scholarly journals Glycine Increases Insulin Sensitivity and Glutathione Biosynthesis and Protects against Oxidative Stress in a Model of Sucrose-Induced Insulin Resistance

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Mohammed El-Hafidi ◽  
Martha Franco ◽  
Angélica Ruiz Ramírez ◽  
José Santamaria Sosa ◽  
José Antonio Pineda Flores ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Receptor ◽  
Redox Status ◽  
Glutathione Biosynthesis ◽  
Stress Markers ◽  
Glutamylcysteine Synthetase ◽  
Key Enzyme ◽  
And Oxidative Stress

Oxidative stress and redox status play a central role in the link between insulin resistance (IR) and lipotoxicity in metabolic syndrome. This mechanistic link may involve alterations in the glutathione redox state. We examined the effect of glycine supplementation to diet on glutathione biosynthesis, oxidative stress, IR, and insulin cell signaling in liver from sucrose-fed (SF) rats characterized by IR and oxidative stress. Our hypothesis is that the correction of glutathione levels by glycine treatment leads to reduced oxidative stress, a mechanism associated with improved insulin signaling and IR. Glycine treatment decreases the levels of oxidative stress markers in liver from SF rats and increases the concentrations of glutathione (GSH) and γ-glutamylcysteine and the amount of γ-glutamylcysteine synthetase (γ-GCS), a key enzyme of GSH biosynthesis in liver from SF rats. In liver from SF rats, glycine also decreases the insulin-induced phosphorylation of insulin receptor substrate-1 (ISR-1) in serine residue and increases the phosphorylation of insulin receptor β-subunit (IR-β) in tyrosine residue. Thus, supplementing diets with glycine to correct GSH deficiency and to reduce oxidative stress provides significant metabolic benefits to SF rats by improving insulin sensitivity.

scholarly journals Nutraceutical Improves Glycemic Control, Insulin Sensitivity, and Oxidative Stress in Hyperglycemic Subjects: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

2020 ◽  
Vol 15 (4) ◽  
pp. 1934578X2091868
Author(s):  
Akkarach Bumrungpert ◽  
Patcharanee Pavadhgul ◽  
Rewadee Chongsuwat ◽  
Surat Komindr
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Clinical Trial ◽  
Glycemic Control ◽  
Lipid Profiles ◽  
Oxidative Stress Markers ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Stress Markers ◽  
And Oxidative Stress

The aim of this research was to investigate the effects of nutraceuticals including bitter melon, fenugreek, cinnamon, alpha-lipoic acid, zinc, biotin, chromium, and cholecalciferol on glycemic control, insulin sensitivity, lipid profiles, oxidative stress, and inflammatory markers in hyperglycemia. The study design was a randomized, double-blind, placebo-controlled trial. Subjects with hyperglycemia were randomly divided into 2 groups. The treatment group ( n = 52) was given a nutraceutical and the control group ( n = 50) was provided with a placebo for 12 weeks. Fasting blood glucose (FBG), hemoglobin A1c (HbA1C), homeostatic model assessment of insulin resistance (HOMA-IR), lipid profiles, biomarkers of oxidative stress, and inflammation were assessed before and after the intervention at 6 weeks and 12 weeks. Nutraceutical supplementation demonstrated a statistically significant decrease in FBG (13.4% and 18.9%), HbA1C (6.5% and 11.3%), and HOMA-IR (28.9% and 35.2%) compared with the placebo. Moreover, low-density lipoprotein-cholesterol (LDL-C) level was significantly reduced in the nutraceutical group (7.1% and 9.3%). Furthermore, the nutraceutical significantly decreased oxidative stress markers, oxidized LDL-C (14.8% and 18.9%) and malondialdehyde (16.6% and 26.2%) compared with the placebo. In conclusion, this nutraceutical can improve glycemic control, insulin resistance, lipid profiles, and oxidative stress markers in hyperglycemic subjects. Therefore, it has the potential to decrease cardiovascular disease risk factors. Clinical trial registration: TCTR20180907001, www.clinicaltrials.in.th.

