Effect of weight loss on blood pressure and insulin resistance in normotensive and hypertensive obese individuals

Su, Hsiu-Yueh; Sheu, Wayne Huey‐Herng; Chin, Hong-Chan; Jeng, Chii; Chen, Y.-D. I.; Reaven, Gerald M.

doi:10.1016/0895-7061(95)00330-r

Cited by 83 publications

(41 citation statements)

References 17 publications

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“…In longitudinal studies, weight gain is known to be associated with rising insulin levels, 33 and weight loss usually leads to some improvement in insulin sensitivity. 32,34 Whether persistence of obesity is associated with changes in insulin resistance is, however, not known.…”

Section: Discussionmentioning

confidence: 99%

Influence of duration of obesity on the insulin resistance of obese non-diabetic patients

et al. 1998

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OBJECTIVE: To investigate whether duration of obesity has an independent impact on insulin resistance. DESIGN: Case-control study. SUBJECTS: 30 non-diabetic obese subjects (age, 34 AE 2 y, body mass index (BMI), 33.5 AE 0.8 kg Á m 72 ) with a range (1±35 y) of self-reported duration of obesity, and 12 age-and gender-matched non-obese controls (BMI, 22.1 AE 0.6 kg Á m 72 ). MEASUREMENTS: Oral glucose tolerance (40 g Á m 72 ), insulin sensitivity (by the euglycaemic insulin clamp technique), and insulin secretion (as the product of post-hepatic insulin clearance and plasma insulin concentration). RESULTS: The obese group presented hyperinsulinaemia in the basal state and after glucose loading (insulin area 58 AE 5 vs 33 AE 3 nmol Á l 71 Á 2 h, P 0.005), insulin resistance (M value 37.4 AE 4.8 vs 50.6 AE 2.6 m mmol Á min 71 Á kg FFM 71 , P 0.002), and insulin hypersecretion (61.9 AE 6.0 vs 33.9 AE 4.0 nmol Á 2 h, P 0.007); endogenous glucose production was similar in the two groups. In the whole dataset, insulin resistance was directly related to BMI, the waist-to-hip ratio (WHR), endogenous glucose production, insulin secretion, and fasting serum triglycerides and uric acid concentrations. When the obese subjects were strati®ed by duration of obesity, insulin resistance was progressively lower with longer obesity duration (P 0.04). When simultaneously adjusting by age, gender and BMI, obesity duration was independently associated with greater insulin sensitivity (P 0.003), lower plasma insulin response to oral glucose (P 0.001), and lower fasting and glucose-stimulated insulin release (P 0.01 for both). CONCLUSIONS: In obese subjects with preserved glucose tolerance, duration of obesity is associated with better insulin sensitivity irrespective of the degree of overweight.

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Section: Discussionmentioning

confidence: 99%

Influence of duration of obesity on the insulin resistance of obese non-diabetic patients

et al. 1998

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“…26 Conversely, weight loss reduces risk in overweight individuals. 27,28 The relation between weight and cardiovascular risk factors is also present during childhood. Waist-to-hip ratio has been positively correlated with serum cholesterol and LDL-C as early as 4 years of age.…”

Section: Discussionmentioning

confidence: 99%

Relation of Weight and Rate of Increase in Weight During Childhood and Adolescence to Body Size, Blood Pressure, Fasting Insulin, and Lipids in Young Adults

et al. 1999

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Background-Weight gain is of concern during early development because adult obesity and its cardiovascular consequences appear to have their origins during childhood. Insulin resistance is known to be related to obesity. Thus, weight gain beginning in childhood may influence the development of insulin-induced cardiovascular risk during adulthood. Methods and Results-We monitored 679 individuals from 7.7Ϯ0.1 years of age with repeated measures of height, weight, and systolic blood pressure (SBP) until 23.6Ϯ0.2 years of age, when blood samples were obtained for measurements of insulin and lipids. Initial childhood weight, body mass index (BMI), and height were significantly correlated with young adult weight, BMI, and height and with fasting insulin, lipids, and SBP. The increases in weight and BMI but not height during childhood were significantly related to the young adult levels of insulin, lipids, and SBP. Conclusions-These data suggest that weight gain in excess of normal growth during childhood is a determinant of adult cardiovascular risk. The finding in multiple linear regression analysis that weight gain during childhood rather than the childhood weight at 7.7 years of age is significantly related to young adult risk factors suggests that a reduction in weight gain could reduce subsequent levels of cardiovascular risk.

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“…5 This observation is supported by data which show a positive linear relationship between BP and body mass index even in the normotensive range, 6 and also by data demonstrating that obese-normotensive individuals almost always reduce BP when they lose weight. 7,8 In contrast, it is possible to study hypertension-independent effects of obesity on cardiovascular function with an animal model of diet-induced obesity, 9 by utilizing a longitudinal analysis wherein a pre-obese BP is determined and subsequently maintained during obesity development. However, the choice of antihypertensive treatment is problematic.…”

Section: Introductionmentioning

confidence: 99%

Hydralazine as antihypertensive therapy in obesity-related hypertension

2004

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OBJECTIVE:The objectives were two-fold: (1) determine whether the use of hydralazine as antihypertensive therapy during obesity development exacerbated obesity-related cardioacceleration and hormonal abnormalities; (2) determine whether the absence of hypertension in obesity attenuated obesity-related abnormalities in hemodynamics, cardiac hypertrophy, and hormonal profile. DESIGN: Female New Zealand White rabbits were divided into lean control (n ¼ 12), lean hydralazine-treated (n ¼ 9), obese control (n ¼ 11), and obese hydralazine-treated (n ¼ 8) groups. Pretreatment mean blood pressure (BP) and heart rate (HR) were determined using telemetry. Pretreatment BP was maintained during 12 weeks of obesity development using hydralazine. MEASUREMENTS: Chronically measured BP and HR; plasma/blood volume; wet and dry ventricular weights; body fat/water; and hormonal profile (plasma renin activity, aldosterone, cortisol, atrial natriuretic peptide, adrenaline, and noradrenaline). RESULTS: Hydralazine treatment in obese animals attenuated obesity-related renin-angiotensin system (RAS) activation. In contrast, RAS was activated in lean hydralazine, as indicated by increased plasma aldosterone. The absence of hypertension in obese hydralazine did not result in attenuation of cardioacceleration, cardiac hypertrophy, or intravascular volumes. CONCLUSIONS: Hydralazine treatment in obese rabbits did not exacerbate obesity-related cardiovascular and hormonal alterations. Cardioacceleration and cardiac hypertrophy persisted in obese hydralazine despite BP control, suggesting hypertension-independent effects of obesity on these variables. Hydralazine's effects on RAS activation differed in lean and obese rabbits, suggesting that the systemic effects of hydralazine as a control therapy in evaluation of antihypertensive medications may differ depending on the underlying pathology.

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Effect of weight loss on blood pressure and insulin resistance in normotensive and hypertensive obese individuals

Cited by 83 publications

References 17 publications

Influence of duration of obesity on the insulin resistance of obese non-diabetic patients

Influence of duration of obesity on the insulin resistance of obese non-diabetic patients

Relation of Weight and Rate of Increase in Weight During Childhood and Adolescence to Body Size, Blood Pressure, Fasting Insulin, and Lipids in Young Adults

Hydralazine as antihypertensive therapy in obesity-related hypertension

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