The role of lipids in the pathogenesis of muscle insulin resistance and beta cell failure in type II diabetes and obesity

2001 ◽  
Vol 109 (Suppl 2) ◽  
pp. S189-S201 ◽  
Author(s):  
E. Kraegen ◽  
G. Cooney ◽  
J.-M. Ye ◽  
A. Thompson ◽  
S. Furler
Keyword(s):  
Insulin Resistance ◽  
Beta Cell ◽  
Type Ii Diabetes ◽  
Type Ii ◽  
Muscle Insulin Resistance ◽  
Beta Cell Failure ◽  
Diabetes And Obesity

Role of lipid oxidation in pathogenesis of insulin resistance of obesity and type II diabetes

Diabetes ◽  
1987 ◽  
Vol 36 (11) ◽  
pp. 1341-1350 ◽  
Author(s):  
J. P. Felber ◽  
E. Ferrannini ◽  
A. Golay ◽  
H. U. Meyer ◽  
D. Theibaud ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Oxidation ◽  
Type Ii Diabetes ◽  
Type Ii

Role of Lipid Oxidation in Pathogenesis of Insulin Resistance of Obesity and Type II Diabetes

Diabetes ◽  
1987 ◽  
Vol 36 (11) ◽  
pp. 1341-1350 ◽  
Author(s):  
J.-P. Felber ◽  
E. Ferrannini ◽  
A. Golay ◽  
H. U. Meyer ◽  
D. Theibaud ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Lipid Oxidation ◽  
Type Ii Diabetes ◽  
Type Ii

Role of resistin in obesity, insulin resistance and Type II diabetes

2005 ◽  
Vol 109 (3) ◽  
pp. 243-256 ◽  
Author(s):  
Christine M. Kusminski ◽  
Philip G. Mcternan ◽  
Sudhesh Kumar
Keyword(s):  
Insulin Resistance ◽  
Type Ii Diabetes ◽  
Disease Risk ◽  
Current Knowledge ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Rodent Models ◽  
Physiological Relevance ◽  
Considerable Controversy

Resistin is a member of a class of cysteine-rich proteins collectively termed resistin-like molecules. Resistin has been implicated in the pathogenesis of obesity-mediated insulin resistance and T2DM (Type II diabetes mellitus), at least in rodent models. In addition, resistin also appears to be a pro-inflammatory cytokine. Taken together, resistin, like many other adipocytokines, may possess a dual role in contributing to disease risk. However, to date there has been considerable controversy surrounding this 12.5 kDa polypeptide in understanding its physiological relevance in both human and rodent systems. Furthermore, this has led some to question whether resistin represents an important pathogenic factor in the aetiology of T2DM and cardiovascular disease. Although researchers still remain divided as to the role of resistin, this review will place available data on resistin in the context of our current knowledge of the pathogenesis of obesity-mediated diabetes, and discuss key controversies and developments.

Beta-cell insensitivity to glucose in the GK rat, a spontaneous nonobese model for type II diabetes

Diabetes ◽  
1991 ◽  
Vol 40 (4) ◽  
pp. 486-491 ◽  
Author(s):  
B. Portha ◽  
P. Serradas ◽  
D. Bailbe ◽  
K. Suzuki ◽  
Y. Goto ◽  
...  
Keyword(s):  
Beta Cell ◽  
Type Ii Diabetes ◽  
Type Ii ◽  
Gk Rat

Abstract P432: Higher Muscle-to-Abdominal Cavity Ratio is Associated with Lower Odds of Type II Diabetes in Older Women

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Britta Larsen ◽  
Matthew Allison ◽  
Eugene Kang ◽  
Sarah Saad ◽  
Gail A Laughlin ◽  
...  
Keyword(s):  
Type Ii Diabetes ◽  
Abdominal Cavity ◽  
Abdominal Muscle ◽  
Normal Weight ◽  
Area Ratio ◽  
Type Ii ◽  
Obese Women ◽  
Abdominal Adipose Tissue ◽  
Race Ethnicity

