Signals from the Adipocytes

Beta Switch Program

The Beta Switch Weight Loss Program by Sue Heintze

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Leptin, Adiponectin and Resistin Leptin is a peptide expressed and secreted by white adipose tissue, proportionally to fat body mass [2, 7]. Both leptin and its receptor have also been isolated in human gastric mucosa [32], suggesting a possible paracrine regulation of the other gastric peptides [10,32].

Leptin plays a central role in the regulation of energy intake and expenditure. Leptin increases some hours before meals in rodents and after several days of overeating in humans [72], while it decreases during fasting [2].

The main activity of leptin is exerted at the central level, in particular in ARC and PVN [7], via the activation of specific receptors named OB-Rb [73]. Specifically, leptin inhibits NPY and AgRP neurons, achieving a decrease in food intake [2,7,32].

Leptin (ob/ob)- or leptin receptor (db/db)-knockout mice are obese, hyperphagic and hyper-insulinaemic [73, 74]. As in mice, genic mutations leading to leptin deficiency have also been described in humans as a rare cause of obesity that fully normalises during leptin replacement therapy [2]. However, not all obese phenotypes derive from leptin deficiency. In fact, in humans obesity is strongly associated with high plasma leptin levels, suggesting a condition of leptin resistance [75].

Leptin secretion is regulated by several hormonal and metabolic signals [2, 14, 15, 76].

Noteworthy, the gastric release of leptin is also stimulated by the activation of vagal afferents, thus suggesting this hormone to be involved not only in the long-term maintenance of weight balance but also in the cephalic phase of gastric function [32,77].

Adiponectin is a peptide produced exclusively by adipocytes [78]; it shows structural homology with the tumour necrosis factor family [32], cytokines characterised by negative effects on energy balance [7].

Unlike leptin, adiponectin levels do not follow circadian rhythms and seem not to be affected by feeding behaviour [79]. However, it is negatively correlated with body mass index [80] and is decreased in ob/ob mice [32]. The evidence, showing lower adiponectin levels in obese diabetic subjects than in obese non-diabetic subjects, suggests its major role in the development of insulin resistance [32].

Resistin is secreted by adipose tissue and exerts its own activity on several peripheral tissues, such as liver and muscle [32]. It seems to possess inversely related effects to adiponectin: higher levels can increase insulin resistance [81].

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