Effect of vitamin E on blood glucose, insulin, lipid peroxides, and antioxidant system of streptozotocin-induced diabetes in rats

There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress which further exacerbates the development and progression of diabetes and its complications. There are multiple sources of oxidative stress in diabetes including non-enzymatic, enzymatic, and mitochondrial pathways. Vitamin E is a fat-soluble vitamin that prevents lipid peroxidation. The present study was carried out to test the effect of vitamin E on blood glucose, insulin, and lipid peroxides in blood and liver tissue of rats in relation to oxidative damage associated with diabetes induced by streptozotocin [STZ]. 24 male albino rats were randomly assigned to control [group I], streptozotocin [STZ]-induced diabetic rats [group II], the third group [vitamin E group] were STZ-induced diabetic rats fed 400 mg of vitamin E/kg diet. After 4 weeks of the induction of diabetes, rats were sacrificed and the following determinations were done on the blood, serum or plasma. Blood glucose, serum insulin, lipid peroxide concentration in plasma as malonyldialdehyde [MDA] level in nmol/g protein, the amount of thiobarbituricp acid reactive materials in plasma [TBARM], serum antioxidant capacity [assayed by measuring the total peroxy radical trapping capacity [TRAP] of serum, and serum superoxide dismutase, enzyme activity [SOD]. In the liver, the following parameters were determined: liver MDA, SOD and Glutathione peroxidase [GSH-Px] enzyme activaties, and Glutathione [GSH] concentration. Hyperglycemia, hypoinsulinemia were regarded in group II which were ameliorated by vitamin E administration. Oxidant stress was found in diabetic rats group II manifested by increase concentration of MDA-plasma and liver, increase TBARM concentration, and TRAP-plasma and serum respectively. Also increased serum SOD, liver SOD, and GSH-Px enzyme activities in these diabetic rats. Administration of vitamin E in the diet decreased the oxidant stress parameters [MDA, TBARM, and TRAP], increased the antioxidant defense parameter [increased GSH concentration in liver], and decreased the oxidant stress as manifested by the decrease in serum SOD enzyme activity; liver SOD; and GSH-Px enzyme activities. Vitamin E was found to be excellent for strengthening the antioxidant defense system in STZ-diabetic rats and it may therefore has a therapeutic role in combating the damaging effect of ROS in diabetes and preventing its complications

Role of oxytocin as regulator of leptin secretion and its relation to biochemical markers [OPG and SRANKL] of bone resorption and formation

Increasing evidences demonstrated many new targets for the hypothalamic hormone oxytocin [OT] supporting the presence of a central neuroendocrine and/or humoral factors that control bone remodeling. The present study was carried out to test the effect of OT on serum leptin level and on the regulation of skeletal homeostasis through measurement of serum levels of osteoprotogerin OPG [secreted glycoprotein of the tumour necrosis receptor superfamily], sRANKL [soluble decoy receptor activator of nuclear factor kappa filigand], calcium and phosphorus. Fifty adult male albino rats used in this study. They were divided into three groups: group I which was subdivided into 3 subgroups, subgroup IA untreated control, IB injected with DM SO [0.16 ml/kg, b.wt x 6 weeks], 1C injected with DMSO [0.08 ml/kg b.wt for 12 weeks]. II OT treated [40 micro/kg b.wt x6 weeks] group. Ill OT [8 micro/kg b.wt x 12 weeks] group. The results obtained showed very high significant increase in OPG level in group [II] compared with subgroups I A and IB and high significant increase of OPG in group [III] compared with subgroup 1C. On the other hand, non significant change was detected in serum levels of sRANKL. As regards serum leptin, a high significant increase was found in group II as compared with subgroups IA and IB and a high significant increase was detected in group [III] compared with IA and 1C subgroups. Serum calcium and phosphorus levels showed very high significant decrease in group [II] compared with IA and IB subgroups and high significant decrease in group [HI] compared with subgroup IA. Also, significant increase in OPG/sRANKL ratio in group [II] compared with IA subgroup. A negative correlation between sRANKL and OPG/sRANKL ratio was obtained in both OT treated groups.The OPG and sRANKL levels obtained in OT treated rats favor increased osteoblast over osteoclast activity and may explain, in part, the imbalance in bone remodeling in favor of bone formation. 'The rise in OPG serum level is probably a homeostatic mechanism to limit bone loss. We can say that leptin should be reappraised as an indicator of energy supplies available for homeostasis, which now includes bone remodeling. We can conclude that the stimulating effect of OT on serum leptin together with increased OPG synthesis indicate anabolic effect on osteoblastic cells to support bone formation and indicate the important role of OPG in bone remodeling and it may be useful for the treatment of osteoporosis associated with increased osteoclast function. OT and leptin can now be added to the array of bone modulating signalling molecules

