Abstract
BackgroundTestosterone deficiency in men is clinically associated with the development of metabolic syndrome, which manifests as obesity, hepatic steatosis, and type-2 diabetes. We investigated the effects of castration-induced testosterone deficiency on body adiposity and the expression of genes related to lipid metabolism and glucose uptake and androgen signaling in male rats fed a normal diet (ND) or a high-fat diet (HFD).MethodsChanges in lipid and glucose metabolism and androgen signaling were investigated at physiological and molecular levels in the muscle, liver, and adipose tissues of non-castrated and castrated rats under ND or HFD feeding.ResultsCastration-induced testosterone deficiency predisposed animals on ND to early development of fatty liver by activating fatty acid (FA) synthesis, whereas HFD activated hepatic FA uptake CD36 expression, leading to the development of hepatic steatosis. In rats fed ND, castration induced muscle fat accumulation by activating CD36 expression. In the subcutaneous fat of ND-fed rats, castration increased adiposity and the expression of FA synthesis-related genes, but it decreased glucose transporter gene expression. In the abdominal fat of rats fed ND, castration increased adiposity by upregulating FA synthesis-related genes, and HFD promoted adiposity by inducing FA uptake, glucose transporter, and FA synthesis-related gene expression. In rats fed ND, castration decreased body growth and muscle weight and downregulated the expression of genes androgen signaling in the longissimus dorsi muscle.ConclusionsTestosterone deficiency increases adiposity in a tissue-specific and diet-dependent manner. Testosterone deficiency decreases body and muscle weights and downregulates androgen signaling.
Highlights
Testosterone plays an important role in lipid and glucose metabolism [1]
We examined the effect of castration on the growth, adiposity, skeletal muscle mass, blood parameters, and expression levels of genes related to lipid metabolism and glucose uptake in the liver, muscle, and sc and ab fat depots in male rats fed a normal diet (ND) or an high-fat diet (HFD) for 9 weeks
Testosterone deficiency increases body adiposity and deregulates expression of genes related to lipid metabolism and glucose uptake in tissue-specific and diet-dependent manners In this study, we found that castration-induced testosterone deficiency increased adiposity in the liver, muscle, and sc and ab fat in rats fed an ND and increased adiposity in the liver and sc and ab fat, but not in the muscle, in rats fed an HFD
Summary
Testosterone plays an important role in lipid and glucose metabolism [1]. Kelly et al [2] suggested that testosterone reduces the deposition of body fat by regulating the expression of genes related to lipid and glucose metabolism. A low testosterone level is predictive of the development of metabolic syndrome, which manifests as obesity, nonalcoholic fatty liver disease, and type-2 diabetes in men [1, 7] and laboratory animals [2, 5]. The effects of testosterone deficiency on adiposity and lipid/ glucose metabolism are controversial. The effects of testosterone deficiency on lipid and glucose metabolism require further investigation. Testosterone deficiency in men is clinically associated with the development of metabolic syndrome, which manifests as obesity, hepatic steatosis, and type-2 diabetes. We investigated the effects of castration-induced testosterone deficiency on body adiposity and the expression of genes related to lipid metabolism and glucose uptake and androgen signaling in male rats fed a normal diet (ND) or a high-fat diet (HFD)
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