Cross-Sectional Associations of Resistin, Coronary Heart Disease, and Insulin Resistance

Burnett, Mary Susan; Devaney, Joseph M.; Adenika, Remi; Lindsay, Robert; Howard, Barbara V.

doi:10.1210/jc.2005-1653

Cited by 127 publications

(86 citation statements)

References 33 publications

(40 reference statements)

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“…A recent study (27) did not find an association between resistin levels and cardiovascular events in Korean diabetic patients, and Pilz et al (28) related resistin levels to inflammatory processes and renal function but not to the incidence of some cardiovascular diseases. In contrast, several other studies (29,30) found that resistin levels are higher in different cardiovascular conditions. More important, the same Pilz et al (28) found an increase in mortality in hyperresistinemic patients, and Lubos et al (31) demonstrated that resistin levels predict cardiovascular mortality in patients with coronary artery disease.…”

Section: Discussioncontrasting

confidence: 60%

Resistin Impairs Insulin-Evoked Vasodilation

et al. 2008

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OBJECTIVE-Since vascular dysfunction is a main trait of obese subjects, in the present study we evaluated the vascular impact of resistin, a recently discovered hormone markedly increased in obesity.RESEARCH DESIGN AND METHODS-We performed our analysis on aortic and mesenteric segments from young and old C57BL/6 mice and on cultured endothelial cells. Resistin-induced vascular effect was evaluated in vitro and in vivo. Molecular analyses were performed by immunoprecipitation and Western blotting.RESULTS-Recombinant murine resistin did not induce changes in either basal vascular tone or phenylephrine-induced vascular contraction. In contrast, both in vivo and in vitro administration of resistin significantly impaired dose-dependent insulin-evoked vasodilation by reducing endothelial nitric oxide synthase (eNOS) enzymatic activity. This effect of resistin was selective for insulin vascular action, since vasodilatation induced by increasing doses of acetylcholine or nitroglycerin was not influenced by the hormone. Molecular analysis of endothelial cells further detailed resistin-induced vascular resistance by showing impairment of insulin-evoked AKT and eNOS phosphorylations after exposure to resistin. Even this latter abnormality is selective of insulin signaling since AKT/eNOS phosphorylations are normally activated during acetylcholine stimulation. More important, the resistin-induced endothelial dysfunction depends on resistin's ability to alter insulin receptor substrate (IRS)-1 tyrosine/serine phosphorylation and its consequent interaction with phosphatidylinositol 3-kinase.CONCLUSIONS-Our results demonstrate that resistin is able to induce a selective vascular insulin resistance-impairing endothelial IRS-1 signaling pathway that leads to eNOS activation and vasodilation. Diabetes 57:577-583, 2008

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Section: Discussioncontrasting

confidence: 60%

Resistin Impairs Insulin-Evoked Vasodilation

et al. 2008

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“…In contrast to the rodent, where resistin appears to be important in modulating hepatic insulin sensitivity (24,25), the contribution of resistin to insulin resistance in human subjects appears to be relatively minor. While a few studies have reported a weak positive association between insulin resistance and resistin levels (14,26,27), the majority of studies have not (23,28 -33). Resistin levels in human subjects are thought to correlate more closely with inflammation than with insulin resistance (28,30,34).…”

Section: The Contribution Of Adipose Tissue To Adipokine Levelsmentioning

confidence: 99%

Ethnicity, Insulin Resistance, and Inflammatory Adipokines in Women at High and Low Risk for Vascular Disease