Glucose-dependent insulin-releasing peptide [GIP] in patients with type 2 diabetes mellitus with and without autonomic neuropathy

This study was conducted to investigate the role of glucose-dependent insulin-releasing peptide or gastric inhibitory polypepetide [GIP] in the control of glycemic state in patients with type 2 diabetes mellitus in the presence and absence of autonomic neuropathy. Twenty patients with type 2 jiabetes mellitus and 10 healthy normal subjects were studied. The diabetic patients were divided into 2 equal groups: one group with autonomic neuropathy [AN] and the other without AN according to cardiovascular autonomic function tests. Patients and controls were subjected to clinical examination and determination of HbA[1c]%, fasting blood sugar and basal insulin level. One-hour after ingestion of standard mixed meal [50 gm carbohydrate and 8% amino acid in 400 ml water] blood samples were collected for determination of glucose, insulin, and GIP plasma levels. Insulin resistance index was calculated from the homeostasis model assessment equation [HOMA]. A significantly impaired postprandial GIP and insulin levels as well as their responses to the ingestion of the mixed meal in the type 2 diabetics with AN was observed compared to those without AN. Postprandial GIP level was found to be correlated negatively with postprandial glucose level [r=-0.54] and positively with postprandial insulin level [r=-0.45], P < 0.05 for all diabetic patients. In diabetic patients with AN, significant -negative correlations were detected between duration of diabetes and postprandial GIP level [r= -0.66], absolute GIP response [r= -0.74], as well as% GIP response [r=- 0.71] [P < /= 0.05 for all.]. GIP plays an important role in the physiologic control of postprandial glucose homeostasis. GIP responses were lower in the diabetics as a group compared with healthy subjects despite similar basal levels. Moreover, In diabetic patients with autonomic neuropathy, there was a delayed and impaired GIP response to the mixed meal. Their absolute and% GIP responses were significantly lower than those of control subjects and patients without autonomic neuropathy

effect of gralic on nitric oxide level in diabetic rats

The increase in number of diabetic patients motivated scientists to find new methods to control such disease. In the present study, the action of Garlic [Allium sativum] was studied on normal and streptozotocin [STZ]-induced diabetic rats. Experimental group included 60 male albino rats divided equally into control group, control group given oral daily dose of garlic [100 mg/kg B.wt] for 16 weeks, STZ-induced diabetic untreated group, and diabetic garlic-treated group included STZ-induced diabetic rats given the daily oral dose of the garlic for 16 weeks. Blood samples were collected for determination of blood glucose, nitric oxide [NO], malondialdehyde [MDA], and lipid profile [triglycerides [TG], cholesterol [C], high density lipoprotein-cholesterol [HDL-C], and low density lipoprotein-cholesterol [LDL-C]]. Supplementation of garlic to non-diabetic rats had produced no significant differences as regards any of the parameters including glucose, lipid profile, nitric oxide, and lipid peroxidation end product malondialdehyde [MDA] levels when compared with the control group. The diabetic rats showed significant elevation in serum glucose, NO, MDA, TG, C, and LDL-C. Concomitantly significant decrease in HDL-C was detected when compared with their corresponding values of controls. However, supplementation of garlic to the diabetic rats had shown a significant decrease in serum glucose, TG, C, LDL-C, NO, [and MDA] levels, while elevation in HDL-C level was detected. Thus, from the present study it is assumed that garlic treatment decreases the blood glucose level. Antioxidant garlic may protect B cells against toxic effect of ROS [reactive oxygen species] provoked due to hyperglycemia. This was indicated by the significant decrease of oxidative stress after garlic treatment in the studied group. It is concluded that garlic supplementation improves blood lipid profiles, strengthens blood oxidant potential, and causes significant reduction in blood glucose; NO; and MDA levels. These results suggest that garlic exerted antioxidant and antihyperglycemic effects