Exercise maintains euglycemia in association with decreased activation of c-Jun NH2-terminal kinase and serine phosphorylation of IRS-1 in the liver of ZDF rats

2010 ◽  
Vol 298 (3) ◽  
pp. E671-E682 ◽  
Author(s):  
Michael A. Király ◽  
Jon Campbell ◽  
Edward Park ◽  
Holly E. Bates ◽  
Jessica T. Y. Yue ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Insulin Receptor ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Rodent Model ◽  
Voluntary Exercise ◽  
Insulin Receptor Substrate ◽  
Markers Of Inflammation ◽  
And Oxidative Stress

Stress-activated systems and oxidative stress are involved in insulin resistance, which, along with β-cell failure, contribute to the development of type 2 diabetes mellitus (T2DM). Exercise improves insulin resistance and glucose tolerance, and these adaptations may, in part, be related to reductions in inflammation and oxidative stress. We investigated circulating and tissue-specific markers of inflammation and oxidative stress and insulin-signaling pathways in a rodent model of T2DM, the Zucker diabetic fatty rat, with and without voluntary exercise. At 5 wk of age, Zucker diabetic fatty rats ( n = 8–9/group) were divided into basal (B), voluntary exercise (E), and sedentary control (S) groups. B rats were euthanized at 6 wk of age, and S and E rats were euthanized 10 wk later. E rats ran ∼5 km/day, which improved insulin sensitivity and maintained fed and fasted glucose levels and glucose tolerance. Ten weeks of exercise also decreased whole body markers of inflammation and oxidative stress in plasma and liver, including lowered circulating IL-6, haptoglobin, and malondialdehyde levels, hepatic protein oxidation, and phosphorylated JNK, the latter indicating decreased JNK activity. Hepatic phosphoenolpyruvate carboxykinase levels and Ser307-phosphorylated insulin receptor substrate-1 were also reduced in E compared with S rats. In summary, we show that, in a rodent model of T2DM, voluntary exercise decreases circulating markers of inflammation and oxidative stress and lowers hepatic JNK activation and Ser307-phosphorylated insulin receptor substrate-1. These changes in oxidative stress markers and inflammation are associated with decreased hyperglycemia and insulin resistance and reduced expression of the main gluconeogenic enzyme phosphoenolpyruvate carboxykinase.

Antihypertensive effects of Tartary buckwheat flavonoids by improvement of vascular insulin sensitivity in spontaneously hypertensive rats

2017 ◽  
Vol 8 (11) ◽  
pp. 4217-4228 ◽  
Author(s):  
Zuoxu Hou ◽  
Yuanyuan Hu ◽  
Xingbin Yang ◽  
Wensheng Chen
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Spontaneously Hypertensive Rats ◽  
Tartary Buckwheat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
And Oxidative Stress

Tartary buckwheat flavonoids alleviate hypertension through attenuating vascular insulin resistance and oxidative stress.

Early experimental obesity is associated with coronary endothelial dysfunction and oxidative stress

2007 ◽  
Vol 292 (2) ◽  
pp. H904-H911 ◽  
Author(s):  
Offer Galili ◽  
Daniele Versari ◽  
Katherine J. Sattler ◽  
Monica L. Olson ◽  
Dallit Mannheim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Microvascular Permeability ◽  
Systemic Oxidative Stress ◽  
Coronary Endothelium ◽  
And Oxidative Stress

