Abstract
Gender differences in the relative risk of developing metabolic complications, such as insulin resistance or non-alcoholic fatty liver disease (NAFLD), have been reported. The deregulation of glycerol metabolism partly contributes to the onset of these metabolic diseases, since glycerol constitutes a key substrate for the synthesis of triacylglycerols (TAGs) as well as for hepatic gluconeogenesis. The present mini-review covers the sex-related differences in glycerol metabolism and aquaglyceroporins (AQPs) and its impact in the control of adipose and hepatic fat accumulation as well as in whole-body glucose homeostasis. Plasma glycerol concentrations are increased in women compared to men probably due to the higher lipolytic rate and larger AQP7 amounts in visceral fat as well as the well-known sexual dimorphism in fat mass with women showing higher adiposity. AQP9 represents the primary route for glycerol uptake in hepatocytes, where glycerol is converted by the glycerol-kinase enzyme into glycerol-3-phosphate, a key substrate for de novo synthesis of glucose and TAG. In spite of showing similar hepatic AQP9 protein, women exhibit lower hepatocyte glycerol permeability than men, which might contribute to their lower prevalence of insulin resistance and NAFLD.
Highlights
GLYCEROL IS AN IMPORTANT VARIABLE IN METABOLIC AND ENERGY HOMEOSTASISGlycerol represents a direct source of glycerol-3-phosphate (G3P), an important metabolite for the control of fat accumulation since it is required for the synthesis of triacylglycerols (TAGs), and for glucose homeostasis, given that it constitutes a major substrate for gluconeogenesis during states of negative energy balance, such as fasting or exercise [1, 2]
Specialty section: This article was submitted to Diabetes, a section of the journal Frontiers in Endocrinology
Plasma glycerol concentrations are increased in women compared to men probably due to the higher lipolytic rate and larger AQP7 amounts in visceral fat as well as the well-known sexual dimorphism in fat mass with women showing higher adiposity
Summary
Glycerol represents a direct source of glycerol-3-phosphate (G3P), an important metabolite for the control of fat accumulation since it is required for the synthesis of triacylglycerols (TAGs), and for glucose homeostasis, given that it constitutes a major substrate for gluconeogenesis during states of negative energy balance, such as fasting or exercise [1, 2]. Circulating free glycerol results from lipolysis, diet-derived glycerol, or glycerol reabsorbed in proximal renal tubules. Intracellular glycerol derives from glucose, via glycolysis, or through the conversion of pyruvate, lactate, and alanine to G3P, a pathway termed glyceroneogenesis occurring in the white and brown adipose tissues, and in the liver to support TAG synthesis, in situations when cycling of TAG is increased [1]
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