Endothelial Dysfunction Is Detectable in Young Normotensive First-Degree Relatives of Subjects With Type 2 Diabetes in Association With Insulin Resistance

Balletshofer, Bernd; Rittig, Kilian; Enderle, Markus D.; Volk, A.; Maerker, Elke; Jacob, Stephan; Matthaei, S.; Rett, K.; Häring, Hans Ulrich

doi:10.1161/01.cir.101.15.1780

Cited by 412 publications

(322 citation statements)

References 38 publications

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“…The endothelium plays a pivotal role in the pathogenesis of atherosclerosis, and impaired endothelial function is considered an early marker for vascular disease [43][44][45][46]. Offspring of diabetic parents are not only at risk for progression to diabetes, they have also previously been suggested to have diminished endothelial function [31,32]. We restricted our analysis to a diabetesprone group as the relatively narrow range of adiponectin and endothelial function in a solely healthy population could miss an important relationship that might be better revealed during progression from normal to the early pathologic state.…”

Section: Discussionmentioning

confidence: 99%

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The role of total and high-molecular-weight complex of adiponectin in vascular function in offspring whose parents both had type 2 diabetes

et al. 2005

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Aims/hypothesis: Adiponectin is an adipokine with insulin-sensitising and anti-atherogenic properties. We studied the role played by total adiponectin and by the bioactive high-molecular-weight (HMW) oligomeric complexes of adiponectin in vascular function in offspring whose parents both had type 2 diabetes, a population at high risk of diabetes and atherosclerosis. Methods: Total and %HMW adiponectin, the cytokines C-reactive protein, interleukin-6 and plasminogen activator inhibitor-1 (PAI-1), as well as lipid profiles were assayed in 19 offspring, each with two type 2 diabetic parents. Subjects underwent OGTTs and IVGTTs. Endothelium-dependent vasodilation (EDV) was assessed by brachial artery ultrasonography. Results: There was a significant relationship between %HMW and total adiponectin levels (r=0.72, p=0.001). Despite an expected strong positive correlation between HDL-cholesterol and adiponectin levels (r=0.52, p=0.04), as well as HDL-cholesterol and EDV (r=0.56, p<0.02), there was no significant relationship between either total adiponectin or % HMW adiponectin and EDV. Adiponectin was inversely associated with PAI-1 (r=0.50, p=0.05), but did not correlate with the inflammatory markers C-reactive protein or interleukin-6. Conclusions/interpretation: In offspring of diabetic parents, a population at high risk of diabetes and atherosclerotic disease, there is no relationship between total or %HMW adiponectin and endotheliumdependent vasodilation. However, low adiponectin was associated with impaired fibrinolysis as manifested by increased levels of plasminogen activator inhibitor-1.

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Section: Discussionmentioning

confidence: 99%

“…Thus, we sought to evaluate the relationship between total and high-molecular-weight adiponectin and measures of vascular function in offspring whose parents both had type 2 diabetes. This group is at risk of diabetes [29,30] and may have early atherosclerotic disease manifested as abnormal endothelial function [31,32].…”

Section: Introductionmentioning

confidence: 99%

The role of total and high-molecular-weight complex of adiponectin in vascular function in offspring whose parents both had type 2 diabetes

et al. 2005

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“…Among the whole group, the 46 patients with restenosis, defined as recurrence and then 50% diameter reduction in the segment treated, showed a minimal lumen diameter (MLD) at follow-up of 0.95Ϯ0.49 versus 2.65Ϯ0.62 mm in the group without restenosis (74 patients). After a standard oral glucose test (75 g), 16 patients with restenosis and 35 patients without restenosis showed plasma glucose concentrations diagnostic for type 2 diabetes at 2 hours postload; 12 patients with restenosis and 14 patients without restenosis had an impaired glucose tolerance (IGT), whereas 18 patients with restenosis and 25 patients without restenosis demonstrated a normal glucose tolerance (NGT).…”

