Effect of obesity on lipolytic activity of adipose tissue in male rats

Obesity has become a major problem in the modern world; it is affected genetically and by lifestyle. Since obesity is associated with multi co-morbidities like dyslipidemia, hypertension, and metabolic syndrome, this work studied the effect of induced obesity on body weight, blood pressure, lipid profile, glycemic state and lipolytic activity of adipose tissue in male rats. Twenty male rats of a body weight ranging from 178 to 200 g were divided equally into two groups, one fed commercial rat chow as a control group [Cgp] and the other fed 10% saturated fat to induce obesity as experimental group [SFgp]. After 3 months the body weight, blood pressure, fasting blood glucose, insulin level, and lipid profile of both groups were measured and the lipolytic activity of adipose tissue was assessed by the amount of free glycerol released. Rats fed saturated fat for 3 months showed significant increase in birth weight, systolic blood pressure, TG, Cholesterol, LDL, fasting blood glucose and insulin levels by 55.3%, 15.86% 24%, 7.92%, 19.58% 20.5% and 26.25% respectively with a significant decline in HDL by 12.9%. Lipolytic activity of SC tissue in the presence of adrenaline decreased significantly by 15%, while in the presence of insulin it increased significantly by 33.33%. It showed a significant increase by 18% and 25.84% in the presence of adrenaline and insulin respectively in visceral adipose tissue. A p value less than 0.05 was considered statistically significant. obesity induced in male rats by high saturated fat diet showed a significant rise in BW and is associated with hypertension, dyslipidemia, hyperglycemia and insulin resistance. The adipose tissue of obese male rats showed a significant decrease in lipolytic activity of SC with a significant rise in the corresponding value in visceral adipose tissue

Effect of insulin resistance on lipolytic activity of adipose tissue in male rats

The excess usage of fructose as a sweetener that we all consume everyday in one way or another has raised the incidence of insulin resistance among the population which is associated with dyslipedemia, hypertension and obesity. This work studied the effect of induced insulin resistance on body weight, blood pressure, lipid profile, glycemic state and lipolytic activity of adipose tissue in male rats. 20 male rats of 129.4 g average body weight were divided equally into two groups. Both had free access to water. The control [Cgp] had pure water, the experimental group [Fgp] had water mixed with 25% of fructose to induce insulin resistance. After 3 months the body weight, blood pressure, fasting blood glucose, insulin levels, lipid profile of both groups were measured and lipolytic activity of adipose tissue was assessed by the amount of free glycerol released. Rats given fructose for 3 months showed significant increase in BW, systolic blood pressure, TG, Cholesterol, LDL, fasting blood glucose and insulin levels by 28.7%, 13.9% 23.9%, 3%, 5.61% 115.49% and 232.8% respectively with a significant decline in HDL by 5.98%. Lipolytic activity of SC and visceral adipose tissue in presence of adrenaline increased significantly by 55.25%, and 78.63% respectively, which runs in parallel with the results obtained in presence of insulin as it showed a significant rise in both SC and visceral adipose tissue by 109.3% and 167.12 respectively. data were statistically significant at p<0.05. Insulin resistance induced in male rat by high fructose consumption showed a significant rise in BW and is associated with hypertension and dyslipidemia with significant rise in lipolytic activity of both SC and visceral adipose tissue

Plasma and cardiac oxytocin during rat gestation and postpartum: evaluation of their effects on the isolated perfused rat heart

Our purpose was to determine the dynamic changes in plasma and cardiac oxytocin during gestation, to study the cardiac effects of oxytocin in the isolated perfused rat heart model and whether pregnancy modifies the hormone's action. Cardiac and plasma oxytocin were evaluated at three stages of gestation [6,13 and 20 days] and at 2 days postpartum. In addition, at the same stages, hearts were excised and attached to a Langendorf's apparatus. Heart rate [HR] and left ventricular developed pressure [LVDP] were measured while being exposed serially to same plasma concentrations of oxytocin observed at each studied stage. Compared with non-pregnant controls, plasma and cardiac oxytocin were significantly and respectively decreased by 41.9%; 38% in early, 42.5%; 36.6% in mid and 8,9%; 47.9% in late gestation, to increase again by 178.1% and 81% postpartum. Hearts from pregnant rats had higher HR, LVDP and delta P/delta t[max] than did hearts from non-pregnant animals. Postpartum, hearts showed lower HR by 9.2%, LVDP by 6.9% and delta P/delta t [max] by 13.9% compared to non-pregnant rats. During pregnancy, reproductive hormones may regulate cardiac oxytocin release and consequently its negative chronotropic and inotropic effects. After parturition, an activated oxytocin system may help the body to get rid of the excess volume

Study of the possible protective role of estrogen in experimentally-induced liver cirrhosis in rats

Chronic liver diseases, such as fibrosis or cirrhosis, are more common in men than in women. This gender difference may be related to the effects of sex hormones on the liver. The aim of the present work was to investigate the effects of estrogen on CCL 4 induced fibrosis of the liver rats. Liver fibrosis was induced in male and female rats by CCL 4 administration in a dose of 2mg/kg/SC/twice weekly. Along with CCL 4 treatment a subgroup of the male rats received estradiol [1mg/kg] twice weekly, while tamoxifen [6mg/kg/day/orally] was given to a female subgroup. At the end of 8 weeks, all the rats were sacrified to study the serum indicators and the livers. The fibrotic response of the female liver to CCL 4 treatment was significantly weaker than that of male liver. In addition, estradiol treatment reduced aspartate aminotransferase [AST] and alanine aminotransferase [ALT] in sera, suppressed hepatic collagen content and malondialdehyde [MDA], decreased the areas of hepatic cirrhosis significantly in male fibrotic rats induced by CCL 4 administration. Whereas, tamoxifen had the opposite effect in female fibrotic rats. We concluded that estradiol reduces CCL 4 induced hepatic fibrosis in rats. The antifibrogenic role of estrogen in the liver may be one reason for the sex associated differences in the progression from hepatic fibrosis to cirrhosis

Role of estrogen on acetylcholine-elicited airway reactivity in ovariectomized rats: study of the possible involved mechanisms

Estrogen replacement therapy [ERT] is frequently prescribed for postmenopausal women. Epidemiological data suggest that sex hormones may play a role in the expression of asthma, but the mechanism[s] whereby this influence is mediated remain[s] unclear. To better understand the role of physiologic doses of estrogens in airway function, we tested the hypothesis that estradiol [E[2], 10 micro g/kg/d for 21 d] given to oophorectomized female rats modifies airway responsiveness to acetylcholine [Ach], compared with oophorectomized rats given placebo. In vitro airway responsiveness was evaluated with the cumulative concentration-response curve [CCRC] of isolated tracheal spirals. Compared with placebo, E[2] treatment significantly increased the EC[50] of Ach but did not alter the CCRC to either carbachol [CCh] or tracheal pre-treatment with physostigmine. In addition, L-arginine pre-incubation of tracheal spirals increased significantly the EC[50] of Ach in the placebo-treated group and this effect was more prominent with E[2]-treatment. L-NAME abolished the effect of L-arginine on the CCRC of the placebo treated spirals, however with E[2]-treatment, this effect was less prominent. We concluded that E[2] treatment decreased airway responsiveness to Ach in ovariectomized rats at least in part by increasing acetylcholine esterase [AChE] activity and by modifying the airway NO production