The aim of this present study was to investigate the effect of bitter gourd extract on insulin sensitivity and proximal insulin signalling pathways in high-fat-fed rats. High-fat feeding of male Wistar rats for 10 weeks decreased the glucose tolerance and insulin sensitivity compared to chow-fed control rats. Bitter gourd extract supplementation for 2 weeks (9th and 10th) of high-fat feeding improved the glucose tolerance and insulin sensitivity. In addition bitter gourd extract reduced the fasting insulin (43 (SE 4·4) v. 23 (SE 5·2) mU/ml, P, 0·05), TAG (134 (SE 12) v. 96 (SE 5·5) mg/dl, P, 0·05), cholesterol (97 (SE 6·3) v. 72 (SE 5·2) mg/dl, P,0·05) and epidydimal fat (4·8 (SE 0·29) v. 3·6 (SE 0·24) g, P, 0·05), which were increased by high-fat diet (HFD). High-fat feeding and bitter gourd supplementation did not have any effect on skeletal muscle insulin receptor, insulin receptor subtrate-1 (IRS-1) and insulin-stimulated insulin receptor tyrosine phosphorylation compared to chow-fed control rats. However high-fat feeding for 10 weeks reduced the insulin-stimulated IRS-1 tyrosine phosphorylation compared to control rats. Bitter gourd supplementation together with HFD for 2 weeks improved the insulin-stimulated IRS-1 tyrosine phosphorylation compared to rats fed with HFD alone. Our results show that bitter gourd extract improves insulin sensitivity, glucose tolerance and insulin signalling in HFD-induced insulin resistance. Identification of potential mechanism(s) by which bitter gourd improves insulin sensitivity and insulin signalling in high-fat-fed rats may open new therapeutic targets for the treatment of obesity/dyslipidemia-induced insulin resistance.
We propose that the oxidative stress response induced by the dengue virus may trigger the inflammatory cytokine responses in dengue severity and thereby contributes to the pathogenesis of the disease; however the interplay between the oxidative response and inflammatory activity in disease virulence needs further study.
The oxidative stress-sensitive c-Jun-N-terminal kinase (JNK) pathway is known to be activated in diabetic condition and is involved in the progression of insulin resistance. However, the effect of antioxidants on JNK pathway and insulin resistance has not been investigated. The present study was aimed to investigate the effect of antioxidants on redox balance, insulin sensitivity, and JNK pathway in high-fat-fed rats. Male Wistar rats were divided into four groups: the control group -received a rodent chow; controlCantioxidant group -fed with rodent chow supplemented with 0 . 2% (w/w) vitamin E, 0 . 3% (w/w) vitamin C, and 0 . 5% (w/w) a-lipoic acid; high-fat groupreceived high-fat diet; and high fatCantioxidant group -fed with high-fat diet supplemented with above antioxidants. Fat feeding to rats for 9 weeks significantly increased IRS-1 serine phoshorylation, reduced insulin-stimulated IRS-1 tyrosine phosphorylation and insulin sensitivity. High-fat diet also impaired redox balance and activated the redox-sensitive serine kinase -JNK pathway. Antioxidant supplementation along with high-fat diet preserved the free radical defense system, inhibited the activation of JNK pathway, and improved insulin signaling and insulin sensitivity. The present study shows for the first time that antioxidants inhibit JNK pathway and IRS-1 serine phosphorylation while improving insulin sensitivity in fat-fed rats. These findings implicate the beneficial effect of antioxidants in obesity-/dyslipidemia-induced insulin resistance in humans.
Oxidative stress in viral infections has been suggested. The study was carried out to assess the oxidative stress in the different clinical spectrums of dengue infection and to evaluate if thrombocytopenia is associated with lipid and protein oxidative injury. Twenty-seven dengue fever (DF), 32 dengue hemorrhagic fever (DHF) and 21 dengue shock syndrome (DSS) cases were studied at 3, 5 and 7 days of illness. Sixty-three healthy subjects were selected as controls. Serum protein carbonyls (PCOs), malendialdehyde (MDA) and total antioxidant status (TAS) were estimated in blood. Dengue infected individuals had significantly high levels of PCOs and MDA on the three days tested in comparison to controls. In DF cases, no significant changes in the levels of MDA and PCOs were found in course of time. However, among DHF and DSS, significant increase in MDA levels was found in the fifth and seventh day samples in comparison to their respective third day sample (P < 0.05). Using one way ANOVA, high PCOs levels were found in DSS in comparison to DF and DHF cases on all the three days tested (P < 0.001). TAS levels were found to be low among DSS on days 5 and 7 and day 7 in DHF when compared with DF cases. Correlation analysis between MDA and hematocrit revealed a significant positive association between them in DHF and DSS on day 5 (DHF r = 0.372; p = 0.024 and DSS r = 0.535; p = 0.0-01) and day 7 (DHF r = 0.412; p = 0.003 and DSS r = 0.765; p < 0.0001). There was an important negative correlation between platelet count and plasma lipid peroxidation levels among DHF and DSS on all three days tested [day 3 (DHF r = -0.392; p = 0.012 and DSS r = -0.453; p = 0.004), day 5 (DHF r = -0.592; p < 0.001 and DSS r = -0.581; p < 0.001) and day 7 (DHF r = -0.418; p = 0.001 and DSS r = -0.515; p = 0.002)]. This study concludes that an increase in oxidative stress was found in dengue viral infection. The level of oxidative stress was maximal in DSS followed by DHF and its severity was minimal in DF. The thrombocytopenia of dengue infection was associated with the extent of lipid peroxidation. Future studies might be carried out to find the role of oxidative damage in the ethiopathogenesis of thrombocytopenia and vascular leakage in dengue infection.
Undergraduate medical students get fewer opportunities to clarify their doubts and to reinforce their understanding of concepts after lecture classes. There is no information available in the literature that addresses the question of usefulness of prior formulation of questions followed by small group discussion by undergraduate medical students as a revision exercise. The purpose of this work is to evaluate the effect of formulation of objective type short answer questions by undergraduate medical students followed by small group discussion on the answers of the questions prepared as a revision exercise on their understanding of the topic "amino acid metabolism" and the retention of the gain after 15 days. At the end of a regular teaching module on the topic of amino acid metabolism, undergraduate medical students were asked to prepare 16 objective type short answer questions on the various aspects of the topic as homework. Small group discussions involving 12-14 students in each group and lasting one hour were conducted on the questions and answers prepared by them in the presence of a faculty member. The effects on low, medium, and high achievers were evaluated with multiple choice questions by pre-test and post-tests before and after the group discussion. Formulation of questions was highly effective in improving understanding on the topic for all the students. The overall mean post-test scores after the formulation of questions (12.6) and after the small group discussion that followed (14.7) were significantly higher than the mean pre-test score (8.5). For high achievers, the gain from formulation of questions was higher than the gain from small group discussion. Small group discussion was highly effective for all students. The gain from small group discussion was higher among the low and medium achievers in comparison with the high achievers. The gain from the exercise was retained among the low, medium, and high achievers after 15 days. In conclusion, formulation of short answer questions followed by small group discussion on the answers of the questions prepared by the undergraduate medical students is an effective revision exercise for improving their understanding on a selected topic.
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