Section: Subjectsmentioning

confidence: 99%

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Piatti¹,

Mario²,

Monti³

2004

ACC Current Journal Review

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Background-Previously undiagnosed diabetes, impaired glucose tolerance, and insulin resistance are common in patients with acute myocardial infarction and coronary heart disease (CHD) and might be involved in early restenosis after stent implantation. To evaluate whether markers of insulin resistance syndrome, including leptin, and endothelial dysfunction are related to increased rate of early restenosis, we studied nondiabetic patients with CHD after successful coronary stenting. Methods and Results-Both patients with CHD undergoing coronary stenting (120 patients) and control subjects (58 patients) were submitted to an oral glucose tolerance test (OGTT). Fasting leptin levels and fasting and postglucose load insulin sensitivity were assessed. Endothelial function was measured by nitrite and nitrate release (NOx) during OGTT. More than 50% of patients treated with stent implantation presented impaired glucose tolerance or type 2 diabetes, which was previously undiagnosed. These patients also had higher glucose, insulin, and leptin levels than control subjects. Among the stented patients, insulin and leptin levels were higher in patients with restenosis than in patients without restenosis. A significant increase in NOx levels was found during OGTT both in patients without restenosis and in control subjects. On the contrary, NOx profiles were blunted in patients with restenosis. At multiple regression analysis, only ⌬AUC-NOx areas and insulin sensitivity index showed an independent correlation with the minimal lumen diameter at follow-up. Conclusions-We demonstrated that insulin resistance and endothelial dysfunction are independent predictors of early restenosis after coronary stenting.

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“…26 Endothelial dysfunction and impaired nitric oxide-mediated vasodilatation have also been suggested to directly lead to reduced insulin delivery to skeletal muscles, resulting in peripheral insulin resistance and hyperglycaemia. 27 The association of insulin resistance with arterial hypertension 28 further suggests that a vascular impairment might precede development of diabetes. The ability of arterial hypertension to predict incident diabetes 8 also confirms that the vascular changes associated with diabetes cannot be simply considered as a consequence of the disease.…”

Section: Discussionmentioning

confidence: 99%

Hypertensive target organ damage predicts incident diabetes mellitus

Izzo

Simone

Trimarco

et al. 2013

European Heart Journal

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See page 3395 for the editorial comment on this article (doi:10.1093/eurheartj/eht365) AimsWhether patients with hypertensive preclinical cardiovascular disease (CVD) are at higher risk of incident diabetes has never been studied. Methods and resultsWe assessed incident diabetes in 4176 hypertensive non-diabetic patients (age 58.7 + 8.9 years, 58% male) with ≥1 year follow-up (median: 3.57 years; inter-quartile range: 2.04-7.25). Left ventricular (LV) hypertrophy (LVH) was defined as LV mass index (LVMi) ≥51 g/m 2.7 . Carotid atherosclerosis (CA) was defined as intima-media thickness .1.5 mm. During follow-up, diabetes developed in 393 patients (9.4%), more frequently in those with than without initial LVH or CA (odds ratio ¼ 1.97 and 1.67, respectively; both P , 0.0001). In the Cox regression, the presence of either initial LVH or CA was associated with higher hazard of diabetes [hazards ratio (HR) ¼ 1.30 and 1.38, respectively; both P ¼ 0.03], independently of the type and number of anti-hypertensive medications, initial systolic blood pressure (P , 0.001), body mass index, fasting glucose, family history of diabetes (all P , 0.0001), and therapy with b-blockers. The presence of one of the, or both, markers of preclinical CVD increased the chance of incident diabetes by 63 or 64%, respectively (both P , 0.002), independently of significant confounders, a result that was confirmed (HR ¼ 1.70 or 1.93, respectively; both P , 0.0001) using ATPIII metabolic syndrome (HR ¼ 2.73; P , 0.0001) in the Cox model. ConclusionInitial LVH and CA are significant predictors of new onset diabetes in a large population of treated hypertensive patients, independently of initial metabolic profile, anti-hypertensive therapy, and other significant covariates. This sequence may be attributable to risk factors common to preclinical CVD and diabetes, but a vascular origin of diabetes cannot be excluded.--

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Endothelial Dysfunction Is Detectable in Young Normotensive First-Degree Relatives of Subjects With Type 2 Diabetes in Association With Insulin Resistance

Cited by 412 publications

References 38 publications

The role of total and high-molecular-weight complex of adiponectin in vascular function in offspring whose parents both had type 2 diabetes

The role of total and high-molecular-weight complex of adiponectin in vascular function in offspring whose parents both had type 2 diabetes

Association of insulin resistance, hyperleptinemia, and impaired nitric oxide release with in-stent restenosis in patients undergoing coronary stenting

Hypertensive target organ damage predicts incident diabetes mellitus

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