Obesity increases prostanoid-mediated vasoconstriction and vascular thromboxane receptor gene expression

Traupe, Tobias; Läng, Matthias; Göettsch, Winfried; Münter, Klaus; Morawietz, Henning; Vetter, W; Barton, Matthias

doi:10.1097/00004872-200211000-00024

Cited by 124 publications

(136 citation statements)

References 40 publications

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“…Similarly, an important aspect of obesity-associated vascular injury obtained from preclinical and clinical studies, is that many of the vascular changes found in obesity are highly similar to those seen with aging [37] , which not only represents a physiological process but in itself represents a strong and independent risk factor for future cardiovascular events [37] . As with aging [37] , experimental or human obesity shows an attenuation of endothelium-dependent vasodilation [38,39] , a decrease in NO bioactivity [38,39] in conjunction with NO synthase uncoupling [37] , an increase in prostanoid-mediated endothelium-dependent contractions [40][41][42] , telomere shortening [43][44][45][46] , increased vascular stiffness [47] , and increased arterial intima-media thickness [26,48] . Obesity also increases tissue levels of endothelin-1 [38,49,50] , a strong vasoconstrictor peptide and atherogenic growth factor and proinflammatory stimulus [51] .…”

Section: Atherosclerosis Begins In Childhoodmentioning

confidence: 99%

Childhood obesity: a life-long health risk

Barton

2012

Acta Pharmacol Sin

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Childhood obesity has become major health concern for physicians, parents, and health agencies around the world. Childhood obesity is associated with an increased risk for other diseases not only during youth but also later in life, including diabetes, arterial hypertension, coronary artery disease, and fatty liver disease. Importantly, obesity accelerates atherosclerosis progression already in children and young adults. With regard to pathophysiological changes in the vasculature, the striking similarities between physiological changes related to aging and obesity-related abnormalities are compatible with the concept that obesity causes "premature" vascular aging. This article reviews factors underlying the accelerated vascular disease development due to obesity. It also highlights the importance of recognizing childhood obesity as a disease condition and its permissive role in aggravating the development of other diseases. The importance of childhood obesity for disease susceptibility later in life, and the need for prevention and treatment are also discussed.

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Section: Atherosclerosis Begins In Childhoodmentioning

confidence: 99%

Childhood obesity: a life-long health risk

Barton

2012

Acta Pharmacol Sin

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“…These two changes weaken the protective role of the endothelium with reduced nitric oxide production and enhanced responsiveness to endothelin. 8,9,10 Summarizing these findings, Traupe et al advocate that obesity related increases in production of EDCFs may contribute to the development of vascular diseases. As insulin resistance advances and patients develop diabetes, comparable vascular abnormalities are present at the endothelial level 11,12 (see Figure 1).…”

Section: Pathobiology Of Atherosclerosismentioning

confidence: 99%

Effect of glitazones on the progression of coronary artery disease in type 2 diabetes patients

Chilton¹

2009

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Abstract:The effect of thiazolidinediones (TZDs) on the progression of atherosclerosis in diabetes patients remains unclear. There has been heightened interest in recent years in this class of diabetes medications due to the non-glycemic lowering effects, such as altering lipids, inflammation and hematologic profiles. There have been several exciting studies over the past few years focused on the mechanism of action of the TZDs with respect to alteration in the cardio-metabolic profile in diabetes patients. New tools such as intravascular ultrasound have been used to follow plaques characteristics over time on a much more sensitive scale than has ever been possible in the past by coronary angiograms. These advances have enabled researchers to follow closely the macrovascular effects of different anti-atherosclerotic medications such as statins and TZDs. This article reviews the pathophysiology of atherosclerosis in diabetes, the role that TZDs play in this process and the imaging trials looking at the progression or regression of atherosclerosis in patients treated with TZDs.

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“…32 The design of the LIFE study does not provide information about mechanisms of obesity-related risk. There is, however, growing evidence that severe obesity is associated with activation of inflammatory mechanisms, 34 -39 increase in vascular thromboxane receptor gene expression, 40 and increased fibrinogen levels 41 that might be involved in precipitating cardiovascular disease events, especially when cardiovascular risk is high or very high. Activation of circulating markers of inflammation is most evident with central body fat distribution.…”

Section: Severe Obesity As An Independent Prognostic Predictormentioning

confidence: 99%

Body Build and Risk of Cardiovascular Events in Hypertension and Left Ventricular Hypertrophy

et al. 2005

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Background-Obesity may independently increase the risk of adverse events in hypertension with target-organ damage.We investigated whether body build was independently associated with higher cardiovascular risk and whether treatment with losartan relative to atenolol influenced the impact of body build on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and on cardiovascular death in patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Methods and Results-The population of 9079 patients was divided as follows: thin (body mass index [BMI] Ͻ20 kg/m 2 , 2%), normal weight (BMI 20 to 24.9, 24%), overweight (BMI 25 to 29.9, 45%), and obese (class I: BMI 30 to 34.9, 21%; class II: BMI 35 to 39.9, 6%; class III: BMI Ն40, 2%). Incident diabetes increased progressively with BMI and was somewhat higher in the atenolol arm. Differences in gender and race were detected among the body build groups. Rates (Cox proportional hazard analysis) of the primary composite end point did not differ among body build groups after adjustment for age, gender, race, smoking habit, prevalent cardiovascular disease, and left ventricular hypertrophy. Cardiovascular death was more frequent among thin (PϽ0.05) and pooled class II-III obesity (both PϽ0.04) than normal-weight groups. Risk was not attenuated significantly by losartan treatment, nor did it interfere with the greater benefit of losartan-as opposed to atenolol-based treatment. Conclusions-In the LIFE study, stratification for classes of body build identified increased risk of cardiovascular mortality in both thin and moderately-to-severely obese individuals. This risk was not attenuated significantly by losartan treatment, nor did it interfere with the greater benefit of losartan-based treatment as opposed to atenolol-based treatment.

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Obesity increases prostanoid-mediated vasoconstriction and vascular thromboxane receptor gene expression

Abstract: These data demonstrate that obesity augments prostanoid-dependent vasoconstriction and markedly increases vascular thromboxane receptor gene expression. These changes are likely to promote the development of vascular disease, hypertension and thrombosis associated with obesity.

Cited by 124 publications

References 40 publications

Childhood obesity: a life-long health risk

Childhood obesity: a life-long health risk

Effect of glitazones on the progression of coronary artery disease in type 2 diabetes patients

Body Build and Risk of Cardiovascular Events in Hypertension and Left Ventricular Hypertrophy

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