Subcutaneous adipose tissue cytokine production is not responsible for the restoration of systemic inflammation markers during weight loss

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Abstract
It has been suggested that weight loss can improve systemic inflammation associated with obesity by decreasing the adipose production of pro-inflammatory cytokines. This suggestion, however, remains controversial. To analyse the effect of weight loss on peripheral inflammatory markers and subcutaneous adipocytokine production. Patients were studied at baseline, at the end of the weight loss period, and after 2 weeks of weight stabilisation. Nineteen morbid obese non-diabetic patients and 20 lean control subjects. During the weight loss period patients followed a 6-week low-calorie diet. Plasma levels of inflammatory markers, maximal in vitro whole-blood cytokine production, subcutaneous adipose tissue expression and content of several cytokines. Obese subjects had higher circulating levels of C reactive protein (CRP), serum amyloid A (SAA), interleukin IL-6, IL-1 and soluble tumor necrosis factor receptors (sTNFR). Weight loss was associated with a significant decrease in CRP, SAA, leucocytes and plasma IL-6. Maximal in vitro cytokine production of IL-1 and sTNFR1 increased during this period. Weight loss did not induce significant changes in the adipose concentrations of IL-6, IL-1 or sTNF-receptors. However, adipose expression of IL-6, IL-1, TNFalpha, membrane cofactor protein-1 and adiponectin increased at the end of the weight loss period. During weight maintenance, circulating inflammatory parameters increased and in some cases returned to baseline. 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.

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