No abstract available.
Animals ; Cyclosporine* ; Rats* ; Streptozocin*

No abstract available.
Animals ; Pertussis Vaccine* ; Rats* ; Streptozocin* ; Whooping Cough*

No abstract available.
Animals ; Apoptosis* ; Collagen* ; Insulin* ; Rats* ; Streptozocin*

ular thickness in comparison to the non-diabetic rat. This was confirmed histologically. In conclusion, this study suggests that in streptozotocin-induced diabetics, the healing process of bone fracture was impaired and delayed about 2-3 weeks comparing to non-diabetics.
Animals ; Fractures, Bone ; Mandibular Fractures* ; Rats* ; Streptozocin

This study determined the effects of palm vitamin E (TRF) diet on the levels of blood glucose, glycated hemoglobin (gHb), serum advanced glycosylation end-products (AGE) and malondialdehyde (MDA) of diabetic Sprague-Dawley rats. The rats received either control (normal rat chow), TRF diet (normal chow fortified with TRF at 1 g/kg) or Vitamin C diet (vitamin E-deficient but contained vitamin C at 45 g/kg). The animals were maintained on the respective diet for 4 weeks, made diabetic with streptozotocin (STZ), then followed-up for a further 8 weeks. At week-4, mean serum AGE levels of rats given TRF diet (0.7 +/- 0.3 units/ml) were significantly lower than those of control or Vitamin C diet rats (p pounds 0.03). The levels increased after STZ and became comparable to the other groups. At week 12, blood glucose (20.9 +/- 6.9 mM) and gHb (10.0 +/- 1.6%) of rats on TRF diet remained significantly low compared to that of control or Vitamin C diet rats (p pounds 0.03). MDA however, was not affected and remained comparable between groups throughout the study. This study showed that TRF may be a useful antioxidant; effectively prevented increase in AGE in normal rats, and caused decrease in blood glucose and gHb in diabetic rats. Further studies are needed to elucidate the mechanisms of action of TRF.
Rattus norvegicus ; Diet ; Protirelin ; control ; Streptozocin

The effects of insulin and exercise on glucose uptake of skeletal muscle were investigated in soleus muscle isolated from low dose streptozotocin induced diabetic rat in vitro. Glucose uptake was assessed by measuring ³H-methylglucose uptake in vitro. Basal glucose uptake in diabetes was reduced by approximately one-third of the control value (5.6±0.73µMol/g/20min. in diabetes versus 8.4±0.77 in control, P<0.01). There was also a significant decrease (P<0.01) in glucose uptake of diabetes at physiologic insulin concentration (200 µIU/ml) by 40% (6.1±1.20 versus 10.0±0.81). Furthermore, maximal insulin (20000 µIU/ml)-stimulated glucose uptake was 36% lower in diabetes as compared with control (7.3±1.29 versus 11.4±1.29, P<0.01). In contrast, exercise (1.0 km/hr, treadmill running for 45 min.) effect on glucose uptake was so dramatic in diabetes that glucose uptake at basal state was 8.+1.09 and insulin stimulated-glucose uptake were 10.2±1.47 and 11.9±1.64, in 200 and 20000 µIU/ml added insulin, respectively. These results suggest that insulin insensitivity develops in skeletal muscle after 2 weeks of streptozotocin-induced diabetes, but these insensitivity was recovered significantly by single session of running exercise.
Animals ; Glucose* ; In Vitro Techniques ; Insulin* ; Muscle, Skeletal* ; Rats* ; Running ; Streptozocin

In the present study, the effects of alpha lipoic acid (ALA) supplementation on glycemic control and lipid profile in streptozotocin (STZ)-induced diabetic rats have been evaluated. Sprague Dawley rats were divided into nondiabetic (NDM), diabetic without supplementation (No Suppl) and diabetic with ALA groups. ALA was orally administered once a day for 8 weeks with a dose of 100 mg/kg BW. Supplementation of ALA to STZ-induced rats prevented the severe damage to the islet cells of the pancreas and lowered the plasma glucose and glycated hemoglobin (HbA1c) levels. Supplementation of ALA also suppressed the increased of total cholesterol (TC), triglycerides and low density lipoprotein-cholesterol (LDL-C) levels in the plasma of diabetic rats as well as increased high density lipoproteincholesterol (HDL-C) levels. In conclusion, this study suggest that ALA may be effective in controlling glycemic status and improving dyslipidemia in streptozotocin-induced diabetic rats and has the potential in reducing cardiovascular complications due to diabetes mellitus.
Rattus norvegicus ; Streptozocin ; Aminolevulinic Acid ; Dyslipidemia ; Thioctic Acid

