Abstract
The aim of the present study was to evaluate the roles of gonadotropin-inhibitory hormone (GnIH) as an endocrine link between increasing adiposity and impaired testicular function in mice. To achieve this, the effect of GnIH on changes in nutrients uptake and hormonal synthesis/action in the adipose tissue and testis was investigated simultaneously by in vivo study and separately by in vitro study. Mice were treated in vivo with different doses of GnIH for 8 days. In the in vitro study, adipose tissue and testes of mice were cultured with different doses of GnIH with or without insulin or LH for 24 h at 37°C. The GnIH treatment in vivo showed increased food intake, upregulation of glucose transporter 4 (GLUT4), and increased uptake of triglycerides (TGs) in the adipose tissue. These changes may be responsible for increased accumulation of fat in white adipose tissue, resulting in increase in the body mass. Contrary to the adipose tissue, treatment with GnIH both in vivo and in vitro showed decreased uptake of glucose by downregulation of glucose transporter 8 (GLUT8) expressions in the testis, which in turn resulted in the decreased synthesis of testosterone. The GnIH treatment in vivo also showed the decreased expression of insulin receptor protein in the testis, which may also be responsible for the decreased testicular activity in the mice. These findings thus suggest that GnIH increases the uptake of glucose and TGs in the adipose tissue, resulting in increased accumulation of fat, whereas simultaneously in the testis, GnIH suppressed the GLUT8-mediated glucose uptake, which in turn may be responsible for decreased testosterone synthesis. This study thus demonstrates GnIH as mediator of increasing adiposity and impaired testicular function in mice.
Highlights
Nutrition has a significant impact on reproductive processes, including steroidogenesis, gametogenesis, early embryonic development, etc. [1, 2]
The results of present study provide the experimental proof suggesting an active participation of gonadotropin-inhibitory hormone (GnIH) in increased food intake and glucose and TGs uptake in adipose tissue results in fat accumulation and increased body mass whereas in testis, GnIH suppressed glucose uptake resulting in decreased testosterone synthesis
The mice treated in vivo with GnIH showed both dose- and duration-dependent increase in food intake
Summary
Nutrition has a significant impact on reproductive processes, including steroidogenesis, gametogenesis, early embryonic development, etc. [1, 2]. Nutrition has a significant impact on reproductive processes, including steroidogenesis, gametogenesis, early embryonic development, etc. [1, 2] This association is because reproductive activities are energetically expensive, and the brain modulates the reproductive processes according to nutritional availability [3, 4]. The reproductive tissues appears to have a number of “nutrient sensing” mechanisms that may link nutrient status to the reproductive system. Glucose is a very important mediator of nutritional effects on reproduction. Blood concentrations are inversely correlated to energy intake [5]. Glucose is transported by the family of facilitative glucose transporters (GLUTs), which are
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