Increased Adipose Angiotensinogen Gene Expression in Human Obesity

Harmelen, Vanessa van; Ariapart, Parisa; Hoffstedt, Johan; Lundkvist, Inger; Bringman, Sven; Arner, Peter

doi:10.1038/oby.2000.40

Cited by 154 publications

(112 citation statements)

References 18 publications

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“…Obesity leads to hypertension and increases the cardiovascular risk (Mikhail et al, 1999). RAS has been implicated in obesity by several authors (Giacchetti et al, 2002), which is supported by recent investigations that show high plasma concentrations of angiotensinogen (ANG) (Umemura et al, 1997) and a rise in the expression of the ANG gene in obese humans (Van Harmelen et al, 2000). The plasma ANG decrease was highly correlated with the WC decline and with one reduction in the systolic ambulatory blood pressure (Engeli et al, 2005).…”

Section: Discussionmentioning

confidence: 84%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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Metabolic Syndrome (MS) is recognized as a cluster of cardiovascular risk factors. All components of MS have a genetic base. Genes of the renin angiotensin system are potential candidate genes for MS. We investigated whether angiotensin converting enzyme (ACE) gene polymorphism increases susceptibility to MS as an entity in a Mexican population. In a cross-sectional study, 514 individuals were studied including 245 patients with MS and 269 subjects without MS criteria. ACE gene polymorphism was detected using PCR. MS was defined according to The National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) criteria, except that the raised fasting plasma glucose ≥ 100 mg/dl criterion for identification of intolerance fasting glucose was modified in accordance with the suggestion of the American Diabetes Association. Patients with MS were significantly different from subjects without MS in relation to mean body mass index (BMI), waist circumference (WC), systolic blood pressure, diastolic blood pressure, glucose, total cholesterol (C), triglycerides, HDL-C, and LDL-C (P ＜ 0.0001). The differences in the mean BMI, WC, glucose, total cholesterol, triglycerides, LDL-C, and HDL-C were maintained in patients with the MS and DD genotypes (P ＜ 0.01). The DD genotype was strongly associated with MS (adjusted OR = 5.48, 95% CI 3.20-9.38, P ＜ 0.0001). We concluded that the DD genotype increases susceptibility to MS in a Mexican population. These results indicate that pharmacological and non-pharmacological treatment and a reduction in body fat will have important therapeutic implications in this disease.

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Section: Discussionmentioning

confidence: 84%

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

et al. 2007

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“…[45][46][47] The renin-angiotensin-aldosterone system (RAAS) is overactivated in overweight obese hypertensive subjects, and plasma renin activity (PRA) and aldosterone concentrations are higher than those in lean subjects. [48][49][50][51][52][53] Activation of the RAAS increases sodium retention and peripheral resistance, thereby contributing to obesity hypertension. Locally produced angiotensin II, arising from adipose tissue itself, and adipocyte-derived proteins modulating aldosterone secretion 51,54,55 may also have a significant etiological role.…”

Section: Discussionmentioning

confidence: 99%

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

et al. 2010

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We evaluated the effects of body weight (BW) loss on blood pressure (BP) in overweight non-obese patients with stage 1 hypertension. We enrolled 376 overweight (body mass index (BMI) X25 and o30 kg m À2 ) stage 1 hypertensive patients in this prospective 12-month trial. Each patient received tailored, low caloric dietary advice. After 6 months, patients with a BW reduction o5% were excluded. Body weight, BMI, BP, fasting plasma glucose (FPG), fasting plasma insulin (FPI), leptin (pL), renin and aldosterone levels were evaluated at baseline and after 6 and 12 months. In 222 patients who completed the study, a mean weight reduction of 8.1 kg reduced systolic blood pressure (SBP) by 4.2 mm Hg and diastolic blood pressure (DBP) by 3.3 mm Hg (Po0.05), which was accompanied by a significant decrease in FPI, pL and aldosterone levels (Po0.05). Larger SBP/DBP reductions were observed in 106 patients with normalized BMI (À5/À4.5 mm Hg, Po0.01) compared with the 116 patients who did not become normalized (À3.3/À1.6 mm Hg). The former also presented with greater decreases in FPG, FPI, pL, renin and aldosterone levels. Of the 106 patients who had normalized BMI, 52 also had normalized BP. Clinical and metabolic characteristics of these patients were similar to those of the 56 patients who did not have normalized BP. In overweight, mild hypertensive patients, weight loss was effective in reducing BP and in reversing some endocrinologic alterations associated with being overweight. Half of the patients who had normalized BMI also had normalized BP, which could indicate that these patients essentially did not have a form of hypertension but that these effects were instead secondary to being overweight. Keywords: blood pressure; overweight; weight-loss INTRODUCTION Excessive body weight (BW), in particular abdominal obesity, increases the risk for cardiovascular disease, stroke, type 2 diabetes, hypertension, lipoprotein disorders, osteoarthritis, certain types of cancers and total mortality. 1-5 An escalating epidemic of overweight (body mass index (BMI) X25 and o30 kg m À2 ) and obesity (BMI 430 kg m À2 ), is affecting both industrialized and many developing countries in the world, and constitutes a major public health problem. 4,6,7 In particular, in the United States, the prevalence of obesity was estimated at 32% of the population. Being overweight was even more prevalent, representing 42% of men and 28% of women, of whom 34 and 39%, respectively, had high blood pressure (BP). 8,9 The coexistence of hypertension and excessive BW greatly enhances cardiovascular risk. 2,10 Recent recommendations suggest the use of stratification tables to calculate the percentage of increased cardiovascular risk in patients with hypertension and excess BW or obesity. 11 The mechanisms underlying hypertension in subjects with excessive BW

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“…Systemic oxidative stress, measured by animals 29,30 . Another proposed cause relates to the abundant synthesis and secretion of angiotensinogen by adipose tissue 31,32 , especially visceral tissue 32,33 . Angiotensinogen is cleaved by rennin to angiotensin I and then converted to angiotensin II by angiotensinconverting enzyme in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Visceral Fat Accumulation is Associated with Oxidative Stress and Increased Matrix Metalloproteinase-9 Expression in Atherogenic Factor-overlapped Model Rats

Tomita¹,

Iwai²,

Kumai

et al. 2010

Showa Univ J Med Sci

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Increased Adipose Angiotensinogen Gene Expression in Human Obesity

Cited by 154 publications

References 18 publications

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Association between angiotensin-1 converting enzyme gene polymorphism and the metabolic syndrome in a Mexican population

Effect of body weight loss and normalization on blood pressure in overweight non-obese patients with stage 1 hypertension

Visceral Fat Accumulation is Associated with Oxidative Stress and Increased Matrix Metalloproteinase-9 Expression in Atherogenic Factor-overlapped Model Rats

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