Association of lipid profile and obesity in patients with polycystic ovary syndrome.

Objective. Abnormal lipid profile and obesity increase the risk of polycystic ovary syndrome (PCOS). PCOS patients may have a greater risk of infertility, metabolic syndrome (MetS) and cardiovascular disease (CVD) due to abnormal lipid profile and obesity. The aim of the study was to find the association between abnormal lipid profile and obesity in patients with PCOS. Methods. In this case-control study, a total of 102 female subjects (51 diagnosed PCOS and 51 age-matched healthy controls) were enrolled, aged between 20-40 years. Biochemical parameters such as total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), very low-density lipoprotein-cholesterol (VLDL-C), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) were estimated. Anthropometric parameters such as body mass index (BMI), waist circumference (WC), hip circumference (HC), and waist-to-hip ratio (WHR) were recorded. A p<0.05 was considered statistically significant. Results. Mean of BMI, WC, WHR, LH, FSH, TC, TG, LDL-C, and VLDL-C was found significantly elevated in patients with PCOS as compared to controls (p<0.01). However, the mean of HDL-C was found significantly reduced in patients with PCOS as compared to controls (p<0.01). BMI has shown a significant positive correlation with WC (r=0.562, p<0.01) and WHR (r=0.580, p<0.01) among PCOS patients. LH has shown a significant positive correlation with FSH (r=0.572, p<0.01) among PCOS patients. TC has shown a significant positive correlation with TG (r=0.687, p<0.01), LDL-C (r=0.917, p<0.01), and VLDL-C (r=0.726, p<0.01) among PCOS patients. Conclusion. The results showed that abnormal lipid profile and obesity have a significant association with PCOS patients. Regular monitoring and treatment of PCOS patients are required to reduce the risk of infertility, MetS, and CVD.

Evaluation of serum adipokines (omentin-1 and visfatin) in coronary artery disease at a North Indian hospital.

Objective. Adipose tissue is considered to be an endocrine organ that secretes bioactive substances known as adipokines that contribute to the pathophysiology of metabolic and coronary diseases related to obesity. In this study, various novel biomarkers, such as inflammatory markers that are pro-inflammatory (visfatin) and anti-inflammatory (omentin-1), as prognostic indicators for people with coronary artery disease (CAD) were investigated. Methods. In this study, 30 diabetic patients with CAD, 30 diabetic patients without CAD, and 30 healthy control counterparts were included. Serum omentin and visfatin concentrations were evaluated by solid-phase enzyme linked immunosorbent assay (ELISA) kit. Patients with established diagnosis of CAD based on angiography, ECG, and elevated cardiac marker level were included into the study. Patients with cardioembolic stroke, cerebral venous sinus thrombosis, CNS vasculitis, and hemorrhage due to trauma, tumor, vascular malformation, and coagulopathy were excluded. Results. The serum omentin-1 levels were significantly higher in the healthy controls in comparison with the diabetic group (p<0.0001) and serum visfatin levels were significantly higher in the diabetic group in comparison with the healthy controls (p<0.0001). The serum omentin levels were significantly higher in the diabetic group in comparison with the cardio-diabetic group (p<0.0001) and serum visfatin levels were significantly higher in the cardio-diabetic group in comparison with the diabetic group (p<0.0001). The serum omentin-1 showed negative correlation with the serum visfatin in the cardio-diabetic group. Conclusion. The adipokines, such as omentin and visfatin, may be good therapeutic candidates in preventing or ameliorating CAD.

The role of kisspeptin in the pathogenesis of a polycystic ovary syndrome.

Hypothalamic-pituitary gonadal (HPG) axis is responsible for the development and regulation of the female reproductive system. In polycystic ovary syndrome (PCOS), there is a disturbance in the HPG axis. Kisspeptin, a neuropeptide produced by the KISS1 gene, plays a vital role in the regulation of HPG axis by binding with its receptors KISS1R/GPR54, and stimulates gonadotropin secretion from the hypothalamus into pituitary to release luteinizing hormone (LH) and follicle stimulating hormone (FSH). Polymorphisms or mutations in the KISS1 gene can cause disturbance in the kisspeptin signaling pathway and is thought to disrupt HPG axis. Altered signaling of kisspeptin can cause abnormal secretion of GnRH pulse, which leads to increased LH/FSH ratio, thereby affecting androgen levels and ovulation. The increased levels of androgen worsen the symptoms of PCOS. In the present article, we review the molecular physiology and pathology of kisspeptin and how it is responsible for the development of PCOS. The goal of this review article is to provide an overview and metabolic profile of kisspeptin in PCOS patients and the expression of kisspeptin in PCOS animal models. In the present article, we also review the molecular physiology and pathology of kisspeptin and how it is responsible for the development of PCOS.

Determination of Serum Zinc and Phosphorus Levels in Patients with Hypothyroidism.

Various studies reported that serum zinc (Zn) and phosphorus (P) levels altered in patients with hypothyroidism and vice versa, but results were found inconsistent. It was aimed to find the association between serum Zn and P in patients with hypothyroidism. In this case-control study, a total of 100 subjects (50 newly diagnosed patients of hypothyroidism and 50 controls) were enrolled aged between 25 and 60 years. Biochemical parameters such as thyroid profile, serum Zn, and P were estimated in each subject. A p < 0.05 was considered statistically significant. The mean level of body mass index (BMI), thyroid-stimulating hormone (TSH), and serum P was found significantly elevated in cases compared to controls (p < 0.001). However, the mean level of total triiodothyronine (T3), thyroxine (T4), and serum Zn was found significantly reduced in cases compared to controls (p < 0.001). The serum Zn has shown a significant negative correlation with T3 and BMI among cases (r = - 0.313 p < 0.05, r = - 0.338 p < 0.05, respectively). However, serum P has shown a significant positive correlation with TSH and BMI among cases (r = 0.310 p < 0.05, r = 0.449 p < 0.01, respectively). Regression analysis indicated that serum Zn significantly predicted hypothyroidism (p < 0.00). Similarly, serum P significantly predicted hypothyroidism (p < 0.007). Results showed that serum Zn levels were significantly reduced and serum P levels were significantly elevated in cases compared to controls. The serum Zn and serum P both significantly associated with hypothyroidism.

