Background:Interaction between advanced glycation end product (AGE) and receptor for AGE (RAGE) triggers the escalation of inflammatory cytokine expressions. High-sensitivity C-reactive protein (hsCRP), an important inflammatory marker, has been reported to be modulated by soluble RAGE (sRAGE). However, the relationship between hsCRP and sRAGE in diabetes was not clearly described. Therefore present study was conducted to determine the relationship between sRAGE with hsCRP in men with central obese diabetic and non-diabetic. Materials and Methods: Adult men aged 25-60 years with central obese diabetes and non-diabetes, were recruited. Patient's profiles were collected before the physical and blood examination. Physical examinations were conducted by measuring waist/abdomen, blood pressure, height, and weight. The routine blood test was performed to obtain concentrations of fasting blood glucose, HbA1c, hsCRP and sRAGE level. Results: Fifty-seven subjects with central obese and waist size ≥90 cm were selected. It was found that hsCRP values were significantly different (p=0.000) in HbA1c <6.5% dan HbA1c ≥6.5% groups. There was an inverse relationship between hsCRP and sRAGE levels for both in HbA1c <6.5% (r=-0.073) and HbA1c≥6.5% (r=-0.022) groups. In HbA1c ≥6.5% group, sRAGE showed strong positive correlation with 1 mg/dL ≤ hsCRP <3 mg/dL group (r>0.5). Conclusion:In the early stages of diabetes with hsCRP <1 mg/dL, the protective function was demonstrated with greater sRAGE levels. However, in further phase with 3 ≤ hsCRP < 10 mg/dL, the level of sRAGE was low, which is assumed to be associated with complications. Hence, sRAGE could be suggested as a complementary marker for hsCRP to evaluate diabetic men with central obesity.

BACKGROUND: Gamma glutamyltransferase (GGT) was reported recently to be associated with inflammation, oxidative stress and increased amino acid. However, role of GGT in insulin resistance pathomechanism is not exactly known. Therefore correlation of GGT with inflammation, oxidative stress and elevated amino acid, in men with central obesity need to be confirmed.METHODS: A cross-sectional study was designed. Men with central obesity were recruited and selected. Anthropometric parameters, creatinine, hs-CRP, fasting glucose, fasting insulin, glutathione peroxidase (GPx) activity, GGT, plasma total cysteine (tCys) and fatty liver were measured. Subjects were then divided in 4 groups based on waist circumference (WC) and fatty liver: Group I: WC ≤100 cm, without fatty liver; Group II: WC ≤100 cm, with fatty liver; Group III: WC >100 cm, without fatty liver; Group IV: WC >100 cm, with fatty liver. All biochemical characteristics in each group were then statistically analyzed.RESULTS: Seventy-two men with central obesity were selected. Numbers of subjects in each group were: Group I: n=33; Group II: n=5; Group III: n=17; Group IV: n=17. We found significant difference of HOMA-IR between Group I and IV, significant correlation between GGT and HOMAIR, and significant negative correlation between tCys with HOMA-IR in Group IV.CONCLUSION: GGT was significantly correlated with HOMA-IR in men with WC >100 cm and fatty liver. Further investigation with more subjects is necessary to determine clear GGT cut-off to distinguish subjects with fatty liver and insulin resistance.KEYWORDS: GGT, hs-CRP, GPx, tCys, HOMA-IR, insulin resistance

