scholarly journals Effects of Fermented Houttuynia cordata Thunb. on Diabetic Rats Induced by a High-Fat Diet with Streptozotocin and on Insulin Resistance in 3T3-L1 Adipocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Wannachai Sakuludomkan ◽  
Ranchana Yeewa ◽  
Subhawat Subhawa ◽  
Chakkrit Khanaree ◽  
Arisa Imsumran Bonness ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Biological Properties ◽  
Diabetic Rats ◽  
Human Consumption ◽  
High Fat ◽  
Houttuynia Cordata ◽  
Houttuynia Cordata Thunb

Houttuynia cordata Thunb. (plukaow in Thai language) exhibits several biological properties, and many products of H. cordata are therefore commercially available for human consumption, such as fermented juice or tablets as food supplements. This study aimed to investigate the antidiabetic effects of fermented H. cordata (HC) in high-fat diets and streptozotocin-induced diabetic rats. Oral administration of HC at a dose of 100 mg/kg.bw not only maintained bodyweight, food intake, and water consumption but also reduced blood glucose levels and improved glucose tolerance ability in the diabetic rats. Moreover, HC also decreased oxidative stress markers in serum and inflammatory-related mediators in pancreas tissues, indicating the improvement of pancreatic beta-cell function in the diabetic rats. In order to clarify the mechanism of HC, the effects of ethanolic extract of HC (HCE) on insulin resistance were determined in 3T3-L1 adipocytes. FHE could recover glucose uptake and decrease lipolysis in palmitate-treated 3T3-L1 adipocytes. Taken together, these results demonstrate that HC can improve diabetic symptoms by enhancing insulin sensitivity, reducing oxidative stress, and suppressing inflammation.

scholarly journals Biochemical and Oxidative Changes in High Fat Diet/Streptozotocin-induced Diabetic Rats Treated with Metformin and the Polyherbal Diawell

2019 ◽  
pp. 1-11
Author(s):  
O. N. Briggs ◽  
E. O. Nwachuku ◽  
D. Tamuno-Emine ◽  
N. Nsirim ◽  
K. N. Elechi-Amadi
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
High Fat Diet ◽  
Diabetic Control ◽  
Negative Control ◽  
Diabetic Rats ◽  
High Fat ◽  
Treatment Groups ◽  
Significant Difference ◽  
Oxidant Status

Diabetes mellitus is an epidemic, with a huge disease burden on the patients. This has led to an increase in the use of herbal remedies and combination therapies to reduce this burden. Aim: This study evaluates the biochemical and oxidative changes in type 2 diabetic rats, treated with metformin and the polyherbal drug diawell. Methodology: A total of 35 male Wistar albino rats weighing between 120-220 g were used for this study. The rats were placed on high fat diet, and diabetes was induced by a single intraperitoneal injection of freshly prepared streptozotocin (STZ) (45 mg/kg body wt). Fasting plasma glucose (FPG) was determined using the glucose oxidase method. Fasting plasma insulin (FPI), total oxidant status (TOS), total antioxidant status (TAS) and superoxide dismutase (SOD) levels were quantitatively determined by a rat-specific sandwich-enzyme linked immunosorbent assay (ELISA) method. Insulin resistance (IR) was determined using the homeostatic model assessment for insulin resistance (HOMA-IR) method. Oxidative stress index (OSI) was determined by the ratio of TOS to TAS. Phytochemical analysis was also done on the herbal tablet. Results: Mean FPG levels were significantly lower (p˂0.05) in all groups, except the group administered diawell, which was not significantly different (p>0.05), compared to the diabetic control. Mean FPG levels were significantly higher (p˂0.05) in the metformin group, diawell group, but showed no significant difference (p>0.05) in the combination group, compared to the negative control. HOMA-IR was significantly higher (p<0.05) in the diabetic control compared to the negative control and treatment groups. The metformin and diawell groups had significantly higher (p˂0.05) HOMA-IR values, whereas the combination (metformin + diawell) showed no significant difference (p>0.05) when compared to the negative control. TOS was significantly higher (p<0.05) in the diabetic control compared to the negative control and treatment groups. The metformin and diawell groups had significantly higher (p˂0.05) TOS values, whereas the combination (metformin + diawell) showed no significant difference (p>0.05) when compared to the negative control. There was significantly lower (p˂0.05) TAS levels in the diabetic and treatment groups, compared to the negative control. OSI values were significantly lower (p˂0.05) in all groups when compared to the diabetic control. Also, OSI values were significantly higher (p˂0.05) in the treatment groups compared to the negative control. Conclusion: There was depletion of antioxidant parameters and an increase in oxidative stress in the diabetic rats. Administration of metformin and the polyherbal tablet diawell individually, were not effective in correcting the pathological and biochemical changes associated with diabetes. However, the combination treatment produced a better glycaemic response and attenuated the oxidant status in the rats. Antioxidant therapy should be incorporated in diabetes management, and anti-diabetic herbals properly evaluated.

scholarly journals Gymnemic acid, a potent antidiabetic agent protects skeletal muscle from hyperglycemia mediated oxidative stress and apoptotic events in High fat and High fructose diet fed adult rats

