Hormones regulating lipid metabolism and plasma lipids in childhood obesity

Abstract

OBJECTIVE: To review the mechanisms by which leptin, insulin and adiponectin influence lipid metabolism and plasma lipids in obesity, as well as to describe the associations between these hormones in prepubertal children. METHOD: Revision of relevant papers published in the last 5 y related to the interactions of leptin, insulin and adiponectin, with special emphasis on those reporting potential mechanisms by which these hormones regulate lipid metabolism and plasma lipids. We also provide original results concerning the relationships found between plasma lipids and leptin, and insulin and adiponectin in prepubertal obese children. RESULTS: Recent data in the literature shed new light to explain the effects of both leptin and adiponectin in the regulation of lipid metabolism in peripheral tissues. Activation of the AMP-dependent kinase pathway and subsequent increased fatty acid oxidation seems to be the main mechanism of action of these hormones in the regulation of lipid metabolism. In addition, we have found that insulin plasma levels are positively associated to leptin but negatively correlated with adiponectin in obese children. Adiponectin is negatively associated to plasma lipid markers of metabolic syndrome but positively related to HDLcholesterol, whereas insulin and leptin show opposite patterns. These results support the effect of adiponectin in increasing insulin sensitivity and decreasing plasma triglycerides. CONCLUSION: Leptin, insulin and adiponectin are associated hormones that regulate lipid metabolism in childhood. Adiponectin appears to be the missing link to explain the alterations in lipid metabolism and plasma lipids seen in obesity.

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

“…While these effects were correlated to increased leptin sensitivity (with food intake suppression as read-out parameter), it remains to be investigated whether increased leptin signaling is a consequence or a cause of these effects. As such, this sort of interactions might have major implications for the aetiology of obesity and diabetes because these diseases are often characterized by dysregulation of the hypothalamic-pituitary-adrenal axis [43], as well as of altered adipocyte hormone secretion and signaling [44,45].…”

Embryonic stem cell-derived pancreatic endoderm transplant with MCT1-suppressing miR-495 attenuates type II diabetes in mice

“…5D and E). Leptin is a hormone produced by adipose tissue and functions to stimulate glucose uptake and control energy expenditure by facilitating fatty acid oxidation and preventing lipid accumulation through activating AMP kinase [32], therefore serves as another indicator of diabetes and obesity in our study. Plasma leptin concentration after fasting in both mice were significantly increased compared to Sham + ND mice (p<0.05), while no significant difference was found in miR-PE + HFD mice (Fig.…”

Therapeutic Applications of Ghrelin Agonists in the Treatment of Gastroparesis

“…Ghrelin influences fat deposition [36], induces food intake through peripheral and central mechanisms [37] and appears to be involved in the rewarding properties of food intake through enhancement of hedonic and incentive responses to food-related cues [38]. Fasting expression of ghrelin has been shown to be increased by a high fat diet in a mouse model [39] and in patients with anorexia nervosa and cachexia, plasma ghrelin levels are increased while lower plasma ghrelin levels are observed in obese individuals compared to lean persons or controls [40,41]. Clinical trials in humans conducted with ghrelin in cachexia associated with cancer, cardiac and chronic lung disease have also shown increases in appetite, weight and cardiac output without significant toxicity [42][43][44].…”