Indriyanti Rafi Sukmawati
Postgraduate Program in Clinical Biochemistry, Hasanuddin University Jl. Perintis Kemerdekaan Km.10, Makassar

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Adiposopathy and Obesity Paradox Indriyanti Rafi Sukmawati; Andi Wijaya
The Indonesian Biomedical Journal Vol 5, No 1 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i1.45

Abstract

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
Pathomechanism of Insulin Resistance in Men with Central Obesity: Correlation of GGT, GPx, hs-CRP and Plasma Total Cysteine Ritawaty Ritawaty; Indriyanti Rafi Sukmawati; Ilhamjaya Patellongi; Ferry Sandra
The Indonesian Biomedical Journal Vol 5, No 2 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i2.58

Abstract

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