Oxidative Stress Is Associated with Adiposity and Insulin Resistance in Men

Abstract To investigate the direct relationship of oxidative stress with obesity and insulin resistance in men, we measured the plasma levels of 8-epi-prostaglandin F2α (PGF2α) in 14 obese and 17 nonobese men and evaluated their relationship with body mass index; body fat weight; visceral, sc, and total fat areas, measured by computed tomography; and glucose infusion rate during a euglycemic hyperinsulinemic clamp study. Obese men had significantly higher plasma concentrations of 8-epi-PGF2α than nonobese men (P < 0.05). The plasma levels of 8-epi-PGF2α were significantly correlated with body mass index (r = 0.408; P < 0.05), body fat weight (r = 0.467; P < 0.05), visceral (r = 0.387; P < 0.05) and total fat area (r = 0.359; P < 0.05) in all (obese and nonobese) men. There was also a significant correlation between the plasma levels of 8-epi-PGF2α and glucose infusion rate in obese men (r = −0.552; P < 0.05) and all men (r = −0.668; P < 0.01). In all subjects, the plasma levels of 8-epi-PGF2α were significantly correlated with fasting serum levels of insulin (r = 0.487; P < 0.01). In brief, these findings showed that the circulating levels of 8-epi-PGF2α are related to adiposity and insulin resistance in men. Although correlation does not prove causation, the results of this study suggest that obesity is an important factor for enhanced oxidative stress and that this oxidative stress triggers the development of insulin resistance in men.

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Body mass index and waist circumference are better predictors of insulin resistance than total body fat percentage in middle-aged and elderly Taiwanese

Medicine ◽

10.1097/md.0000000000008126 ◽

2017 ◽

Vol 96 (39) ◽

pp. e8126 ◽

Cited By ~ 19

Author(s):

Yiu-Hua Cheng ◽

Yu-Chung Tsao ◽

I-Shiang Tzeng ◽

Hai-Hua Chuang ◽

Wen-Cheng Li ◽

...

Keyword(s):

Insulin Resistance ◽

Body Mass Index ◽

Waist Circumference ◽

Body Mass ◽

Body Fat ◽

Body Fat Percentage ◽

Middle Aged ◽

Fat Percentage ◽

Total Body Fat ◽

Total Body

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A1 adenosine receptor partial agonist lowers plasma FFA and improves insulin resistance induced by high-fat diet in rodents

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00573.2006 ◽

2007 ◽

Vol 292 (5) ◽

pp. E1358-E1363 ◽

Cited By ~ 47

Author(s):

Arvinder K. Dhalla ◽

Mei Yee Wong ◽

Peter J. Voshol ◽

Luiz Belardinelli ◽

Gerald M. Reaven

Keyword(s):

Insulin Resistance ◽

Insulin Sensitivity ◽

Adenosine Receptor ◽

Infusion Rate ◽

Glucose Infusion ◽

Glucose Infusion Rate ◽

Oral Glucose ◽

Acute Administration ◽

High Fat ◽

Adenosine Receptor Agonist

There is substantial evidence in the literature that elevated plasma free fatty acids (FFA) play a role in the pathogenesis of type 2 diabetes. CVT-3619 is a selective partial A1 adenosine receptor agonist that inhibits lipolysis and lowers circulating FFA. The present study was undertaken to determine the effect of CVT-3619 on insulin resistance induced by high-fat (HF) diet in rodents. HF diet feeding to rats for 2 wk caused a significant increase in insulin, FFA, and triglyceride (TG) concentrations compared with rats fed chow. CVT-3619 (1 mg/kg) caused a time-dependent decrease in fasting insulin, FFA, and TG concentrations. Acute administration of CVT-3619 significantly lowered the insulin response, whereas glucose response was not different with an oral glucose tolerance test. Treatment with CVT-3619 for 2 wk resulted in significant lowering of FFA, TG, and insulin concentrations in rats on HF diet. To determine the effect of CVT-3619 on insulin sensitivity, hyperinsulinemic euglycemic clamp studies were performed in C57BL/J6 mice fed HF diet for 12 wk. Glucose infusion rate was decreased significantly in HF mice compared with chow-fed mice. CVT-3619 treatment 15 min prior to the clamp study significantly ( P < 0.01) increased glucose infusion rate to values similar to that for chow-fed mice. In conclusion, CVT-3619 treatment lowers FFA and TG concentrations and improves insulin sensitivity in rodent models of insulin resistance.

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Lipoprotein Metabolism, Insulin Resistance, and Adipocytokine Levels in Japanese Female Adolescents With a Normal Body Mass Index and High Body Fat Mass

Circulation Journal ◽

10.1253/circj.cj-08-0381 ◽

2009 ◽

Vol 73 (3) ◽

pp. 534-539 ◽

Cited By ~ 6

Author(s):

Noriaki Kishimoto ◽

Koichi Okita ◽

Shingo Takada ◽

Ichiro Sakuma ◽

Yasuaki Saijo ◽

...

Keyword(s):

Insulin Resistance ◽

Body Mass Index ◽

Body Mass ◽

Body Fat ◽

Fat Mass ◽

Lipoprotein Metabolism ◽

Female Adolescents ◽

Normal Body Mass Index ◽

Body Fat Mass ◽

Japanese Female

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Ginsenoside Re Reduces Insulin Resistance through Inhibition of c-Jun NH2-Terminal Kinase and Nuclear Factor-κB

Molecular Endocrinology ◽

10.1210/me.2007-0119 ◽

2008 ◽

Vol 22 (1) ◽

pp. 186-195 ◽

Cited By ~ 47

Author(s):

Zhiguo Zhang ◽

Xiaoying Li ◽

Wenshan Lv ◽

Yisheng Yang ◽

Hong Gao ◽

...

Keyword(s):

Insulin Resistance ◽

Glucose Uptake ◽

Insulin Signaling ◽

Infusion Rate ◽

Glucose Infusion ◽

Signaling Cascades ◽

Glucose Infusion Rate ◽

Nuclear Factor ◽

Phosphatidylinositol 3 Kinase ◽

Ginsenoside Re

Abstract Ginsenoside Re (Re), a compound derived from Panax ginseng, shows an antidiabetic effect. However, the molecular basis of its action remains unknown. We investigated insulin signaling and the antiinflammatory effect by Re in 3T3-L1 adipocytes and in high-fat diet (HFD) rats to dissect its anti-hyperglycemic mechanism. Glucose uptake was measured in 3T3-L1 cells and glucose infusion rate determined by clamp in HFD rats. The insulin signaling cascade, including insulin receptor (IR) β-subunit, IR substrate-1, phosphatidylinositol 3-kinase, Akt and Akt substrate of 160 kDa, and glucose transporter-4 translocation are examined. Furthermore, c-Jun NH2-terminal kinase (JNK), MAPK, and nuclear factor (NF)-κB signaling cascades were also assessed. The results show Re increases glucose uptake in 3T3-L1 cells and glucose infusion rate in HFD rats. The activation of insulin signaling by Re is initiated at IR substrate-1 and further passes on through phosphatidylinositol 3-kinase and downstream signaling cascades. Moreover, Re demonstrates an impressive suppression of JNK and NF-κB activation and inhibitor of NF-κBα degradation. In conclusion, Re reduces insulin resistance in 3T3-L1 adipocytes and HFD rats through inhibition of JNK and NF-κB activation.

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