been observed between serum leptin levels and several components of the metabolic syndrome. The association of leptinemia and hypertension or diabetes is inconsistent. Leptin levels are higher in females versus males and obese versus lean individuals. We investigated if correlations exist between leptin levels and several indices of the metabolic syndrome in obese and lean Moroccan subjects with (63 males, 129 females) and without (123 males, 234 females) diabetes and/or hypertension. Plasma glucose and insulin and systolic and diastolic blood pressures were higher in obese versus lean individuals. Obesity had no effect on lipid profile, plasma IGF-1, or C-peptide levels. Leptin levels were higher in females versus males and in obese versus lean individuals. The levels correlated significantly with body mass index. Serum leptin concentration did not correlate with either systolic or diastolic blood pressure, although there was a trend for higher blood pressure with increased leptin levels in females. There was no significant difference in leptin levels between NIDDM patients and healthy controls. However, in hypertensive patients, leptin levels were significantly higher in both lean males and females with diabetes as compared to those without diabetes. Similarly, the higher leptin levels paralleled elevated insulin levels in obese nondiabetic males and females, and in male and female diabetics with hypertension. Correlations were observed between leptin levels and C-peptide (an estimate of endogenous insulin secretion), but not with serum IGF-1. The calculated values of HOMA-IR, a marker of insulin resistance, were somewhat higher, parallel with elevated leptin levels, in obese male and female individuals compared to their lean counterparts. There was no relationship between leptin levels and serum lipids. There was a trend for increased serum uric acid levels with higherleptin concentrations. Thus, leptinemia is related to some components of metabolic syndrome, and in turn, it may contribute to the syndrome. This study is novel in that relationships were determined between leptin levels and various indices of metabolic syndrome in a large population of the same ethnic/regional background.

Endurance training increases the beta-adrenergic lipolytic response in subcutaneous adipose tissue in obese subjects.

The aim of this study was to assess, by longitudinal follow-up, the influence of aerobic training on the in vivo lipolytic activity of adipose tissue in obese male subjects. Eleven obese non-diabetic males, aged 41.5+/-5.77 (range 27-49 y) with body mass index (BMI) 36.5+/-4.5 kg/m2 (range 29.4-47.1 kg/m2) participated in the study. Subjects took part in a 12-week aerobic training program. Before and after training, microdialysis of abdominal subcutaneous adipose tissue (SCAT) was carried out, using perfusion with graded doses of the beta-adrenergic agonist isoprenaline and a single dose of the phosphodiesterase inhibitor theophylline. In addition, the response of plasma glycerol and free fatty acids (FFAs) to intravenous infusion of graded doses of isoprenaline was tested. The training did not induce significant weight loss and promoted an increase in maximum aerobic capacity (P<0.05). The increase of extracellular glycerol in SCAT in response to isoprenaline perfusion was enhanced after the training (P<0.05), while no change in the response of interstitial glycerol to theophylline action was observed. The training did not elicit a change in the isoprenaline-induced changes of blood flow in adipose tissue. The increases of plasma FFAs and glycerol in response to intravenous isoprenaline infusion, were significantly enhanced after training. The present study shows that aerobic training induced an increase in the response of plasma and subcutaneous adipose tissue concentration of glycerol to beta-adrenergic stimulation. The effect of an agent acting at the post-receptor level (theophylline) in SCAT was not modified by training.

ACTH and cortisol response to combined corticotropin releasing hormone-arginine vasopressin stimulation in obese males and its relationship to body weight, fat distribution and parameters of the metabolic syndrome.

To investigate the activity of the hypothalamic-pituitary-adrenal (HPA) axis in male obesity and its relationship with several prominent parameters of the metabolic syndrome. A cross-sectional clinical study of the activity of the HPA axis in groups of obese males and normal-weight controls. Seventeen obese non-diabetic males with a body mass index (BMI) >28 and eight normal-weight controls were examined. Fat free mass (FFM) and fat mass (FM) were measured by bioelectrical impedance, and the waist-to-hip circumference ratio (WHR) was calculated in all subjects. Baseline samples were taken for sex hormone and lipid determination, and an oral glucose tolerance test (OGTT) was performed for glucose and insulin determination. The activity of the HPA axis was determined by the combined administration of human corticotropin releasing hormone (CRH) (100 microg) and arginine vasopressin (AVP) (0.3 IU). As expected, FFM and FM and the WHR were higher in obese men than in controls, as were fasting insulin and stimulated (as area under the curve (AUC)) glucose and insulin concentrations. Baseline adrenocorticotropin (ACTH) and cortisol concentrations were similar in both groups, but stimulated (as AUC), ACTH was higher (P < 0.05) in obese subjects than in controls, whereas no significant difference in cortisolAUC was present. Since the main differences between obese subjects and controls were present during the early 30 min of the test, the correlation coefficients between total and incremental ACTH(AUC 0-30 min) and CortisolAUC 0-30 min and all other variables were analyzed. A significant correlation coefficient was present between them and all anthropometric parameters, fasting insulin and insulinAUC, but not with androgens and gonadotrophins. In addition, a significant correlation was present between total and incremental ACTH(AUC 0-30 min) and triglyceride concentrations. However, after adjusting for BMI or FM values, all correlation coefficients became non-significant, except the one between incremental ACTH(AUC 0-30 min) and insulinAUC (P < 0.05). These findings indicate that obese men may also have an altered pituitary response to combined CRH/AVP stimulation, which appears to be predominantly related to body size and total body fat. ACTH hyperresponsiveness after CRH/AVP stimulation also appears to be related to hyperinsulinaemia, but underlying mechanisms of this relationship remain to be elucidated.