2020 ◽  
Vol 11 (2) ◽  
pp. 1526-1538
Author(s):  
Porkodi Karthikeyan ◽  
Lakshmi Narasimhan Chakrapani ◽  
Thangarajeswari Mohan ◽  
Bhavani Tamilarasan ◽  
Pughazhendi Kannan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Diabetic Rats ◽  
High Fat ◽  
Gymnemic Acid ◽  
High Fructose ◽  
Type 2 Diabetic

Type 2 diabetes is delineated by impaired metabolic flexibility, and intramyocellular lipid accumulation, causing insulin resistance, particularly in skeletal muscle by reducing insulin-stimulated glucose uptake. High-fat diet and high fructose (HFD and HF) administration in rodents bestows a model for hyperlipidemia, insulin resistance, and Type 2 diabetes. The current study is focused on elucidating the role of Gymnemic acid in combating hyperglycemia mediated oxidative stress and apoptotic events in the skeletal muscle of HFD and HF induced Type 2 diabetes in Wistar albino rats by boosting antioxidant defense system. Gymnemic acid, a saponin of triterpene glycoside contained in leaves of Gymnema Sylvestre, has potent anti-diabetic properties. Treatment with Gymnemic acid restored the antioxidant status (Gpx, SOD, CAT, GR, Vit C & Vit E) with significant (p<0.05) decrease in free radical levels and reinvigorated the expression of apoptotic and antiapoptotic proteins in Type 2 diabetic rats. Histopathological data demonstrate that oral administration of Gymnemic acid protects skeletal muscle fibers from an oxidative niche in HFD and HF in Type 2 diabetic rats. In accordance with this, Gymnemic acid might be regarded as a promising therapeutic agent against Type 2 diabetes, thereby restoring skeletal muscle integrity and function.

scholarly journals Effect of polyherbal drug on oxidative stress and insulin resistance in high-fat diet-induced type 2 diabetic rats

All Life ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 310-320
Author(s):  
Rahul Gopalakrishnan ◽  
Nandhakumar Elumalai ◽  
Renuka Alagirisamy
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
High Fat ◽  
Type 2 Diabetic

scholarly journals Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

2010 ◽  
Vol 299 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Jill K. Morris ◽  
Gregory L. Bomhoff ◽  
John A. Stanford ◽  
Paige C. Geiger
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Locomotor Activity ◽  
Substantia Nigra ◽  
High Fat Diet ◽  
Model Assessment ◽  
High Fat

Despite numerous clinical studies supporting a link between type 2 diabetes (T2D) and Parkinson's disease (PD), the clinical literature remains equivocal. We, therefore, sought to address the relationship between insulin resistance and nigrostriatal dopamine (DA) in a preclinical animal model. High-fat feeding in rodents is an established model of insulin resistance, characterized by increased adiposity, systemic oxidative stress, and hyperglycemia. We subjected rats to a normal chow or high-fat diet for 5 wk before infusing 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our goal was to determine whether a high-fat diet and the resulting peripheral insulin resistance would exacerbate 6-OHDA-induced nigrostriatal DA depletion. Prior to 6-OHDA infusion, animals on the high-fat diet exhibited greater body weight, increased adiposity, and impaired glucose tolerance. Two weeks after 6-OHDA, locomotor activity was tested, and brain and muscle tissue was harvested. Locomotor activity did not differ between the groups nor did cholesterol levels or measures of muscle atrophy. High-fat-fed animals exhibited higher homeostatic model assessment of insulin resistance (HOMA-IR) values and attenuated insulin-stimulated glucose uptake in fast-twitch muscle, indicating decreased insulin sensitivity. Animals in the high-fat group also exhibited greater DA depletion in the substantia nigra and the striatum, which correlated with HOMA-IR and adiposity. Decreased phosphorylation of HSP27 and degradation of IκBα in the substantia nigra indicate increased tissue oxidative stress. These findings support the hypothesis that a diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure.

Triterpenoid-Rich Fraction from Ilex hainanensis Merr. Attenuates Non-Alcoholic Fatty Liver Disease Induced by High Fat Diet in Rats

