Abstract
Late-onset hypogonadism (i.e. androgen deficiency) raises the risk for abdominal obesity in men. The mechanism for this obesity is unclear. Here, we demonstrated that hypogonadism after castration caused abdominal obesity in high-fat diet (HFD)-fed, but not in standard diet (SD)-fed, C57BL/6J mice. Furthermore, the phenotype was not induced in mice treated with antibiotics that disrupt the intestinal microflora. In HFD-fed mice, castration increased feed efficiency and decreased fecal weight per food intake. Castration also induced in an increase of visceral fat mass only in the absence of antibiotics in HFD-fed mice, whereas subcutaneous fat mass was increased by castration irrespective of antibiotics. Castration reduced the expression in the mesenteric fat of both adipose triglyceride lipase and hormone-sensitive lipase in HFD-fed mice, which was not observed in the presence of antibiotics. Castration decreased thigh muscle (i.e. quadriceps and hamstrings) mass, elevated fasting blood glucose levels, and increased liver triglyceride levels in a HFD-dependent manner, whereas these changes were not observed in castrated mice treated with antibiotics. The Firmicutes/Bacteroidetes ratio and Lactobacillus species increased in the feces of HFD-fed castrated mice. These results show that androgen (e.g. testosterone) deficiency can alter the intestinal microbiome and induce abdominal obesity in a diet-dependent manner.
Highlights
IntroductionLate-onset hypogonadism (i.e. androgen deficiency) raises the risk for abdominal obesity in men
Late-onset hypogonadism raises the risk for abdominal obesity in men
The degree of digestion, determined by a ratio of dried fecal weight-to-food intake, was decreased by castration in the high-fat diet (HFD)-fed, but was not affected in the standard diet (SD)-fed group (Fig. 1e, p = 0.0040 and 1j). These results indicate that castration-induced hypogonadism caused obesity in a HFD-dependent manner by increasing feed efficiency but not by increasing hyperphagia
Summary
Late-onset hypogonadism (i.e. androgen deficiency) raises the risk for abdominal obesity in men. The Firmicutes/Bacteroidetes ratio and Lactobacillus species increased in the feces of HFD-fed castrated mice These results show that androgen (e.g. testosterone) deficiency can alter the intestinal microbiome and induce abdominal obesity in a dietdependent manner. Hypogonadism (i.e. low testosterone level) increases in men the risk of obesity, cardiovascular diseases, and even mortality[10,11,12,13] through the increase of body fat, in particular visceral fat[14,15]; and testosterone treatment reduces the amount of visceral fat[16] Androgen deprivation therapies, such as either castration or an leteinizing hormone-releasing hormone analog for prostate cancer patients, promote the development of obesity[17,18,19].
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have