Background: Excess abdominal adipose tissue has been identified as an important factor in the development of type II diabetes. Lean muscle tissue also plays an important role in glucose regulation, yet research on the role of muscle in diabetes etiology is limited. Abdominal muscle mass could be particularly relevant for normal weight diabetics, for whom excessive abdominal adipose tissue may play less of a role. Objective: To explore the association between muscle-to-abdominal cavity area ratio and prevalent diabetes in older community-dwelling women in the Rancho Bernardo Study, UCSD Filipino Women’s Health Study, and the Health Assessment Study of African-American Women. Methods: Participants were 421 women (40% Caucasian, 28% Filipina, 32% African American) with a mean age of 64 (6.9) years. Abdominal muscle and fat areas were measured using computed tomography (CT) scans, and were used to compute a muscle-to-abdominal cavity area ratio (MACR). Based on body mass index (BMI), participants were classified as normal weight (18-24.9 kg/m2), overweight (25-29.9), or obese (30+). Prevalent diabetes was defined as self-report of physician diagnosis, anti-diabetes medication use, fasting morning glucose ≥ 126 mg/dL or 2 hour glucose ≥ 200mg/dL. MACR was modeled per standard deviation (SD) and logistic regression was used to examine the association with diabetes while adjusting for relevant covariates. Results: Prevalent diabetes was seen in 12.8% of the sample (54 of 421). In age and race/ethnicity adjusted models, each SD increase in MACR was associated with significant reduced odds of diabetes (OR = 0.62, CI: 0.43-0.89, p = 0.01), which remained significant after further adjustment for BMI category, smoking, physical activity, hypertension, anti-hypertensive drugs, and estrogen use (OR = 0.64, CI: 0.41-0.98, p = .041). The association was modestly attenuated after further adjusting for visceral fat area (OR = 0.70, CI: 0.44-1.10, p = 0.12). Normal weight women with diabetes had significantly less total muscle (p = 0.045) and smaller MACR’s (p = 0.001) than those without diabetes, while this was not seen for overweight or obese women with diabetes. Stratified by BMI category, MACR was significantly associated with lower odds of diabetes for normal weight women across all three models (fully adjusted OR = 0.37, CI: 0.15-0.90, p =.03), yet was not associated with diabetes in any models for women who were overweight or obese (all p > 0.50). Interactions of MACR with race/ethnicity were not significant. Conclusions: Muscle-to-abdominal cavity ratio is associated with reduced likelihood of type II diabetes in women. This association differs by BMI category, with muscle showing the greatest protection in normal weight women, and no effect in overweight or obese women. This highlights the potential role of low muscle mass as a risk factor for diabetes, particularly in women who may appear to be at low risk.

scholarly journals The Nrf2/Keap1/ARE Pathway and Oxidative Stress as a Therapeutic Target in Type II Diabetes Mellitus

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Joshua A. David ◽  
William J. Rifkin ◽  
Piul S. Rabbani ◽  
Daniel J. Ceradini
Keyword(s):  
Diabetes Mellitus ◽  
Oxidative Damage ◽  
Therapeutic Target ◽  
Type Ii Diabetes ◽  
Animal Studies ◽  
Cell Types ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
And Oxidative Stress

Despite improvements in awareness and treatment of type II diabetes mellitus (TIIDM), this disease remains a major source of morbidity and mortality worldwide, and prevalence continues to rise. Oxidative damage caused by free radicals has long been known to contribute to the pathogenesis and progression of TIIDM and its complications. Only recently, however, has the role of the Nrf2/Keap1/ARE master antioxidant pathway in diabetic dysfunction begun to be elucidated. There is accumulating evidence that this pathway is implicated in diabetic damage to the pancreas, heart, and skin, among other cell types and tissues. Animal studies and clinical trials have shown promising results suggesting that activation of this pathway can delay or reverse some of these impairments in TIIDM. In this review, we outline the role of oxidative damage and the Nrf2/Keap1/ARE pathway in TIIDM, focusing on current and future efforts to utilize this relationship as a therapeutic target for prevention, prognosis, and treatment of TIID.

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