No abstract

A low-calorie diet is associated with an improvement in the systemic inflammatory status. This seems to be due to energy restriction rather than to adipose mass loss, since inflammatory levels return to baseline soon after weight stabilisation. Furthermore, a negative energy balance and fat mobilisation are associated with increased subcutaneous cytokine adipose expression.

Plasma α-ketoglutarate is superior to common liver function tests in obese patients as a surrogate biomarker of NAFLD. The measurement of this biomarker may potentiate the search for a therapeutic approach, may decrease the need for liver biopsy and may be useful in the assessment of disease progression.

INTRODUCTION:Tumor necrosis factor (TNFa) has been invoked as an adipostat. Accordingly, the adipose tissue expression of TNFa has been shown to be proportional to the degree of adiposity. The regulatory role of TNFa in obesity may be controlled by several mechanisms. These include the inhibitory effect on LPL activity, the mediation on glucose homeostasis or the effect on leptin. To assess the role of TNFa in obesity we measured adipocyte TNFa expression in 96 females with a wide range of adiposity and with or without type 2 diabetes. We analysed the relationship between TNFa expression, adipocyte LPL activity, insulin resistance and leptin in this population. RESULTS: The TNFa and leptin expression of the adipose tissue in obese and morbid obese patients were significantly higher than in controls. Obese and morbid obese patients had slightly higher levels of LPL activity, but these differences were not significant. We observed a significant relationship between adipose TNFa expression and body mass index (r ¼ 0.35, P < 0.001). TNFa expression was negatively related to LPL activity (r ¼ 7 0.28, P < 0.05) and positively related to leptin expression (r ¼ 0.35, P < 0.001). CONCLUSION: Our results indicate that obese women, even those with morbid obesity, over-express TNFa in subcutaneous adipose tissue in proportion to the magnitude of the fat depot and independently of the presence of type 2 diabetes. The TNFa system may be a homeostatic mechanism that prevents further fat deposition by regulating LPL activity and leptin production.