Polycystic ovary syndrome (PCOS) is a heterogeneous condition which is related to an endocrine reproductive disorder of females. It affects females of 18–44 age. The persistent hormonal disbalance leads to the complexities such as numerous cysts, an irregular menstrual cycle that ultimately leads to infertility among females. Many candidate genes have been identified to be one of the causes of PCOS. Different studies have been carried out to find the genetic correlation of PCOS. It is essential to carry out such studies that identify the clear cause of PCOS and its genetic association and hormonal disbalance. This review has highlighted different genes and their correlation with PCOS that leads to hormonal disbalance. Yet not in-depth but an attempt to study the genetic predisposition of PCOS.

The present study deals with the diabetic neuropathies prevailing in the male population. In this investigation 100 insulin-dependent diabetes mellitus (IDDM) and 314 non-insulin-dependent diabetes mellitus (NIDDM) patients with and without an objective evidence of neuropathy, having an age span of 15 to 80 years and the duration of diabetes distributed over 1-33 years were included along with age-matched nondiabetic controls. The diabetic subjects were evaluated for semen analysis. Results of semen analysis showed a highly significant increase (p > .0005) in total sperm output and sperm concentration in both IDDM and NIDDM neuropathic diabetic men. On the other hand, sperm motility and semen volume were found to be about 30 and 60% less, respectively, in IDDM and NIDDM patients, where as sperm morphology and quality of sperm motility remained unaffected. A comparison between IDDM and NIDDM neuropathic and non-neuropathic diabetic groups further indicated a nonsignificant difference in the parameters of semen analysis, thus suggesting an endocrine basis for the sexual disturbances of diabetic neuropathy. A significant rise in total sperm output in both IDDM and NIDDM neuropathic diabetic patients and a significant decrease in semen volume in both types of diabetic patients thus suggests some kind of Leydig cell hyperplasia, which in turn may stimulate spermatogenesis and atonia of the bladder and urethra, resulting in retrograde ejaculation.

Diabetic neuropathies were studied in 100 insulin-dependent diabetes mellitus patients, 314 non-insulin-dependent diabetes mellitus patients with and without an objective evidence of neuropathy (age span, 15-80 years; duration of diabetes distributed over 1-33 years), and their age-matched nondiabetic controls. Serum and urinary levels of pituitary-gonadal hormones were evaluated in the diabetic subjects. There were striking results, i.e., a significantly low serum total and serum free (urinary) testosterone level (p < .0005) and a significantly high serum and urinary FSH and LH and serum prolactin level (p < .0005), specifically in the neuropathic diabetic patients, suggesting a series of pathological reactions in the smooth musculature of genital organs characterized by an increase in the interstitial thickness of seminiferous tubules, peritubular and intertubular fibrosis, and tubular sclerosis. Testicular necrosis, probably due to neuropathy, provided an additional aid to confirm these findings. A decrease in semen volume and sperm motility in the diabetic neuropathic patients further suggested the involvement of the entire smooth musculature of the reproductive tract, leading to atonia of the bladder and urethra. Such complications are purely neurogenic. The low serum and urinary testosterone levels and increased serum and urinary FSH and LH and serum prolactin levels in the diabetic men with neuropathy suggest gonadal disorder (hypogonadotropic hypogonadism), which may be due to testicular necrosis and thickening of seminiferous tubules, causing autonomic lesion.

Introduction: Diabetes mellitus (DM) has been a growing epidemic worldwide and poses a major socio-economic challenge. The leading cause of DM death is nephropathy due to end-stage renal disease (ESRD). This study aims to identify the possible association of I/D variants of the ACE gene and M268T (rs699) of the AGT gene of renin-angiotensinaldosterone system (RAAS). Materials and methods: Study subjects include 115 patients with DM, 110 with diabetic nephropathy (DN) and 110 controls. Fasting blood samples were collected for biochemical analyses and PCR amplification of specific regions of the ACE and AGT genes using primers. Results: The distribution of ACE (I/D) II 28.8%, ID 35.6% and DD 35.6% while in DN II 24.5%, ID 41% and DD 34.5%. The AGT (M268T) genotypes were distributed in DM as TT 30.4%, MT 66.9% and MM 2.6% while in DN subjects TT 56.4%, MT 42.7% and MM 0.9%. Conclusion: Significant differences were observed in the DD genotype and D allele of the ACE gene and the TT genotype and T allele of AGT genes between diabetic patients with and without nephropathy. The study may conclude that the D allele polymorphism in the ACE gene and the T allele polymorphism in AGT gene may be considered as genetic risk factors for the development of nephropathy in diabetes.