In order to study the effects of Chungpyesagantang(淸肺瀉肝湯) on the diabetic rats induced by streptozotocin, during 15 days rats were administered Chungpyesagantang extract after streptozotocin injection (50mg/kg) (sample group). On 2nd, 9th, and 15th day, I investigated the levels of body weight, serum glucose, serum total cholestrol, serum triglyceride. The last day, I killed rats and investigated hepatic lipid peroxidase. The results were obtained as follows: 1. Body weight of the diabetic rats induced by streptozotocin and Chungpyesagantang, as compared with the control group on the 15th day, increased effectively. (p〈0.05 respectively) 2. Glucose levels in serum of the diabetic rats induced by streptozotoc in and Chungpyesagantang, as compared with the control group on the 9th and 15th day, decreased effectively.(p〈0.05 respectively) 3. Total cholesterol levels in serum of the diabetic rats induced by streptozotocin and Chungpyesagantang, as compared with the control group on the 9th and 15th day, decreased effectively.(p〈0.05 respectively ) 4. Triglyceride levels in serum of the diabetic rats induced by streptozotocin and Chungpyesagantang, as compared with the control group on the 9th and 15th day, decreased effectively.(p〈0.05 respectively) 5. On hepatic lipid peroxidethe of the diabetic rats induced by streptozotocin and Chungpyesagantang, as compared with the control group on the 9th and 15th day, decreased effectively.(p〈0.01 respectively)
This study was conducted to investigate the effects of streptozotocin-induced (STZ) diabetes on insulin-like growth factor-I (IGF-I), insulin-like growth factor binding proteins (IGFBPs), and IGF-I carrier proteins in serum, liver, and kidney. The levels of total and free IGF-I were measured by radioimmunoassay (RIA). The patterns of IGFBPs were determined by western ligand blotting (WLB) analysis. The profiles of IGF-I carrier proteins in serum were determined by column chromatography. The levels of total and free IGF-I in serum were lower in STZ-induced diabetic rat than normal rat (p<0.01). Similarly, the levels of total IGF-I in liver was lowered in STZ-induced diabetic rats. On the other hand, the levels of total IGF-I in kidney were increased in STZ-induced diabetic rats compared with normal rats (p<0.01). In serum and liver from STZ-induced diabetic rats, the amount of IGFBP-3 was decreased and the amount of IGFBP-2 was increased compared with normal rats. There was a not difference in amount of IGFBP-4 in serum between STZ-induced diabetic rats and normal rats. The serums of normal rats have higher 150kDa carrier proteins than in STZ-induced diabetic rats, whereas, most of 50kDa carrier proteins were found in STZ-induced diabetic rats. These results demonstrate that in STZ-induced diabetic rats, IGF-I/IGFBPs system that included functional bioactivity was changed in serum as well as tissues, and these changes may play an important role in pathogenesis of diabetes.
Growing evidence indicates that enhanced generation or actions of nitric oxide (NO) are implicated in the pathogenesis of hypertension in spontaneously hypertensive rats and diabetic nephropathy in streptozotocin (STZ)-induced diabetic rats. We investigated whether inducible nitric oxide synthase (iNOS) expression in STZ-induced diabetic rats is responsible for the alterations of vascular reactivity. Diabetic state was confirmed 28 days after injection of STZ (i.p) in rats by measuring blood glucose. In order to evaluate whether short term (4 weeks) diabetic state is related with altered vascular reactivity caused by iNOS expression, isometric tension experiments were performed. In addition, plasma nitrite/nitrate (NOx) levels and expression of iNOS in the lung and aorta of control and STZ-treated rats were compared by using Griess reagent and Western analysis, respectively. Results indicated that STZ-treated rats increased the maximal contractile response of the aorta to phenylephrine (PE), and high $K^+,$ while the sensitivity remained unaltered. Endothelium-dependent relaxation, but not SNP-mediated relaxation, was reduced in STZ-treated rats. Plasma nitrite/nitrates are significantly increased in STZ-treated rats compared to controls. The malondialdehyde (MDA) contents of liver, serum, and aorta of diabetic rats were also significantly increased. Furthermore, nitrotyrosine, a specific foot print of peroxynitrite, was significantly increased in endothelial cells and smooth muscle layers in STZ-induced diabetic aorta. Taken together, the present findings indicate that enhanced release of NO by iNOS along with increased lipid peroxidation in diabetic conditions may be responsible, at least in part, for the augmented contractility, possibly through the modification of endothelial integrity or ecNOS activity of endothelium in STZ-diabetic rat aorta.
