Clustering of Insulin Resistance With Vascular Dysfunction and Low-Grade Inflammation in Type 2 Diabetes

Natali, Andrea; Toschi, Elena; Baldeweg, Stephanie E; Ciociaro, Demetrio; Favilla, Stefania; Saccà, Luigi; Ferrannini, Ele

doi:10.2337/diabetes.55.04.06.db05-1076

Cited by 174 publications

(143 citation statements)

References 55 publications

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“…TNF-␣ levels have been reported to be significantly elevated in insulinresistant type 2 diabetic subjects (39,40). Although First Nation and control women had similar levels of TNF-␣, a weak correlation was found between TNF-␣ and HOMA-IR but only in the First Nation individuals.…”

Section: The Contribution Of Adipose Tissue To Adipokine Levelsmentioning

confidence: 78%

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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Section: The Contribution Of Adipose Tissue To Adipokine Levelsmentioning

confidence: 78%

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

et al. 2007

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“…These pro-inflammatory markers also positively correlated with insulin resistance and the features of the metabolic syndrome, in most cases, independently of the degree of obesity [6,7,[12][13][14].…”

Section: Inflammatory Markers In Obesity Metabolic Syndrome and T2dmmentioning

confidence: 84%

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Esser

Legrand-Poels

Piette

et al. 2014

Diabetes Research and Clinical Practice

1,632

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:It is recognized that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes. Systemic inflammatory markers are risk factors for the development of type 2 diabetes and its macrovascular complications. Adipose tissue, liver, muscle and pancreas are themselves sites of inflammation in presence of obesity. An infiltration of macrophages and other immune cells is observed in these tissues associated with a cell population shift from an anti-inflammatory to a pro-inflammatory profile. These cells are crucial for the production of pro-inflammatory cytokines, which act in an autocrine and paracrine manner to interfere with insulin signaling in peripheral tissues or induce β-cell dysfunction and subsequent insulin deficiency. Particularly, the pro-inflammatory interleukin-1β is implicated in the pathogenesis of type 2 diabetes through the activation of the NLRP3 inflammasome. The objectives of this review are to expose recent data supporting the role of the immune system in the pathogenesis of insulin resistance and type 2 diabetes and to examine various mechanisms underlying this relationship. If type 2 diabetes is an inflammatory disease, anti-inflammarory therapies could have a place in prevention and treatment of type 2 diabetes.

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“…Using the forearm technique, we have previously shown that EDV is reduced in diabetic patients in proportion to their degree of insulin resistance [46]. Insulin resistance, however, does not cluster with EDV in nondiabetic normotensive participants [47] or in patients with essential hypertension [48].…”

Section: Discussionmentioning

confidence: 97%

Effects of glucose tolerance on the changes provoked by glucose ingestion in microvascular function

et al. 2008

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Aims/hypothesis Hyperglycaemia and hyperinsulinaemia have opposite effects on endothelium-dependent vasodilatation in microcirculation, but the net effect elicited by glucose ingestion and the separate influence of glucose tolerance are unknown. Methods In participants with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or diabetic glucose tolerance, multiple plasma markers of both oxidative stress and endothelial activation, and forearm vascular responses (plethysmography) to intra-arterial acetylcholine (ACh) and sodium nitroprusside (SNP) infusions were measured before and after glucose ingestion. In another IGT group, we evaluated the time-course of the skin vascular responses (laser Doppler) to ACh and SNP (by iontophoresis) 1, 2 and 3 h into the OGTT; the plasma glucose profile was then reproduced by means of a variable intravenous glucose infusion and the vascular measurements repeated. Results Following oral glucose, plasma antioxidants were reduced by 5% to 10% (p<0.01) in all patient groups. The response to acetylcholine was not affected by glucose ingestion in any group, while the response to SNP was attenuated, particularly in the IGT group. The ACh:SNP ratio was slightly improved therefore in all groups, even in diabetic participants, in whom it was impaired basally. A time-dependent improvement in ACh:SNP ratio was also observed in skin microcirculation following oral glucose; this improvement was blunted when matched hyperglycaemia was coupled with lower hyperinsulinaemia (intravenous glucose). Conclusions/interpretation Regardless of glucose tolerance, oral glucose does not impair endothelium-dependent vasodilatation either in resistance arteries or in the microcirculation, despite causing increased oxidative stress; the endogenous insulin response is probably responsible for countering any inhibitory effect on vascular function.

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Clustering of Insulin Resistance With Vascular Dysfunction and Low-Grade Inflammation in Type 2 Diabetes

Cited by 174 publications

References 55 publications

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

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

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes

Effects of glucose tolerance on the changes provoked by glucose ingestion in microvascular function

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