et al. 2007

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OBJECTIVE -We sought to compare the relationship between body composition, insulin resistance, and inflammatory adipokines in Aboriginal Canadian women, who are at high risk of vascular disease, with white women. RESEARCH DESIGN AND METHODS -A subgroup of the First Nations Bone HealthStudy population, consisting of 131 Aboriginal women and 132 matched white women, was utilized. Body composition was determined by whole-body dual X-ray absorptiometry, and blood analytes were measured after an overnight fast.RESULTS -After excluding individuals with diabetes, A1C, BMI, percent trunk fat, and homeostasis model assessment of insulin resistance (HOMA-IR) were greater in First Nation women compared with white women, whereas adiponectin, retinol binding protein (RBP)4, and insulin-like growth factor binding protein-1 (IGFBP-1) were lower. First Nation women had more trunk fat for any given level of total fat than white women. There were no differences in resistin, leptin, tumor necrosis factor (TNF)-␣, or C-reactive protein (CRP) levels between First Nation and white women. Insulin resistance correlated with leptin and inversely with adiponectin levels in both First Nation and white women. There were weak correlations between insulin resistance and TNF-␣, interleukin-6, and CRP, but these were not significant after correction for body fat. No correlation was found between RBP4 and insulin resistance. ANCOVA revealed a higher HOMA-IR adjusted for total body fat in First Nation women than in white women (P ϭ 0.015) but not HOMA-IR adjusted for trunk fat (P Ͼ 0.2).CONCLUSIONS -First Nation women are more insulin resistant than white women, and this is explained by trunk fat but not total fat. Despite the increased insulin resistance, inflammatory adipokines are not significantly increased in First Nation women compared with white women. Diabetes Care 30:286 -291, 2007A n increased prevalence of vascular disease in insulin-resistant states such as pre-diabetes, type 2 diabetes, and the metabolic syndrome has been long recognized (1). There is considerable debate whether insulin resistance is the primary event in atherosclerosis, with consequent activation of proinflammatory signaling pathways, or, alternatively, whether low-grade inflammation and subsequent insulin resistance accounts for the association of diabetes and vascular disease (2).Aboriginal Canadian populations, which include First Nation, Metis, and Inuit individuals (3), have an increased prevalence of atherosclerosis and cardiovascular and peripheral vascular disease (4,5). First Nations are Aboriginal individuals signatory to treaties and/or recognized by the Canadian Federal Government as a fiduciary responsibility and represent the large majority of Aboriginal individuals living in Canada (3). While type 2 diabetes is more prevalent among Canadian men than women in the general population, the reverse is true for the First Nation population (6,7). In the First Nation population, obesity is more prevalent among men than women, but the prevalence of metabolic ...

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“…Supporting this theory, adults with MetS tend to have higher resistin levels than their healthy counterparts. 29 However, the correlation between insulin resistance and plasma resistin in adult humans remains controversial, supported by some studies 25,[35][36][37] and not in others, 4,21,34,38,39 and this therefore weakens the relation between resistin and MetS.…”

Section: Introductionmentioning

confidence: 99%

Serum resistin correlates with central obesity but weakly with insulin resistance in Chinese children and adolescents

Fisette

et al. 2009

Int J Obes

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Objective: Resistin has been linked with obesity and hypothesized as a potential marker of insulin resistance in addition to being linked with acute inflammation. However, these links are still highly controversial in humans. Our goal was to examine resistin levels in relation to obesity, insulin resistance and inflammation markers in a large population of Asian children and adolescents. Methods: Children and adolescents (n ¼ 3472) aged 6-18 years, boys (n ¼ 1765) and girls (n ¼ 1707), were assessed for body size parameters, pubertal development, blood lipids, glucose, insulin, resistin, C-reactive protein (CRP), adiponectin and complement C3 (C3) levels. Results: Resistin increased with central obesity in both genders but not with simple adiposity in boys. Several markers associated with central obesity correlated in a gender-specific fashion with plasma resistin. Waist circumference, fat-mass percentage, waistto-height ratio and body mass index (BMI) positively correlated with resistin in both genders. Blood lipids such as triglycerides, nonesterified fatty acids (NEFA) and low-density lipoprotein cholesterol, diastolic and systolic blood pressure correlated positively with resistin in boys. NEFA, high-density lipoprotein cholesterol (negatively) and inflammation markers, such as CRP and C3, positively correlated with resistin in girls. There was no correlation between resistin and adiponectin, and no association of adiponectin with resistin quintiles in either boys or girls. In both boys and girls, resistin tended to decrease with age, with girls having higher levels than boys. Few indices of insulin resistance were linked with plasma resistin in either gender. Conclusion: In this population, plasma resistin levels are a weak biochemical marker of metabolic dysfunction defined by central obesity, adiposity and inflammation and does not predict insulin resistance. Only a small proportion of resistin variation can be explained by factors related to metabolic syndrome, suggesting that resistin is not strongly implicated in a concentrationdependent fashion in any of the examined pathologies.

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Cross-Sectional Associations of Resistin, Coronary Heart Disease, and Insulin Resistance

Abstract: Resistin is not independently associated with CHD. Resistin is elevated in survivors of myocardial infarction; however, this reflects a novel association of raised resistin with diabetic nephropathy.

Cited by 127 publications

References 33 publications

Resistin Impairs Insulin-Evoked Vasodilation

Resistin Impairs Insulin-Evoked Vasodilation

Ethnicity, Insulin Resistance, and Inflammatory Adipokines in Women at High and Low Risk for Vascular Disease

Serum resistin correlates with central obesity but weakly with insulin resistance in Chinese children and adolescents

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