Endocrine Abstracts

Obesity, a new world syndrome, is defined as excessive white adipose tissue accumulation, that may impair health leading to severe metabolic and reproductive complications affecting millions of people of different age groups. Recent studies have shown that incidence of male obesity induced fertility issues are rising in couples undergoing assisted reproductive technologies suggesting that obesity is emerging as an established risk factor for male infertility or subfertility. Obesity is a multifactorial condition with predominantly genetic and/or environmental causes. No studies have compared genetically inherited and high fat diet induced obesity effects on spermatogenesis. Thus, our present study aims to delineate effects of obesity on spermatogenesis using two male rat models: genetically inherited obese (GIO) – WNIN/Ob and diet induced obese (DIO) – High fat diet. Terminal body weights were similar in both groups, but, differential effects on adiposity index were observed in both the groups. We observed a significant decrease in caudal sperm counts in GIO group but not in DIO group despite body weights being similar in both the groups. To study the specific cause of reduced sperm counts in GIO group, not in DIO group, flow cytometry and germ cell specific marker expression studies in testis revealed that both genetically inherited and diet induced obesity affects mitosis process by increasing spermatogonial proliferation. In GIO group, both meiosis and differentiation process was affected by decreasing spermatocyte population and increasing round spermatid population as well as decrease in elongated spermatid population confirming the decrease in caudal sperm counts whereas in DIO group, it was unaffected. Further, gene expression studies in testis in GIO and DIO group revealed differential expression of genes involved in various aspects of spermatogenesis mainly primary spermatocyte progression and spermiogenesis process, reproductive hormone receptors, leptin signaling molecular players, pro-inflammatory cytokines and cell cycle mediators. Taken together, our study shows that the differences in the effects of genetically inherited and diet induced obesity on spermatogenesis is based on the difference in adiposity index and not due to high terminal body weights. This suggests that the discrepancies in the literature concerning human obesity induced fertility issues could be due to combination of both genetic and environmental factors as well as due to the difference in the amount and distribution of white adipose tissue which could be leading to infertility in some obese individuals but not in all.