Transgenic zero-erucic and high-oleic mustard oil improves glucose clearance rate, erythrocyte membrane docosahexaenoic acid content and reduces osmotic fragility of erythrocytes in male Syrian golden hamsters

Brassica juncea, the Indian mustard variety has high erucic acid (22:1 n-9) in its oil, which causes several deleterious effects. The Centre for Genetic Manipulation of Crop Plants (India) has developed a zero-erucic and high-oleic acid transgenic mustard variety having 67% oleic acid, which is almost equivalent to that of olive oil, i.e. 71%. Therefore, we assessed its impact on erythrocyte osmotic fragility, fluidity and activities of membrane-bound enzymes and insulin sensitivity. 40 male Syrian golden hamsters of 6–8 weeks age, were divided into five groups, consisting of 8 hamsters in each and fed diet containing any one of the oils, i.e. groundnut (GNO), conventional mustard (OCM), low-erucic mustard (OLM), zero-erucic high-oleic transgenic mustard (OTM) and olive (OLO) at 10% level for 16 weeks. At the end, compared to OLO group, OTM-fed hamsters resisted osmotic shock-induced erythrocyte-haemolysis, which corroborated with higher docosahexaenoic acid (DHA; 22:6 n-3) levels in their erythrocyte membranes. However, it did affect neither the fluidity nor the activities of membrane-bound enzymes. Although fasting plasma glucose, insulin and free fatty acid levels were comparable among the various groups; during glucose challenge, OTM diet-fed animals displayed higher disposal rate of circulatory glucose, without altering the insulin levels, when compared to the conventional mustard; OCM. In conclusion, the consumption of oil from zero-erucic high-oleic transgenic mustard improved the DHA content of erythrocyte membrane, which possibly resisted haemolysis and enhanced glucose clearance during glucose overload. However, it did not affect the activities of erythrocyte membrane-bound enzymes and fluidity compared to olive oil. Keywords: Dietary fat, Membrane lipids, Insulin resistance, PUF

Human Papillomavirus (HPV) Infection in Early Pregnancy: Prevalence and Implications

Introduction. Young women (20-35 years) are at high risk of HPV infection, although the majority of the infections are asymptomatic and are cleared spontaneously by the host immune system. These are also the group of women who are sexually active and are in the population of pregnant women. During pregnancy, the changes in the hormonal milieu and immune response may favor persistence of HPV infection and may aid in transgenerational transmission thereby furthering the cancer risk. In the present study, we determined the prevalence of vaginal HPV infection in early pregnancy and attempted to relate with pregnancy outcome. Material and Methods. Vaginal cytology samples were collected from the condoms used to cover the vaginal sonography probe during a routine first trimester visit to the hospital. All women were followed up throughout pregnancy and childbirth. Maternal and neonatal outcomes were recorded. Results. We found a prevalence of HPV infection around 39.4% in our population. Interestingly all HPV positive women were infected with one or more high risk HPV viruses with an overlap of intermediate and low risk in 43% and 7.3%, respectively. Women with preterm prelabor rupture of membranes (PPROM) showed a statistically higher incidence in HPV positive (7.3%) group as compared to the HPV negative (3.2%) group. Conclusion. The prevalence of genital HPV infection is high during pregnancy (around 40%) and was associated with higher incidence of PPROM

Carbenoxolone treatment ameliorated metabolic syndrome in WNIN/Ob obese rats, but induced severe fat loss and glucose intolerance in lean rats.

BACKGROUND: 11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11β-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11β-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity. METHODOLOGY/PRINCIPAL FINDINGS: Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n = 6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11β-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment. CONCLUSIONS/SIGNIFICANCE: We conclude that 11β-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11β-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11β-HSD1 inhibition may lead to insulin resistance in normal conditions

Carbenoxolone Treatment Ameliorated Metabolic Syndrome in WNN/Ob Obese Rats but induced Severe Fat Loss and Glucose Intolerance in Learn Rats

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Effect of carbenoxolone on food intake, body weight and organ weights in WNIN/Ob lean and obese rats.

<p>Values represent means ± SEM of 6 rats per group. LC, Lean control; OC, Obese control; LT, Lean- treated; OT, Obese- treated. Parameters were measured after four weeks of treatment with carbenoxolone (50 mg/kg/body weight/day) or vehicle (same volume of phosphate buffer saline).</p>#<p><i>p</i><0.05,</p>##<p><i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats.</p>*<p><i>p</i><0.05,</p>**<p><i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone- treated animals with vehicle-treated animals of the same phenotype. </p

Effect of carbenoxolone on plasma biochemical parameters in WNIN/Ob lean and obese rats.

<p>(A). Fed-state corticosterone. (B). Fasting corticosterone. (C). Fed-state triglycerides. (D). Fasting triglycerides. (E). Fed-state total cholesterol. (F). Fasting total cholesterol. (G). Fed-state HDL cholesterol. (H). Fasting HDL cholesterol. Plasma parameters were measured after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg bodyweight/day). Empty bars indicate lean phenotype where as filled bars indicate obese phenotype. Values are means ± SEM for 6 animals for group. #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p

Effect of carbenoxolone on adipose tissue morphology and glycogen content.

<p>(A). Adipocyte size (number of cells/16sq.mm). (B). Photographs of adipose tissue sections stained with haematoxylin and eosin (to observe adipocyte cell size). (C). Photographs of adipose tissue sections with Haematoxylin and Eosin (to observe adipose tissue inflammation characterized by presence of ‘crown like structures’-indicated by arrows). (D). Photographs of adipose tissue sections stained with Masson's trichrome stain (to observe fibrosis-indicated by arrows). (E). Tissue glycogen content. Parameters were measured after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg body weight/day). Empty bars indicate lean phenotype, where as filled bars indicate obese phenotype. OC, Obese control; OT, Obese- treated. Images were taken at Magnification of 10X. Values are means ± SEM for 6 animals for group. . #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p

Effect of carbenoxolone on adipose tissue gene expression quantified by semi quantitative reverse transcription PCR.

<p>(A). Stearoyl CoA desaturase 1 (SCD1). (B). Malic enzyme 1 (ME1). (C). Macrophage expressed gene (MPEG). (D). Lysosomal acid lipase (LIPA). (E). Beta3-Adrenergic receptor (β3-AR). Parameters were measured after 4weeks of treatment with carbenoxolone or vehicle (50 mg/kg body weight/day). Empty bars indicate lean phenotype where as filled bars indicate obese phenotype. Relative gene expression was measured using calnexin gene as internal control. Relative expression of gene of interest in lean control was taken as 1. Values are means ± SEM for 4 animals for group. . #<i>p</i><0.05, ##<i>p</i><0.01 and ### <i>p</i><0.001 comparing vehicle-treated lean and obese rats. *<i>p</i><0.05, **<i>p</i><0.01 and *** <i>p</i><0.001 comparing carbenoxolone-treated animals with vehicle-treated animals of the same phenotype.</p