The purpose of this study was to investigate the effect of vitamin B6 deficiency on the concentration of energy metabolite in streptozotocin-induced diabetic rats. Thirty rats were fed a vitamin B6 deficient diet(-B6) or a control diet(+B6) for 5 weeks and then subdivided into 3 groups respectively ; base group, one day diabetic group and three day diabetic group. Diabetes of rats were induced by streptozotocin injection into the tail vein. Glucose, glycogen, protein, alanine, triglyceride and free fatty acids were compared in plasma, liver skeletal muscle of rats. Also, the total urinary nitrogen and glucose excretion were compared. Compared with +B6 rats, the increase of plasma glucose in -B6 rats due to the diabetes was smaller. After diabetes was induced, the level of plasma alamine was not changed in -B6 rats while increased significantly(p<0.05) in +B6 rats. The increase of urinary nitrogen excretion was smaller and the increase of muscle protein was larger in -B6 rats at the first day diabetes was induced. The levels of plasma free fatty acid and liver triglyceride were significantly (p<0.05) higher in -B6 rats after diabetes was induced. These results suggest that vitamin B6 deficiency may impair the adaptation of animals to the energy metabolism related due to a decrease of the body protein catabolism of fatty acid oxidation in diabetes and aggravate fatty liver which is one of the chronic complications of diabetes.
Oxidative stress is caused by an imbalance between the production of reactive oxygen and an ability of a biological system, to readily detoxify the reactive intermediates or easily repair the resulting damage. It has been suggested that developmental alloxan-induced liver damage is mediated through increases in oxidative stress. The anti-diabetic effect and antioxidant activity of Phaleria macrocarpa (PM) fractions were investigated in alloxan-induced diabetic rats. After two weeks administration of PM, the liver antioxidant enzyme and hyperglycemic state were evaluated. The results showed that oral administration of PM treatments reduced blood glucose levels in diabetic rats by oral administration (P < 0.05). Serum glutamic-oxaloacetic transaminase (sGOT) and serum glutamic-pyruvate-transaminase (sGPT) were also diminished by PM supplementation. The superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GPx) activities, and glutathione (GSH) level in the alloxan-induced diabetic rats were significantly decreased (P < 0.05) compared to those in the normal rats but were restored by PM treatments. PM fractions also repressed the level of malondialdehyde (MDA) in the liver. Glutathione reductase (GR), glutathione-S-transferase (GST) and $\gamma$-glutamylcysteine synthase (GCS) were also reduced in alloxan-induced diabetic rats. PM fractions could restore the GR and GST activities, but the GCS activity was not affected in rat livers. From the results of the present study, the diabetic effect of the butanol fraction of PM against alloxan-induced diabetic rats was concluded to be mediated either by preventing the decline of hepatic antioxidant status or due to its indirect radical scavenging capacity.
In this study, we investigated the antioxidative effects of So-Dang-Tang (SDT) on streptozotocin (STZ)-induced diabetic rats. Diabetes was induced by intraperitoneal injection of STZ (45 mg/kg body weight) into Sprague-Dawley rats. The SDT (200 mg/kg) and the reference drug, glibenclimide (1mg/kg), were orally administered once a day for 28 days in STZ-induced diabetic rats. The activity of antioxidant enzymes, including those of superoxide dismutase (SOD) and catalase, and the levels of glutathione (GSH) and production of malondialdehyde (MDA) were measured in the liver, kidney, and pancreas of diabetic rats. Treatment with SDT in STZ-induced diabetic rats significantly increased the activities of antioxidant enzymes and GSH levels in the liver, kidney, and pancreas when compared to those of the STZ-control group. SDT also significantly decreased lipid peroxidation product and MDA levels in STZ-induced diabetic rats. These results indicate that SDT has an antioxidative action in STZ-induced diabetic rats.
The number of diabetics in Korea is about 3 to 5 percent of the population, and the incidence is increasing yearly due to changes of life style and food intake. Diet is a key element in the management of diabetes, yet the appropriate diet for diabetes remains controversial. We have recently shown that a diet rich in protein of animal origin(casein) seems beneficial to controling plasma glucose and lipids in streptozotocin-induced diabetic rats. It therefore seemed desirable to find out whether the beneficial effect of high casein diet in experimental diabetes could also be reproduced with a vegetable source of protein(soy). The purpose of this study is to compare these results with the results of our previous study. In the present study, non-diabetic and streptozotocin-induced diabetic rats were studied in order to examine the effects of altering the level(20% vs 60%) of dietary soy protein on blood glucose, lipids, and hormones. Results of the present study showed that a high soy protein diet decreased triglyceride concentration in diabetic rats. However, diabetic rats fed a high soy protein diet were not hypocholesterolemic compared to rats fed a control diet. Moreover, diabetic rats fed a high soy protein diet had significantly increased plasma glucose concentration compared to rats fed a control diet. This study was not able to discern a specific effect of dietary protein level on insulin, glucagon, or insulin/glucagon ratio. Except for the hypotriglyceridemic effect, the results were not similar to the findings of our previous study which showed a beneficial effect on streptozotocin-induced diabetic rats fed a high casein diet.
