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Review
. 2018 Apr 15:465:92-102.
doi: 10.1016/j.mce.2017.09.001. Epub 2017 Sep 4.

The impact of androgen actions in neurons on metabolic health and disease

Jamie J Morford  1 , Sheng Wu  2 , Franck Mauvais-Jarvis  3
Affiliations
Review

The impact of androgen actions in neurons on metabolic health and disease

Jamie J Morford et al. Mol Cell Endocrinol. .

Abstract

The male hormone testosterone exerts different effects on glucose and energy homeostasis in males and females. Testosterone deficiency predisposes males to visceral obesity, insulin resistance and type 2 diabetes. However, testosterone excess predisposes females to similar metabolic dysfunction. Here, we review the effects of testosterone actions in the central nervous system on metabolic function in males and females. In particular, we highlight changes within the hypothalamus that control glucose and energy homeostasis. We distinguish the organizational effects of testosterone in the programming of neural circuitry during development from the activational effects of testosterone during adulthood. Finally, we explore potential sites where androgen might be acting to impact metabolism within the central nervous system.

Keywords: Androgen receptor (AR); Arcuate nucleus (ARC); Central nervous system (CNS); Hypothalamus; Insulin resistance; Metabolism; Obesity; Polycystic ovarian syndrome (PCOS); Sex differences; Testosterone.

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Figures

Figure 1
Figure 1. Testosterone excess during development predisposes females to Type 2 Diabetes (T2D) and Obesity
During development, testosterone acts in the brain to predispose females to T2D by causing insulin resistance. Testosterone excess during development also predisposes females to obesity by enhancing sympathetic output to white adipose tissue (WAT), increasing WAT mass and increasing food intake.
Figure 2
Figure 2. Testosterone deficiency predisposes males to type 2 diabetes and obesity
Testosterone deficiency during adulthood predisposes males to T2D by acting in the brain to contribute to insulin resistance, decreased glucose tolerance, and predisposing to fatty liver. Testosterone deficiency in adult males predisposes to obesity by acting in the brain to increase white adipose tissue mass, decrease energy expenditure, and cause leptin resistance
Figure 3
Figure 3. During adulthood, testosterone excess predisposes females to T2D by causing insulin resistance
Testosterone excess in adult females predisposes them to increased visceral WAT mass, decreased energy expenditure, leptin resistance and decreased locomotor activity.
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