BACKGROUND: Central obesity is known as a risk factor for type 2 diabetes mellitus (T2DM). Its development is influenced by many factors such as a progressive failure of pancreatic beta cell function. The beta cells increase their function to secret insulin along T2DM development to compensate before it becomes exhausted. Zinc (Zn) plays a crucial role in beta cell function and insulin secretion. The majority of Zn in serum are bound to protein which is not readily available interact with cells. The free Zn in serum has been suggested as being more representative than total Zn in beta cell function. This research aimed to investigate the correlation between serum free Zn and homeostasis model assessment for beta cell function (HOMA-B) and to predict the pancreatic beta cell function in the development of T2DM.METHODS: This study was designed as an observational with a cross-sectional approach. The subjects were centrally obese men aged 30-50 years and who had met the inclusion and exclusion criteria from the screening tests. Control subjects were lean men without T2DM. Serum free Zn and serum total Zn were measured by using inductively coupled plasma-mass spectrometry (ICP-MS).RESULTS: There was positive correlation between serum free Zn and HOMA-B (R=0.361, p-value<0.001) but there was no correlation between serum total Zn and HOMA-B (R=-0.062, p-value=0.563). This study found that if the concentration of serum free Zn >1.7 ug/dL in central obese men was suggested as an excessive function of pancreatic beta cell and as an early warning before its exhausted.CONCLUSION: This study suggested that serum free Zn had a correlation with beta cell function and had a predictive ability for beta cell excessive function before its exhausted.KEYWORDS: Type 2 diabetes mellitus, HOMA-B, serum free zinc, central obesity

BACKGROUND: Obesity has reached global epidemic proportions in both adults and children and is associated with numerous comorbidities, including hypertension, type 2 diabetes mellitus (T2DM), dyslipidemia and major cardiovascular diseases (CVD).CONTENT: Adiposity may cause adipocyte and adipose tissue anatomic and functional abnormalities, termed adiposopathy (adipose-opathy) or "sick fat," that result in endocrine and immune derangements. Adiposopathy may directly contribute to CVD through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD through promoting or worsening major CVD risk factors such as T2DM, high blood pressure, and dyslipidemia. Despite this adverse association, numerous studies have documented an obesity paradox in which overweight and obese people with established CVD, including hypertension, heart failure, coronary heart disease, and peripheral arterial disease, have a better prognosis compared with nonoverweight/nonobese patients. These paradoxical findings are made less paradoxical when the pathogenic potential of excessive body fat is assessed based on adipose tissue dysfunction rather than simply on increased fat mass alone.SUMMARY: Adiposopathy is defined as pathological adipose tissue function that may be promoted and exacerbated by fat accumulation (adiposity) and sedentary lifestyle in genetically susceptible patients. Adiposopathy is a root cause of some of the most common metabolic diseases observed in clinical practice, including T2DM, hypertension and dyslipidemia.KEYWORDS: adiposopathy, adiposity, obesity paradox, adipocyte dysfunction, adipose hypertrophy, adipose hyperplasia

BACKGROUND: Ghrelin has many biological activities such as regulating energy homeostasis and recent studies have shown its effects in the cardiovascular system. Ghrelin concentration decreases in obese man that indicates relatioship between ghrelin and energy homeostasis. Ghrelin also improves endothelial function by increasing the bioavaibility of nitric oxide (NO). The bioavaibility of NO is also influenced by ADMA. ADMA is an endogenous competitive inhibitor of endothelial nitric oxide synthase (eNOS), which is significantly elevated during endothelial dysfuction. This study aimed to evaluate the relationship of ADMA and ghrelin with central obesity based on waist circumference and to evaluate the relationship of total ghrelin and ADMA in centrally obese men. METHODS: Total ghrelin and ADMA were measured in 20 non-obese men (waist circumference (WC) 78.85±4.40 cm) and 60 centrally obese men (WC 97.54±5.94 cm). Anthropometric measurements (height, weight, BM, waist circumference and blood pressure) were also recorded. Statistic were carried out by the Spearman and Pearson bivariate correlation analysis and independent sample T test. RESULTS: ADMA concentrations were significantly higher in centrally obese men than in normal weight controls (p-value <0.05), whereas total ghrelin concentrations were not significantly lower in centrally obese men than in normal weight controls (p-value >0.05). Ghrelin total concentrations were significantly lower in centrally obese men with metabolic syndrome than in normal weight controls (p-value <0.05). No significant correlation existed between total ghrelin and ADMA.CONCLUSIONS: No correlation existed between ADMA and total ghrelin. The pathway of ghrelin in altering vascular function may not involve ADMA.KEYWORDS: ghrelin, ADMA, endothelial dysfunction, obese