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Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

Authors
  • Baik, Myunggi1, 2, 3
  • Jeong, Jin Young4
  • Park, Seung Ju1, 2
  • Yoo, Seon Pil1, 2
  • Lee, Jin Oh.1, 2
  • Lee, Jae Sung1, 2
  • Haque, Md Najmul1, 2
  • Lee, Hyun-Jeong4
  • 1 Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Republic of Korea , Seoul (South Korea)
  • 2 Seoul National University, Seoul, Republic of Korea , Seoul (South Korea)
  • 3 Institutes of Green Bio Science Technology, Pyeongchang-daero, Daehwa-myeon, Pyoengchang-gun, Gangwon-do, 25354, Republic of Korea , Pyoengchang-gun (South Korea)
  • 4 Rural Development Administration, Wanju-gun, Jeollabuk-do, 55365, Republic of Korea , Wanju-gun (South Korea)
Type
Published Article
Journal
Genes & Nutrition
Publisher
Springer-Verlag
Publication Date
Aug 17, 2020
Volume
15
Issue
1
Identifiers
DOI: 10.1186/s12263-020-00673-1
Source
Springer Nature
Keywords
License
Green

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.

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