Obesity is independently associated with increased cardiovascular risk. However, since established obesity clusters with various cardiovascular risk factors, configuring the metabolic syndrome, the early effects of obesity on vascular function are still poorly understood. The current study was designed to evaluate the effect of early obesity on coronary endothelial function in a new animal model of swine obesity. As to method, juvenile domestic crossbred pigs were randomized to either high-fat/high-calorie diet (HF) or normal chow diet for 12 wk. Coronary microvascular permeability and abdominal wall fat were determined by using electron beam computerized tomography. Epicardial endothelial function and oxidative stress were measured in vitro. Systemic oxidative stress, renin-angiotensin activity, leptin levels, and parameters of insulin sensitivity were evaluated. As a result, HF pigs were characterized by abdominal obesity, hypertension, and elevated plasma lysophosphatidylcholine and leptin in the presence of increased insulin sensitivity. Coronary endothelium-dependent vasorelaxation was reduced in HF pigs and myocardial microvascular permeability increased compared with those values in normal pigs. Systemic redox status in HF pigs was similar to that in normal pigs, whereas the coronary endothelium demonstrated higher content of superoxide anions, nitrotyrosine, and NADPH-oxidase subunits, indicating increased tissue oxidative stress. In conclusion, the current study shows that early obesity is characterized by increased vascular oxidative stress and endothelial dysfunction in association with increased levels of leptin and before the development of insulin resistance and systemic oxidative stress. Vascular dysfunction is therefore an early manifestation of obesity and might contribute to the increased cardiovascular risk, independently of insulin resistance.

scholarly journals Maternal Fructose Intake Induces Insulin Resistance and Oxidative Stress in Male, but Not Female, Offspring

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Lourdes Rodríguez ◽  
Paola Otero ◽  
María I. Panadero ◽  
Silvia Rodrigo ◽  
Juan J. Álvarez-Millán ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Female Offspring ◽  
Female Rats ◽  
Male Rats ◽  
Female Progeny ◽  
Added Sugars ◽  
Stress Markers ◽  
Fructose Intake

Objective. Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny.Methods. Blood samples from fed and 24 h fasted female and male 90-day-old rats born from fructose-fed, glucose-fed, or control mothers were used.Results. After fasting, HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents from fructose-fed mothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats from carbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers.Conclusion. Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny.

scholarly journals Metformin alleviates insulin resistance in obese-induced mice via remodeling gut microbiota and intestinal metabolites

2020 ◽  
Author(s):  
Ya Zhang ◽  
Yang Cheng ◽  
Jihui Zuo ◽  
Liping Yan ◽  
Qiaojuan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Underlying Mechanism ◽  
Liver Inflammation ◽  
High Fat ◽  
Intracellular Ros ◽  
And Oxidative Stress

AbstractMetformin is widely used to surmount insulin resistance (IR) and diabetes. Evidence indicates that metformin remodels gut microbiota but the underlying mechanism remain unclear. Present results showed that metformin effectively improved insulin sensitivity and alleviated liver inflammation and oxidative stress in high fat diet (HFD)-induced mice. Metabolomics analysis showed that metformin increased tauroursodeoxycholic acid (TUDCA) production by increasing the expression of bile acid synthase Cyp7a1 and Baat. In the palmitic acid (PA)-induced cell, TUDCA activated Nrf2/ARE pathway, thereby reducing intracellular ROS and improving insulin signaling. Further gut microbiota analysis showed that metformin increased the proportion of Akkermanisia muciniphlia in the HFD-fed mice, while TUDCA promoted the proliferation of A. muciniphlia but metformin did not. These findings reveal that metformin remodels the gut microbiota, reduces oxidative stress and enhances insulin sensitivity by increasing the production of TUDCA. This provides a novel mechanism by which metformin alleviates diet-induced IR and improves metabolism.

Oxidative stress markers in women with polycystic ovary syndrome without insulin resistance

2018 ◽  
Author(s):  
Reveka Gyftaki ◽  
Sofia Gougoura ◽  
Nikolaos Kalogeris ◽  
Vasiliki Loi ◽  
George Koukoulis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Oxidative Stress Markers ◽  
Ovary Syndrome ◽  
Stress Markers
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