This study was performed to investigate the effect of a raw diet (RD) on blood glucose and immune function in non-diabetic (normal) and streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley rats were assigned to four groups (normal control, normal RD, diabetic control and diabetic RD). The control groups and the RD groups were fed an AIN-diet and RD for four weeks, respectively. Weight gain was statistically lower in the RD groups than in the controls. Fasting plasma glucose was significantly lower in the diabetic RD group than in the diabetic control group. The $CD4^+$ T-cell population was higher along with the $CD4^+/CD8^+$ ratio of the mesenteric lymph nodes in the normal RD group compared to the other groups. It can be concluded that RD may reduce the plasma fasting glucose concentration in diabetic rats and improve mesenteric lymph node immune function in normal rats.
Diabetes mellitus is associated with vascular complications, including an impairment of vascular function and alterations in the reactivity of blood vessels to vasoactive substances in various vasculature. In the present study, the authors have observed endothelin-B ($ET_B$) receptor agonist-induced relaxation in precontracted mesenteric arterial segments from streptozotocin (STZ)-induced diabetic rats, which was not shown from control rats or in other arterial segments from diabetic rats. Accordingly, the goal of this study was to investigate in what way STZ-induced diabetes altered reactivity of the mesenteric arterial bed and to examine the causal relaxation, if any, between this $ET_B$ receptor-mediated relaxation and endothelial paracrine function, especially nitric oxide (NO) production. The relaxation induced by $ET_B$ agonists was not observed in mesenteric arteries without endothelium. The relaxation to $ET_B$ agonists was completely abolished by pretreatment with BQ788, but not by BQ610. $N_{\omega}-nitro-L-arginine$ methyl ester and soluble guanylate cyclase inhibitors, methylene blue or LY83583 significantly attenuated the relaxant responses to $ET_B$ agonists, respectively. When the expression of eNOS and iNOS was evaluated on agarose gel stained with ethidium bromide, the expression of eNOS mRNA in diabetic rats was significantly decreased, but the expression of iNOS was increased compared with control rats. Furthermore, the iNOS-like immunostaining was densely detected in the endothelium and slightly in the arterial smooth muscle of diabetic rats, but not in control rats. These observations suggest that $ET_B$ receptor may not play a role in maintaining mesenteric vascular tone in normal situation. However, the alterations in $ET_B$ receptor sensitivity were found in diabetic rats and lead to the $ET_B$ agonist-induced vasorelaxation, which is closely related to NO production. In the state of increased vascular resistance of diabetic mesenteric vascular bed, enhanced NO production by activation of iNOS could lead to compensatory vasorelaxation to modulate adequate perfusion pressure to splanchnic area.
Kang, Shin-Jyung;Bao, Cun Liu;Park, Soo-Jin;Kim, Ae-Jung
Nutrition Research and Practice
/
v.4
no.5
/
pp.438-442
/
2010
Rhemannie Radix Preparata (RRP) has been previously employed in traditional oriental medicine as a treatment for diabetic thirst and improving blood flow. The aim of this study was to evaluate its hypoglycemic control by assaying the activities of key enzymes of carbohydrate metabolism in streptozotocin-(STZ)-induced diabetic rats. Further, RRP extracts were prepared in water (RRPW), in 50% ethanol (RRP50), and in 100% ethanol (RRP100), respectively, and compared for their actions in diabetic rats. The oral treatment of RRP (5 mg/kg b.w./d) to diabetic rats for 21 days resulted in a significant decline in blood glucose by 67% compared to diabetic control rats (P < 0.05). The altered activities of glucokinase, glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), and acetyl CoA carboxylase (ACC) in the livers of diabetic rats were reversed significantly to near-normal levels by the administration of RRP (P < 0.05). Among the three RRP extracts, RRP100 was the most effective in terms of hypoglycemic action. However, the administration of RRP to diabetic rats did not improve insulin production. The modulatory effects of RRP100 on the attenuation of carbohydrate enzyme activities appear to hold promise for widespread use for the treatment of diabetes in the future.
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