Abstract
The growth hormone (GH)/insulin-like growth factor I (IGF-I) axis is involved in metabolic control. Malnutrition reduces IGF-I and modifies the thermogenic capacity of brown adipose tissue (BAT). Leptin has effects on the GH/IGF-I axis and the function of BAT, but its interaction with IGF-I and the mechanisms involved in the regulation of thermogenesis remains unknown. We studied the GH/IGF-I axis and activation of IGF-I-related signaling and metabolism related to BAT thermogenesis in chronic central leptin infused (L), pair-fed (PF), and control rats. Hypothalamic somatostatin mRNA levels were increased in PF and decreased in L, while pituitary GH mRNA was reduced in PF. Serum GH and IGF-I concentrations were decreased only in PF. In BAT, the association between suppressor of cytokine signaling 3 and the IGF-I receptor was reduced, and phosphorylation of the IGF-I receptor increased in the L group. Phosphorylation of Akt and cyclic AMP response element binding protein and glucose transporter 4 mRNA levels were increased in L and mRNA levels of uncoupling protein-1 (UCP-1) and enzymes involved in lipid anabolism reduced in PF. These results suggest that modifications in UCP-1 in BAT and changes in the GH/IGF-I axis induced by negative energy balance are dependent upon leptin levels.
Highlights
Our results suggest a possible relationship between the reduction in inflammatory factors and the activation of insulin-like growth factor I (IGF-I) signaling in leptin-treated rats that may be associated with an increase in the expression and activity of enzymes implicated in fatty acid synthesis in Brown adipose tissue (BAT)
We found a reduction in signal transducer and activator of transcription 5 (STAT5) activation in the liver of pair-fed rats, parallel to the pattern of growth hormone (GH) levels, which is in accordance with the reduction of serum insulin-like growth factor (IGF)-I found in these rats
Our results indicate that leptin infused rats had a chronic reduction in food intake, the high leptin preserved the expression of uncoupling protein-1 (UCP-1) in BAT, which seem be related with changes in the Akt pathway, while in the pair-fed rats the negative energy balance and the physiological reduction in leptin levels results in decreased UCP-1 in this tissue
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Brown adipose tissue (BAT) is specialized in heat production. Its thermogenic capacity is due to the presence of uncoupling protein-1 (UCP-1) in the inner mitochondrial membrane, which disconnects mitochondrial oxidation of fuel, mainly fatty acids and glucose, from ATP synthesis, dissipating heat [1]. Brown adipocytes have a high number of mitochondria and multilocular lipid stores that provide a rapid source of fatty acids
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