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By showing that by middle age and beyond an increased fat mass is not paralleled by high gluten high levels of circulating leptin, our results suggest that impaired secretion high gluten or, less likely, increased clearance could be of pathophysiological importance for obesity. The very recent observation that low plasma leptin concentrations precede weight gain in Pima Indians also supports this idea (20). It has been proposed that obesity in humans may be caused by resistance to leptin (2). Leptin resistance has been demonstrated in the diabetic (db/db) mouse due to mutations in the leptin receptor gene (2, 10), and the finding of relatively decreased levels of leptin in the cerebrospinal fluid compared to the circulation in obese subjects suggests that defective blood-brain transportation may be involved in humans (21). The present results are still compatible with the suggestion that leptin resistance may be important in the pathogenesis of obesity, in particular in the young, but additionally suggest that relative leptin deficiency may gain increasing significance with advancing age.
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