Role of adipokines (omentin and visfatin) in coronary artery disease.

AIMS: Adipose tissue is considered as an endocrine organ that releases bioactive factors known as adipokines which contribute to the pathogenesis of rotundity-linked metabolic and cardiovascular complications. Rotundity is a major predisposer for the development and progression of coronary artery disease (CAD). DATA SYNTHESIS: The literature survey from various databases such as Pubmed/Medline, DOAJ, Scopus, Clarivate analytics/Web of Science and Google Scholar were used to prepare this article. The epidemic of rotundity has gained significant attention to understand the biology of adipocytes and the metabolism of adipose tissue in obese individuals. In CAD, visfatin/NAMPT was primarily indicated as a clinical marker of atherosclerosis, endothelial dysfunction and vascular injury having a prognostic significance. Visfatin/NAMPT is a factor that promotes vascular inflammation and atherosclerosis. Omentin is an anti-inflammatory and anti-atherogenic adipokine regulating cardiovascular functions. CONCLUSIONS: This review highlights and summarizes the scientific information pertaining to the role of the adipokines - omentin and visfatin in CAD.

Validity of Indian Diabetes Risk Score and its association with body mass index and glycosylated hemoglobin for screening of diabetes in and around areas of Lucknow.

OBJECTIVES: The present study aimed to assess the validity of Indian Diabetes Risk Score (IDRS) and its association with body mass index (BMI) and glycosylated hemoglobin (HbA1c) for screening of diabetes and obesity. METHODOLOGY: A cross-sectional study was designed, and samples were randomly enrolled from Lucknow and its adjoining areas. Totally, 405 subjects were included in the study. We used diabetes risk factors (age, waist circumference, physical activity, and family history of diabetes) for screening of diabetes and abdominal obesity (AO) and BMI for screening of general obesity. HbA1c was used for confirming the diabetes patients in this population. Statistical analysis was applied to all data using SPSS software (version 20.0). P < 0.05 was considered statistically significant. RESULTS: All 405 subjects were assessed for diabetic risk factors, BMI, and glycated hemoglobin. Of these, 56.3% subjects were aged ≥50 years. 1° and 2° AO was found in 47.9% and 40% subjects, respectively. About 27.1% subjects were found to have sedentary lifestyle, and 72.6% were found to have no family history of diabetes. According to IDRS, 272 subjects (67.2%) were found at high risk of diabetes (score ≥60). Based on BMI calculation, 198 subjects were obese, of which 79.3% were found at high risk for diabetes. A significant association was found between subjects with higher risk score and BMI (P < 0.001). Assessment of HbA1c showed that 97 (23.9%) were prediabetic and 204 (50.4%) were diabetic, of which 63.9% and 77%, respectively was at high risk for diabetes as per IDRS. A significant association was found between subjects with higher risk score and HbA1c (P < 0.001). CONCLUSION: Our study fully supports the validity of IDRS, as it can be used as a cost-effective tool for primary mass screening of diabetes. Moreover, its combination with BMI value and HbA1c can be used for strict monitoring for diabetes and obesity at primary health care centers to reduce the early development of diabetes complications and severe obesity comorbidities.

Oxidatively Damaged DNA: A Possible Antigenic Stimulus for Cancer Autoantibodies.

Reactive oxygen species (ROS) are cytotoxic at higher concentration resulting in cell death, mutations, chromosomal aberrations or carcinogenesis. In this study DNA was modified by singlet oxygen and superoxide anion radicals generated by illumination of riboflavin under 365 nm UV-light. The modified DNA induced high titre antibodies in experimental animals. In enzyme immunoassay, serum antibodies from cancer patients (n = 34) showed a higher recognition of the modified DNA, as compared to the native form. This was further confirmed by the gel-shift assay. Immune IgG were used as a probe to detect oxidative lesions in the DNA of cancer patients. DNA isolated from lymphocytes of cancer patients proved to be an appreciable inhibitor of the experimentally induced antibodies against the ROS-DNA. This indicates the presence of oxidative lesions in the DNA obtained from cancer patients. The results show that ROS induced oxidative damage to DNA in cancer patients generate neo-epitopes that are alien for the immune system, resulting in autoantibody formation.

Oxygen free radical modified DNA: Implications in the etiopathogenesis of Systemic lupus erythematosus.

The present study was designed to probe the possible role of singlet oxygen and superoxide anion radical modified DNA in the etiopathogenesis of Systemic lupus erythematosus. These species were generated by the exposure of riboflavin to 365 nm UV light. Modified DNA showed single strand breaks, hyperchromicity at 260nm and decrease in Tm. The modified DNA induced high titer antibodies in experimental animals. The antibodies showed reactivity with various nucleic acid polymers, a property commonly associated with Systemic lupus erythematosus anti-DNA autoantibodies. Systemic lupus erythematosus sera showed preferential binding of modified DNA over native DNA in direct binding and competitive binding solid phase immunoassays and band shift assays. The results suggest for the possible involvement of the singlet- superoxide modified DNA as a potential trigger for anti- DNA autoantibody production in SLE and thus in the etiopathogenesis of the disease.