PCOs is a heterogeneous disorder with anovulation/oligo ovulation usually taken as oligo menorrhoea or amenorrhoea, hyperandrogenemia, hirsutism, acne, androgen alopecia and polycystic ovaries as the key diagnostic feathers. The study was undertaken to investigate the possible protective and ameliorating effects of GABA in Letrozole induced PCOS model in rats by targeting insulin resistance.PCOs in Adult female rat was induced by the daily gastric administration of letrozole (1 mg/kg/day) in CMC (0.5%) for 36 days. Rats were given metformin (2 mg/kg), GABA (100 mg/kg/day) and GABA (500 mg/kg/day) along with letrozole. One group severed as vehicle control. On the 37 day, the animals were euthanized, and anthropometrical, biochemical (glucose, insulin, lipids, testosterone, Estradiol, Progesterone, oral glucose tolerance test, total protein content in ovary, cholesterol level, triglyceride, HDL, LDL), Antioxidants (CAT, POD, GSR, ROS, GSH, TBARS), and histopathological evaluation of ovaries were carried out. Daily colpocytological examination was also carried out until the termination.Both the doses of GABA significantly reduced body weight, body mass index and testosterone. While the levels of CAT, SOD, POD and Estradiol (E2) were significantly increased in the both doses of GABA. A favourable lipid profile, normal glucose tolerance, and decreased in the percentage of estrus smears were observed. Histopathological examination of ovary revealed a decreased in the number of cystic follicles, and decreased in the adipocytes respectively. The effects observed with GABA were comparable to that with metformin.The results suggest that GABA treatment has shown protective effect in PCOs and provide beneficial effect either by reducing insulin resistance or by inducing antioxidant defence mechanisms.
A high-fat diet (HFD) is linked with cytokines production by non-neuronal cells within the hypothalamus, which mediates metabolic inflammation. These cytokines then activate different inflammatory mediators in the arcuate nucleus of the hypothalamus (ARC), a primary hypothalamic area accommodating proopiomelanocortin (POMC) and agouti-related peptide (AGRP) neurons, first-order neurons that sense and integrate peripheral metabolic signals and then respond accordingly. These mediators, such as inhibitor of κB kinase-β (IKKβ), suppression of cytokine signaling 3 (SOCS3), c-Jun N-terminal kinases (JNKs), protein kinase C (PKC), etc., cause insulin and leptin resistance in POMC and AGRP neurons and support obesity and related metabolic complications. On the other hand, inhibition of these mediators has been shown to counteract the impaired metabolism. Therefore, it is important to discuss the contribution of neuronal and non-neuronal cells in HFD-induced hypothalamic inflammation. Furthermore, understanding few other questions, such as the diets causing hypothalamic inflammation, the gender disparity in response to HFD feeding, and how hypothalamic inflammation affects ARC neurons to cause impaired metabolism, will be helpful for the development of therapeutic approaches to prevent or treat HFD-induced obesity.
Non-alcoholic fatty liver disease (NAFLD) is an acquired metabolic disease characterized by triglycerides (TGs) deposition in liver induced by other factors rather than alcohol consumption.NAFLD significantly contributes to liver diseases in children and adults.NAFLD pathogenesis is associated with age, gender, race and ethnicity.Insulin resistance, hyperinsulinemia, elevated plasma free fatty acids (FFAs), fatty liver, hepatocyte injury, liver inflammation, oxidative stress, mitochondrial dysfunction, imbalanced pro-inflammatory cytokines, and fibrosis are the characteristics of NAFLD.Factors including genetic and epigenetic pathways, sedentary lifestyle, sleep, and diet composition affect NAFLD pathogenesis.In this review, we discuss the aetiology, risk factors and pathogenesis of NAFLD.Special focus is given to macro and micro nutrition as causing factors and their role in the prevention of NAFLD pathogenesis.
Objective: To establish the correlation between IMT (presence and severity) of carotid and femoral artery detected on Doppler study and presence of subclinical CAD in asymptomatic patients for early detection of CAD and risk stratification by a non-invasive method. Methodology: This cross-sectional analytic study was conducted in the Cardiology department of Mayo Hospital Lahore for a period of 1 year. One hundred and twenty asymptomatic subjects with and without conventional risk factors for CAD were included The thickness of the intima-media of carotid and the femoral artery was assessed by high-resolution B mode Ultrasonography. The patients enrolled in our study underwent coronary angiography. Data was entered and analyzed through SPSS (Statistical package for social science) version 16. Results: There were a total of 120 patients with a male-to-female ratio of 1.8:1 The mean age of patients was 32.40 ± 10.74 years, minimum age of patients was 20years while the maximum age was 40 years. Most of our patients were overweight, smokers, and had established family history of heart disease. Most of the patients had a single-vessel disease and had severe CAD at the time of presentation. There were 93 patients whose IMT was >0.8 mm. There were 16 patients whose CMIT was <0.8 mm. Sensitivity, specificity, PPV, NPV and diagnostic accuracy of B-mode USG (using CIMT and FA-IMT) were calculated as 85.32%, 72.73%, 96.88%, 33.33% and 84.17% respectively for CMIT. For FA-IMT sensitivity, specify, PPV, NPV and Diagnostic accuracy of B-mode USG was 84.4%, 54.55%, 94.85%, 26.09% and 81.67% respectively. Conclusion: The increased IMT is a predictor of coronary vascular disease, measured non-invasively with B-mode ultrasound. It can be used to predict future cardiovascular events and risk stratification. If patients are diagnosed in the earlier stages then timely treatment can prevent or regress the progression of the disease.
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