2013 ◽  
Vol 41 (03) ◽  
pp. 487-502 ◽  
Author(s):  
Wei-Xi Cui ◽  
Jie Yang ◽  
Xiao-Qing Chen ◽  
Qian Mao ◽  
Xiang-Lan Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Cyp2e1 Expression ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) has become a major challenge to the healthcare system. This study was designed to evaluate the effect of the triterpenoid-rich fraction (TF) from Ilex hainanensis Merr. on NAFLD. Male Sprague-Dawley (SD) rats were fed a normal diet (control) or high fat diet (NAFLD model). After four weeks, the high fat diet group was orally administrated TF (250 mg/kg) for another two weeks. High fat diet fed rats displayed hyperlipidemia and a decline in liver function compared with control. However, administration with TF could effectively improve these symptoms, as demonstrated by decreasing the plasma levels of triglyceride (p <0.05), total cholesterol (p < 0.01), low-density lipoprotein cholesterol (p < 0.05), alanine transaminase (p < 0.05), aspartate aminotransferase (p < 0.01), liver index (p < 0.05) and insulin resistance index (p < 0.05) while increasing the high-density lipoprotein cholesterol (p < 0.05). Meanwhile, histopathological examination of livers also showed that TF could reduce the incidence of liver lesions induced by high fat diet. Furthermore, TF could alleviate oxidative stress and inflammation status indicated by the decline malondialdehyde and superoxide dismutase levels (p < 0.01, both) and levels of interleukin 6 and tumor necrosis factor-α (p < 0.05). In addition, immunohistochemistry showed TF evidently elevated the peroxisome proliferator-activated receptor (PPARα) expression (p < 0.01), while it diminished the Cytochrome P450 2E1 (CYP2E1) expression (p < 0.01) in liver. These results demonstrate that TF has potential ability to protect liver against NAFLD by regulating lipids metabolism and alleviating insulin resistance, inflammation and oxidative stress. This effect might be associated with regulating PPARα and CYP2E1 expression.

scholarly journals Maternal high-fat diet induces insulin resistance and deterioration of pancreatic β-cell function in adult offspring with sex differences in mice

2014 ◽  
Vol 306 (10) ◽  
pp. E1163-E1175 ◽  
Author(s):  
Hisashi Yokomizo ◽  
Toyoshi Inoguchi ◽  
Noriyuki Sonoda ◽  
Yuka Sakaki ◽  
Yasutaka Maeda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Sex Differences ◽  
High Fat Diet ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Plasma Estradiol ◽  
Β Cell Function ◽  
Estradiol Levels

Intrauterine environment may influence the health of postnatal offspring. There have been many studies on the effects of maternal high-fat diet (HFD) on diabetes and glucose metabolism in offspring. Here, we investigated the effects in male and female offspring. C57/BL6J mice were bred and fed either control diet (CD) or HFD from conception to weaning, and offspring were fed CD or HFD from 6 to 20 wk. At 20 wk, maternal HFD induced glucose intolerance and insulin resistance in offspring. Additionally, liver triacylglycerol content, adipose tissue mass, and inflammation increased in maternal HFD. In contrast, extending previous observations, insulin secretion at glucose tolerance test, islet area, insulin content, and PDX-1 mRNA levels in isolated islets were lower in maternal HFD in males, whereas they were higher in females. Oxidative stress in islets increased in maternal HFD in males, whereas there were no differences in females. Plasma estradiol levels were lower in males than in females and decreased in offspring fed HFD and also decreased by maternal HFD, suggesting that females may be protected from insulin deficiency by inhibiting oxidative stress. In conclusion, maternal HFD induced insulin resistance and deterioration of pancreatic β-cell function, with marked sex differences in adult offspring accompanied by adipose tissue inflammation and liver steatosis. Additionally, our results demonstrate that potential mechanisms underlying sex differences in pancreatic β-cell function may be related partially to increases in oxidative stress in male islets and decreased plasma estradiol levels in males.

scholarly journals Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiac Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Serum Adiponectin ◽  
Diabetic Rat ◽  
Lv Function ◽  
High Dose ◽  
And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

Prenatal androgen excess impairs beta cell function by decreased Sirtuin3 expression

2021 ◽  
Author(s):  
Yu Zhou ◽  
Min Gong ◽  
Yingfei Lu ◽  
Jianquan Chen ◽  
Rong Ju
Keyword(s):  
Oxidative Stress ◽  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Female Offspring ◽  
Sirtuin 3 ◽  
Prenatal Testosterone ◽  
Pancreatic Beta Cell Function ◽  
Prenatal Androgen

Prenatal androgen exposure induces metabolic disorders in female offspring. However, the long-term effect of maternal testosterone excess on glucose metabolism, especially on pancreatic beta cell function, is rarely investigated. Our current study mainly focused on the effects of prenatal testosterone exposure on glucose metabolism and pancreatic beta cell function in aged female offspring. By using maternal mice and their female offspring as animal models, we found that prenatal androgen treatment induced obesity and glucose intolerance in aged offspring. These influences were accompanied by decreased fasting serum insulin concentration, elevated serum triglyceride and testosterone concentrations. Glucose stimulated insulin secretion in pancreatic beta cells of aged female offspring was also affected by prenatal testosterone exposure. We further confirmed that increased serum testosterone contributed to down regulation of Sirtuin 3 expression, activated oxidative stress and impaired pancreatic beta cell function in aged female offspring. Moreover, over-expression of Sirtuin 3 in islets isolated from female offspring treated with prenatal testosterone normalized the oxidative stress level, restored cyclic adenosine monophosphate and adenosine triphosphate generation, which finally improved glucose stimulated insulin secretion in beta cells. Taken together, these results demonstrated that prenatal testosterone exposure caused metabolic disturbance in aged female offspring via suppression of Sirtuin 3 expression and activation of oxidative stress in pancreatic beta cells.

Sign in / Sign up

Export Citation Format

Share Document