Obesity, in general, is associated with decreased adiponectin expression in adipose tissue and plasma levels (7,13). In both men and women, overall obesity, assessed by parameters such as body mass index (BMI) and fat mass, is negatively correlated to adiponectin, although prolonged weight reduction leads to increased adiponectin levels (7,14-17). Nutritional intake does not seem to explain this relationship. Although fasting decreases adiponectin messenger ribonucleic acid (mRNA) levels in mice, serum levels remain unchanged (18). In humans, short-term fasting also does not change plasma levels of adiponectin, although prolonged caloric restriction does result in weight loss and increased adiponectin levels (14,19). Additionally, daily caloric intake, macronutrient intake, or a high-fat meal is not related to any immediate change in circulating adiponectin levels in humans except possibly in obese individuals (20-22).
Instead of food intake, the distribution of adipose tissue may be more closely associated with adiponectin. There is a strong inverse correlation between adiponectin levels and visceral or central fat, compared to subcutaneous fat (9,19). In contrast to subcutaneous adipocytes, human omental adipose tissue had a significant negative correlation with BMI, and only it responded to insulin and PPAR-a agonist administration with increased adiponectin production (23). These findings suggest that adipose tissue, particularly in the visceral distribution, may have an inhibitory mechanism for its own production of adiponectin, perhaps mediated by other factors produced by fat cells such as TNF-a (13).
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