Animals ; Dental Implants ; Diabetes Mellitus ; Osseointegration ; Rats ; Streptozocin ; Tibia ; Titanium

In order to elucidate the molecular mechanism of the intracellular Ca2+ overload frequently reported from diabetic heart, diabetic rats were induced by the administration of streptozotocin, the membrane vesicles of junctional SR (heavy SR, HSR) were isolated from the ventricular myocytes, and SR Ca2+ uptake and SR Ca2+ release were measured. The activity of SR Ca2+-ATPase was 562 +/- 14 nmol/min/mg protein in control heart. The activity was decreased to 413 +/- 30 nmol/min/mg protein in diabetic heart and it was partially recovered to 485 +/- 18 nmol/min/mg protein in insulin-treated diabetic heart. A similar pattern was observed in SR 45Ca2+ uptakes; the specific uptake was the highest in control heart and it was the lowest in diabetic heart. In SR 45Ca2+ release experiment, the highest release, 45% of SR 45Ca2+, was observed in control heart. The release of diabetic heart was 20% and it was 30% in insulin-treated diabetic heart. Our results showed that the activitiesof both SR Ca2+-ATPase and SR Ca2+ release channel were decreased in diabetic heart. In order to evaluate how these two factors contribute to SR Ca2+ storage, the activity of SR Ca2+-ATPase was measured in the uncoupled leaky vesicles. The uncoupling effect which is able to increase the activity of SR Ca2+-ATPase was observed in control heart; however, no significant increments of SR Ca2+-ATPase activities were measured in both diabetic and insulin-treated diabetic rats. These results represent that the Ca2+ storage in SR is significantly depressed and, therefore, Ca2+-sequestering activity of SR may be also depressed in diabetic heart.
Animals ; Heart ; Membranes ; Muscle Cells ; Rats* ; Sarcoplasmic Reticulum* ; Streptozocin

Cataracts often occur in diabetic patients or as a consequence of diabetes experimentally induced with alloxan or streptozotocin. In mammals, the transparency of the lens depends on its Ca++ level, and many researchers have proven experimentally that cataracts may occur in cases of increased lens calcium level. In 1981 Fleckenstein et al. were the first to demonstrate experimentally that the cause of cataracts in the alloxan induced diabetic rat is due to an increased lens calcium level, and this calcium induced cataract may be suppressed by the calcium channel blocker-verapamil which prevents lenticular calcium overload. However, they did not determine the mechanism of verapamif on the inhibitory action of lenticular calcium overload. In this experiment verapamil was administrated to control rats and to streptozotocin induced diabetic rats to discover by what mechanism verapamil prevents the occurrence of cataracts as a complication in experimental diabetic rats. The authors compared lens calcium level and measured active 45Ca efflux from the lens, Na+ - Ca++ exchange and Ca++ - ATPase activity in the lens between the control and experimental groups. Their conclusions are as follows: 1. The calcium level of the lens was significantly increased in SDR(Streptozotocin injected diabetic rat) as compared to NDC(Nondiabetic control rat), VNDC(Verapamil treated nondiabetic control rat) and SVDR(Streptozotocin injected verapamil treated diabetic rat). 2. Active 45Ca efflux across the lens membrane was significantly decreased in SDR as compared to NDC, VNDC and SVDR. 3. The Ca++ - ATPase activity was significantly suppressed in SDR as compared to NDC, VNDC and SVDR. 4. Verapamil had no influence on the Na+ - Ca++ exchange transport system in all groups of NDC, VNDC, SDR and SVDR. Thus, our results suggest that verapamil prevents the occurrence of cataracts in diabetic rats probably by controlling the Ca++ transport system in the lens membrane.
Adenosine Triphosphatases ; Alloxan ; Animals ; Calcium Channels ; Calcium* ; Cataract ; Humans ; Mammals ; Membranes ; Rats* ; Streptozocin ; Verapamil*