Reciprocally, adipocyte tissue activity itself depends on the hormonal and nutritional influences that cause fat cells to either store excess nutrients as intracellular lipid, or release stored energy as heat. Adipose tissue modulates energy regulation both by endocrine secretion and by modification of blood nutrient concentrations and quality. The data thus suggest that the changes in adipose tissue differentiation and inflammatory status seen in long-lived mutant mice reflect interruption of GH-dependent irisin inhibition, with consequential effects on metabolism and thermogenesis.Īdipose tissue constitutes the largest endocrine organ in mammals and plays a crucial role in regulating energy homeostasis. Muscles deprived of GH signals, either globally (GKO) or in muscle only (MKO), produce higher levels of circulating irisin and its precursor FNDC5. Experiments with mice with tissue-specific disruption of GHR showed that these adipocyte and macrophage changes were not due to hepatic IGF1 production nor to direct GH effects on adipocytes, but instead reflect GH effects on muscle. Both kinds of long-lived mice show lower levels of inflammatory M1 macrophages and higher levels of anti-inflammatory M2 macrophages in BAT and WAT, with correspondingly lower levels of TNFα, IL-6, and MCP1. These imply increased thermogenesis and are expected to lead to improved glucose control. We report here that white (WAT) and brown (BAT) fat have elevated UCP1 in both kinds of mice, and that adipocytes in WAT depots turn beige/brown. Altered adipose tissue may contribute to the longevity of Snell dwarf and growth hormone receptor (GHR) knock-out mice.
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