Additive effects of obesity, hypertension, and type 2 diabetes on insulin resistance.

Abstract

Resistance to insulin-mediated glucose disposal has been previously shown to be increased in association with obesity, high blood pressure, and non-insulin-dependent diabetes mellitus. We initiated the present study to quantify the separate effects of hypertension and non-insulin-dependent diabetes mellitus on insulin resistance in both nonobese and obese subjects. To accomplish this, 88 subjects were divided into the following five experimental groups: normal blood pressure, nonobese (n=17); normal blood pressure, obese (n=18); high blood pressure, nonobese (n=18); high blood pressure, obese (n=19); and high blood pressure, obese, noninsulin-dependent diabetes mellitus (n=16). Plasma glucose and insulin concentrations were measured before and after a 75-g oral glucose load. Resistance to insulin-mediated glucose disposal was estimated by determining the steady-state plasma insulin and glucose concentrations during the last 30 minutes of a continuous infusion of somatostatin (5 jug/min), exogenous insulin (25 mU/m 2 per minute), and glucose (240 mg/m 2 per minute). Since the steady-state plasma insulin concentrations I n the past several years it has become apparent that the ability of insulin to stimulate glucose disposal can vary widely from person to person. 12 In addition, it has also been shown 3 -8 that insulin resistance is a common feature in patients who are obese or have either hypertension or non-insulin-dependent diabetes mellitus (NIDDM). Patients with high blood pressure and/or NIDDM tend to be overweight, and it has been suggested that obesity plays a central role in the development of insulin resistance and its associated abnormalities.9 ' 10 Thus, obesity can be viewed as the cause of insulin resistance in patients with high blood pressure and/or NIDDM or simply as a factor that modulates insulin-mediated glucose disposal in any individual, thereby making that individual more likely to develop hypertension or NIDDM. We initiated the present study to address these issues. MethodsThis study was performed in 88 volunteers in good general health with the exception of hypertension with or without the codiagnosis of NIDDM. Subjects were recruited to create the following five experimental groups: (1) are similar in all subjects, the higher the steady-state plasma glucose, the more insulin resistant the individual. Nonobese subjects with normal blood pressure had the lowest plasma glucose and insulin responses and steady-state plasma glucose concentrations, and their values were significantly different from the other four groups. Obese or nonobese subjects with high blood pressure had significantly higher plasma glucose responses and steady-state plasma glucose concentrations than did their respective weight-matched control subjects. Finally, plasma glucose responses and steady-state plasma glucose concentrations were significantly higher in obese subjects with both high blood pressure and non-insulin-dependent diabetes mellitus. These results support the view that the effects of obesity, high...

Plasma insulin, plasminogen activator inhibitor, and ankle-brachial systolic blood pressure ratio in overweight hypertensive subjects

“…21 A weaker correlation has been observed between brachial systolic blood pressure and the fat distribution in obese and non-obese subjects. 7,21,31,32 In the present study, we found that the degree of abdominal fat deposition was strongly associated with the decrease in ABI ratio. The validity of this relationship was based on two important findings: (i) the ABI ratio was no significantly correlated with body weight or body mass index, and (ii) the observed correlation did not result from a significant correlation between the WHR and brachial systolic blood pressure but rather from a negative correlation between the WHR and ankle systolic blood pressure.…”

“…The validity of this relationship was based on two important findings: (i) the ABI ratio was no significantly correlated with body weight or body mass index, and (ii) the observed correlation did not result from a significant correlation between the WHR and brachial systolic blood pressure but rather from a negative correlation between the WHR and ankle systolic blood pressure. Finally, because the degree of abdominal obesity is known to be strongly associated with the presence of insulin resistance, 7,12 we tried to correlate the ABI ratio with all the other major biological markers of resistance to insulin, ie, hypertriglyceridaemia, low HDL-cholesterol, hyperglycaemia and hyperinsulinaemia and finally PAI antigen. 1 Significant negative correlation coefficients were observed with each of these metabolic disorders, indicating that all these biological markers were significantly associated with the observed changes in pressure wave transmission of lower limbs.…”

“…[1][2][3] In patients with essential hypertension, insulin resistance may be exacerbated by antihypertensive drug therapy, mainly when diuretics and beta-blocking agents are involved. [4][5][6][7][8] Resistance to insulin is also a predictor of cardiovascular complications, particularly for the coronary circulation. 1,5,6,9,10 The ratio between ankle on brachial systolic blood pressure (ABI) is a well established index allowing bution, but also with the usual biological features of resistance to insulin: plasma triglycerides and cholesterol; plasma glucose and insulin; and plasminogen activator inhibitor (PAI) antigen.…”

Insulin resistance and upper-normal glucose levels in hypertension: a review

“…7 The insulin suppression test has also been employed to test for the presence of insulin resistance in hypertension. 3,[8][9][10] The procedure requires the use of three simultaneous intravenous infusions.…”

Differential blood pressure effects of oral glucose and intravenous L-arginine in healthy lean normotensive and obese hypertensive subjects

“…[10][11][12][13] Insulin resistance with compensatory hyperinsulinaemia has been observed in lean hypertensives, obese normotensives and hypertensives and in patients with type 2 diabetes mellitus. 2,[14][15][16][17][18] Infusions of insulin have been shown to increase blood pressure (BP) in rats. 19,20 In addition to insulin, glucose per se may play a role in hypertension.…”