Quercetin and quercetin-3-O -glucuronide are equally effective in ameliorating endothelial insulin resistance through inhibition of reactive oxygen species-associated inflammation

2013 ◽  
Vol 57 (6) ◽  
pp. 1037-1045 ◽  
Author(s):  
Xu-Dan Guo ◽  
Dong-Yan Zhang ◽  
Xue-Jiao Gao ◽  
John Parry ◽  
Kang Liu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Fanconi Anemia Links Reactive Oxygen Species to Insulin Resistance and Obesity

2012 ◽  
Vol 17 (8) ◽  
pp. 1083-1098 ◽  
Author(s):  
Jie Li ◽  
Jared Sipple ◽  
Suzette Maynard ◽  
Parinda A. Mehta ◽  
Susan R. Rose ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Fanconi Anemia ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Targeting mitochondrial biogenesis: a potential approach for preventing and controlling diabetes

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ritika Singh ◽  
Lucy Mohapatra ◽  
Alok Shiomurthi Tripathi
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Mitochondrial Biogenesis ◽  
Diabetic Complications ◽  
Reactive Oxygen ◽  
Main Body ◽  
Oxygen Species ◽  
Treatment And Prevention ◽  
Skeletal Muscle Insulin Resistance ◽  
Mitochondrial Number

Abstract Background Diabetes mellitus is a lingering hyperglycemic ailment resulting in several life-threatening difficulties. Enduring hyperglycemia often persuades the buildup of reactive oxygen species that are the significant pathological makers of diabetic complications. The mitochondrial dysfunction, with mitochondrial damage and too much production of reactive oxygen species, have been proposed to be convoluted in the progress of insulin resistance. Numerous studies advocate that agents that enhance the mitochondrial number and/or decrease their dysfunction, could be greatly helpful in management of diabetes and its complications. Main body Mitochondrial biogenesis is an extremely delimited procedure arbitrated by numerous transcription influences, in which mitochondrial fusion and fission happen in synchronization in a standard vigorous cell. But this synchronization is greatly disturbed in diabetic condition designated by modification in the working of several important transcription factors regulating the expressions of different genes. Numerous preclinical and clinical investigations have suggested that, the compromised functions of mitochondria play a significant protagonist in development of pancreatic β-cell dysfunction, skeletal muscle insulin resistance and several diabetic complications. However, there are several phytoconstituents performing through numerous alleyways, either unswervingly by motivating biogenesis or indirectly by constraining or averting dysfunction and producing a beneficial effect on overall function of the mitochondria. Conclusion This review describes standard mitochondrial physiology and anomalous modifications that transpire in answer to persistent hyperglycemia in diabetes condition. It also discusses about the different phytoconstituents that can affect the biogenesis pathways of mitochondria and thus can be used in the treatment and prevention of diabetes.

Endothelium-specific insulin resistance leads to accelerated atherosclerosis in areas with disturbed flow patterns: A role for reactive oxygen species

2013 ◽  
Vol 230 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Matthew C. Gage ◽  
Nadira Y. Yuldasheva ◽  
Hema Viswambharan ◽  
Piruthivi Sukumar ◽  
Richard M. Cubbon ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Flow Patterns ◽  
Oxygen Species ◽  
Disturbed Flow ◽  
Accelerated Atherosclerosis ◽  
Specific Insulin

scholarly journals Aldosterone Inhibits Insulin-Induced Glucose Uptake by Degradation of Insulin Receptor Substrate (IRS) 1 and IRS2 via a Reactive Oxygen Species-Mediated Pathway in 3T3-L1 Adipocytes

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1662-1669 ◽  
Author(s):  
Tsutomu Wada ◽  
Satoshi Ohshima ◽  
Eriko Fujisawa ◽  
Daisuke Koya ◽  
Hiroshi Tsuneki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Glucocorticoid Receptor ◽  
Insulin Receptor ◽  
Receptor Antagonist ◽  
Glucose Uptake ◽  
Reactive Oxygen ◽  
Insulin Receptor Substrate ◽  
Oxygen Species ◽  
Metabolic Signaling

Serum aldosterone level is clinically known to correlate with body weight and insulin resistance. Because the underlying molecular mechanism is largely unknown, we examined the effect of aldosterone on insulin-induced metabolic signaling leading to glucose uptake in 3T3-L1 adipocytes. Aldosterone reduced the amounts of insulin receptor substrate (IRS) 1 and IRS2 in a time- and dose-dependent manner. As a result, insulin-induced phosphorylation of Akt-1 and -2, and subsequent uptake of 2-deoxyglucose were decreased. Degradation of IRSs was effectively prevented by a glucocorticoid receptor antagonist and antioxidant N-acetylcysteine, but not by a mineralocorticoid receptor antagonist. Because aldosterone induced phosphorylation of IRS1 at Ser307, responsible kinases were investigated, and we revealed that rapamycin and BMS345541, but neither SP600125 nor calphostin C, conferred for degradation of IRSs. Although lactacystin prevented the degradation of IRSs, glucose uptake was not preserved. Importantly, sucrose-gradient-sediment intracellular fraction analysis revealed that lactacystin did not effectively restore the reduction of IRS1 in the low-density microsome fraction, important for the transduction of insulin’s metabolic signaling. These results indicate that aldosterone deteriorates metabolic action of insulin by facilitating the degradation of IRS1 and IRS2 via glucocorticoid receptor-mediated production of reactive oxygen species, and activation of IκB Kinase β and target of rapamycin complex 1. Thus, aldosterone appears to be a novel key factor in the development of insulin resistance in visceral obesity.

scholarly journals Insulin-Induced Generation of Reactive Oxygen Species and Uncoupling of Nitric Oxide Synthase Underlie the Cerebrovascular Insulin Resistance in Obese Rats

2012 ◽  
Vol 32 (5) ◽  
pp. 792-804 ◽  
Author(s):  
Prasad VG Katakam ◽  
James A Snipes ◽  
Mesia M Steed ◽  
David W Busija
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Cerebral Arteries ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Fluorescence Studies ◽  
Oxide Synthase

Hyperinsulinemia accompanying insulin resistance (IR) is an independent risk factor for stroke. The objective is to examine the cerebrovascular actions of insulin in Zucker obese (ZO) rats with IR and Zucker lean (ZL) control rats. Diameter measurements of cerebral arteries showed diminished insulin-induced vasodilation in ZO compared with ZL. Endothelial denudation revealed vasoconstriction to insulin that was greater in ZO compared with ZL. Nonspecific inhibition of nitric oxide synthase (NOS) paradoxically improved vasodilation in ZO. Scavenging of reactive oxygen species (ROS), supplementation of tetrahydrobiopterin (BH4) precursor, and inhibition of neuronal NOS or NADPH oxidase or cyclooxygenase (COX) improved insulin-induced vasodilation in ZO. Immunoblot experiments revealed that insulin-induced phosphorylation of Akt, endothelial NOS, and expression of GTP cyclohydrolase-I (GTP-CH) were diminished, but phosphorylation of PKC and ERK was enhanced in ZO arteries. Fluorescence studies showed increased ROS in ZO arteries in response to insulin that was sensitive to NOS inhibition and BH4 supplementation. Thus, a vicious cycle of abnormal insulin-induced ROS generation instigating NOS uncoupling leading to further ROS production underlies the cerebrovascular IR in ZO rats. In addition, decreased bioavailability and impaired synthesis of BH4 by GTP-CH induced by insulin promoted NOS uncoupling.

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