Experimental approach for metabolic disorders as a tool to investigate impact of environment on reproductive health

The epidemics of obesity and diabetes have occurred contemporaneously with increasing use and exposure to environmental endocrine disrupting chemicals. Metabolic disorders affect male reproductive potential due to low sperm count and quality, reduced sperm motility and suppression of testosterone production. In this respect our study aimed to evaluate testiscular cell populations and steroidogenic function in tandem with expression of cell marker tACE (testiscular angiotensin converting enzyme) for delayed germ cell development in experimental conditions of diabetes mellitus (DM) induced on day 1 (neonatally, NDM) or day 10 (prepubertally, PDM) in rats; short and long high-fat diet (HFD) induced obesity in rats since puberty. Our data indicate that metabolic disorders (DM and HFD) affected macro-parameters (decreased gonado-somatic index, increased fat accumulation). Long-term obesity negatively influenced Leydig cell number and testosterone production. Expression of tACE in postmeiotic germ cells showed that prepubertal DM but not neonatal DM caused delay in the first spermatogenesis associated with suppressed Leydig cell development and steroidogenesis in adulthood. Our data indicate that metabolic syndrome involving obesity and diabetes exert negative impact on male reproductive development and function and therefore environmental aspects of endocrine disorders should be considered as a risk factor for male reproductive health.