Insulin Resistance, Hyperinsulinemia, and Blood Pressure

Ferrannini, Ele; Natali, Andrea; Capaldo, Brunella; Lehtovirta, Mikko; Jacob, Stephan; Yki-Järvinen, H

doi:10.1161/01.hyp.30.5.1144

Cited by 261 publications

(89 citation statements)

References 33 publications

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“…[15][16][17][18] Some investigators have reported that chronic administration of insulin might contribute to a sympathetically mediated increase in BP in animal models of obesity hypertension. 19,20 On the other hand, it has been reported that insulin administered acutely causes vasodilation and does not increase BP in animal or humans models.…”

Section: Discussionmentioning

confidence: 99%

Weight Gain–Induced Blood Pressure Elevation

Masuo¹,

Mikami²,

Ogihara³

et al. 2000

Hypertension

131

102

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Abstract-This study was conducted to evaluate the mechanisms in weight gain-induced blood pressure (BP) elevation focusing, in particular, on the contributions of sympathetic nervous system activity, fasting plasma insulin, and leptin to BP levels. The study design was longitudinal with a cohort of 1897 men. BP, pulse rate, body mass index (BMI), fasting plasma norepinephrine (NE), insulin, and leptin were measured at 6 and 12 months in those 172 lean normotensive, 79 obese normotensive, 64 lean untreated hypertensive, and 38 obese untreated hypertensive men whose BMI increased Ͼ10% during the first 6 months. At entry, levels of BP, pulse rate, plasma NE, insulin, and leptin in obese subjects, regardless of BP status, were significantly greater than those in lean subjects. The levels of plasma NE, insulin, and leptin increased with weight gain in the 4 study groups. In the subjects with BP elevation, the increase in pulse rate and plasma NE was significantly greater than that in the subjects without BP elevation at both 6 and 12 months for each of the 4 study groups, although the increase in BMI was similar between the subjects with and without BP elevation. In obese but not lean subjects, whether normotensive or hypertensive, the increases in plasma insulin and plasma leptin with weight gain were greater in the subjects with accompanying BP elevation compared with the subjects without BP elevation. On the other hand, at 6 months in lean subjects, the increase in plasma insulin with weight gain in the subjects with BP elevation was actually lower than that in the subjects without BP elevation. These results suggest that weight gain-induced sympathetic overactivity is more tightly linked to weight gain-induced BP elevation than the changes in plasma insulin and leptin that also accompany weight gain. It is probable that sympathetic nervous activation with weight gain is a major mechanism of blood pressure elevation. Hyperinsulinemia and hyperleptinemia may be ancillary factors that contribute to sympathetic nervous stimulation with weight gain. Key Words: obesity Ⅲ body mass index Ⅲ hypertension, obesity Ⅲ investigative techniques Ⅲ sympathetic nervous system Ⅲ leptin Ⅲ insulin O besity and obesity related-hypertension are major and growing, international health problems, described by the World Health Organization (WHO) in its "Global Burden of Disease" report. 1 Furthermore, it is well known that obesity is a leading risk factor for chronic arterial hypertension and coronary heart disease. 2 The plasma concentration of the adipocyte hormone, leptin, is elevated in human obesity, which is thought to represent a state of leptin "resistance." 3 Leptin has been shown to influence sympathetic nerve activity. 4,5 Collins et al reported that leptin increased norepinephrine (NE) turnover in intercapsular brown adipose tissue. 3 Shek et al 6 reported that in the animal models, chronic leptin infusion caused an increase in heart rate and blood pressure, suggesting a possible role for leptin in the development of obesity-r...

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Section: Discussionmentioning

confidence: 99%

Weight Gain–Induced Blood Pressure Elevation

Masuo¹,

Mikami²,

Ogihara³

et al. 2000

Hypertension

131

102

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“…25,26 The quantity and distribution of body fat is an important confounder in the insulin -BP relationship. 27,28 Although the positive association between IR and a high BP has been reported to be independent of obesity in some studies, 26,29 other studies have suggested that obesity, in particular central obesity, may be the cause of this association. 24,28,30,31 However, the present study showed that the level of IR, BMI and waist circumference were independent risk factors of a high BP in normoglycemic Koreans.…”

Section: Discussionmentioning

confidence: 99%

In Normoglycemic Koreans, Insulin Resistance and Adipocity are Independently Correlated With High Blood Pressure

Sung

Kim

et al. 2004

Circ J

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yperinsulinemia is known to be associated with various cardiovascular risk factors, including high triglyceride concentrations, low high-density lipoprotein (HDL) cholesterol concentrations, high blood pressure (BP), and obesity. 1-3 However, there is some controversy about the role of insulin resistance (IR) in the regulation of BP. Several prospective studies have linked insulin concentrations to the incidence of hypertension [4][5][6] and it has been suggested that hyperinsulinemia and/or IR plays a role in the pathophysiology of hypertension. [7][8][9][10][11] But the association between insulin and hypertension remains contentious, 12 with a number of studies reporting no association between insulin and BP. 13,14 Moreover, to our knowledge a large study of the association between BP and IR has not been conducted in normal glucose tolerance Asians. Therefore, we decided to investigate the relationships between BP and IR using a homeostasis model (HOMA-IR) and further, to evaluate the association between body fat distribution and high BP in nondiabetic normoglycemic Koreans. Methods Subjects and MeasurementsThe total number of subjects involved was 53,477, all of whom presented for a routine health status check up at the Kangbook Samsung Hospital, College of Medicine in Sungkyunkwan University in 2002, and who were without specific medical complaints. Based on the results obtained, patients suspected of having acute inflammatory diseases, other malignancies and those taking BP-lowering medication were excluded. In addition we also excluded those taking antidiabetic agents and those with a fasting glucose over 110 mg/dl. Finally, 49,076 subjects (31,820 men; 17,256 women) were included in this study. Anthropometric indices of adiposity, metabolic variables (including fasting serum insulin and homeostasis model assessment (HOMA) index of insulin sensitivity), BP and several cardiovascular risk factors were measured. The BP was determined using a mercury manometer, between 08.00 h and 10.00 h, after the subject had been sitting upright for at least 10 min.When the systolic or diastolic BP exceeded 140 mmHg or 90 mmHg, it was re-measured twice after a rest and averaged. A high BP was defined as a SBP ≥140 mmHg or a DBP ≥90 mmHg.The body mass index (BMI: kg/m 2 ), the waist circumference and the waist -hip ratio were also measured. The subjects were asked questions concerning the risk factors for general cardiovascular disease (ie, past medical history, life style, such as alcohol consumption, smoking, and Background There is some controversy about the role of insulin resistance (IR) in the regulation of blood pressure (BP). Moreover, a large study of the association between BP and IR has not been conducted in normal glucose tolerance Asians. The present study investigated the relationships between IR, body mass index (BMI) and waist circumference and BP in normoglycemic Koreans. Methods and ResultsAnthropometric indices of adiposity, metabolic variables (fasting serum insulin and a homeostasis model assessment (H...

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“…These include the evaluation of fasting glucose and insulin ratio, the analysis of glucose and insulin profiles after oral glucose load using 75 g dextrose (OGTT) and the so-called 'gold standard' method, which is the euglycemic hyperinsulinemic clamp technique. 21,22 Three indices were obtained using different procedures: (1) homeostasis model assessment (HOMA 23 ): fasting glucose (mmol l -1 ) Â fasting insulin (mU l -1 ); (2) Matsuda index of glucose and insulin profiles after OGTT: 24 10 000 OG0 Â I0x G mean Â I mean , where G and I represent the plasma glucose (mg per 100 ml) and insulin (mU l -1 ) concentrations, respectively, expressing fasting (0) and mean OGTT concentrations; (3) euglycemic, hyperinsulinemic clamp technique (M-value) as described recently in the EU-RISC protocol: 19,25 Exogenous insulin is administered as a primed-continuous infusion at a rate sufficient to maintain a pre-set hyperinsulinemic plateau; simultaneously, the glucose concentration is clamped at the normal fasting level by means of an exogenous infusion of glucose. With this latter technique, the insulin action is measured in vivo under comparable conditions of stimulus (the plasma insulin concentration) and substrate (the plasma glucose concentration 26 ).…”

Section: Methodsmentioning

confidence: 99%

“…Blood samples were obtained from a wrist vein heating the hand to 60 1C on a heating pad (for intermittent blood sampling of arterialized venous blood), for measurement of plasma and insulin concentrations. 25 …”

Section: Methodsmentioning

confidence: 99%

Nocturnal blood pressure but not insulin resistance influences endothelial function in treated hypertensive patients

et al. 2010

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The impact of insulin sensitivity, casual blood pressure and 24-h ambulatory blood pressure on endothelial function was studied in treated hypertensive subjects. Flow-mediated dilatation of the brachial artery after reperfusion was used to determine endothelial function. Insulin sensitivity indices were obtained by using the homeostasis model assessment, after 75 g Dextrose oral glucose tolerance tests (Matsuda index) and the euglycemic hyperinsulinemic clamp (M-value) in 49 patients with arterial hypertension. The insulin sensitivity indices were compared with healthy controls matched for body weight, age and sex (n ¼ 23). Hypertensive patients under therapy were insulin resistant, had higher LDL-cholesterol levels, higher blood pressure and lower endothelial function than healthy controls. Flow-mediated dilatation showed, in the study population being treated for arterial hypertension, no relationships of all insulin sensitivity indices with flow-mediated dilatation, casual blood pressure in the morning before the tests and 24-h ambulatory blood pressure. Flow-mediated dilatation was strongly influenced by nocturnal systolic and diastolic 24-h ambulatory blood pressure (systolic: R 2 ¼ 0.0943, Po0.05; diastolic: R 2 ¼ 0.0947, Po0.05). Therefore, endothelial function in these patients is predominantly influenced by nocturnal systolic and diastolic blood pressure and not by insulin sensitivity.

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Insulin Resistance, Hyperinsulinemia, and Blood Pressure

Cited by 261 publications

References 33 publications

Weight Gain–Induced Blood Pressure Elevation

Weight Gain–Induced Blood Pressure Elevation

In Normoglycemic Koreans, Insulin Resistance and Adipocity are Independently Correlated With High Blood Pressure

Nocturnal blood pressure but not insulin resistance influences endothelial function in treated hypertensive patients

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