Insulin resistance in offspring of hypertensive subjects

D, Mino; Wacher, Niels H.; Amato, Dante; Búrbano, Gabriel; Me, Fonseca; Revilla, C; Gordon, Frank J.; Lifshitz, Alberto

doi:10.1097/00004872-199610000-00006

Cited by 13 publications

(7 citation statements)

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“…Some studies noted that body weight was a factor in FHϩ. 24,29,30 The present study extends previously reported data 9 to examine, on a longitudinal basis, the influence of an FHϩ on insulin, plasma NE, and rise in BP (ie, BPE) for 10 years in subjects who were normotensive at entry. The protocol measured BP, pulse, BMI, and plasma NE and insulin for 10 years in young (Ͻ50 years), nonobese (BMI Ͻ26.0 kg/m 2 ), normotensive Japanese men.…”

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confidence: 78%

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Familial Hypertension, Insulin, Sympathetic Activity, and Blood Pressure Elevation

et al. 1998

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Abstract-This study evaluated the effects of a positive family history of hypertension (FHϩ) on the contributions of sympathetic nervous system (SNS) activity and insulin to blood pressure elevation (BPE). The study design was longitudinal and evaluated BP, body mass index (BMI), and fasting plasma insulin and norepinephrine (NE) levels for 10 years in 557 young, nonobese Japanese men who were normotensive at entry. FHϩ was defined as hypertension in first-degree relatives as verified by historical records or direct determination. BPE was defined as a Ն10% rise in systolic and diastolic BP over entry levels during the 10-year period. In the total group FHϩ was noted in 16%, and BPE occurred in 18% of normotensive subjects. When evaluated by FH, the prevalence of BPE was 33% in FHϩ compared with 16% in FHϪ (PϽ0.05). BP levels were greater both at entry and at year 10 in the FHϩ group. The absolute increment in plasma NE over 10 years was greater in the BPE group than in those without BPE (PϽ0.01). Of note, the rise in plasma NE levels in BPE individuals was identical in FHϩ and FHϪ subjects. Plasma insulin increments were also greater in normotensive subjects with BPE than in normotensive subjects without BPE. However, compared with NE, development of hyperinsulinemia was more pronounced in the FHϩ subjects. The results indicate that SNS hyperactivity may be a less genetically determined predictor of hypertension than is hyperinsulinemia. Because SNS changes in this initially normotensive population appeared more closely related to the development of hypertension than to hyperinsulinemia, environmental rather than genetic factors may be the main determinant of early BPE in nonobese normotensive subjects. (Hypertension. 1998;32:96-100.)Key Words: family history Ⅲ sympathetic nervous system Ⅲ insulin Ⅲ blood pressure T he association of hypertension with hyperinsulinemia and SNS hyperactivity is well established. [1][2][3][4][5][6][7] What is less certain is whether increases in SNS activity and insulin precede or follow the development of hypertension. Increases in SNS activity and metabolic abnormalities may be closely aligned with the rise in BP. For example, in a cross-sectional study, our group found that SNS hyperactivity and abnormal blood glucose and insulin responses to glucose administration characterized the early phase of hypertension. 8 In a 10-year longitudinal study, we also noted that increases in SNS activity preceded the hyperinsulinemia and rise in BP in subjects who were normotensive at entry. 9 In the Normative Aging Study of 752 nondiabetic, middle-aged, male participants, it was also found that insulin levels and urinary NE excretion were related to BP levels. 7 The study concluded that insulin levels and urinary NE excretion were independent predictors of hypertension. In analyzing the relationship of SNS activity and insulin to the development of coronary risk in hypertension, Julius et al 10,11 commented on the "chicken-and-egg" question of whether SNS and insulin abnormalities precede the...

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confidence: 78%

“…28 A recent study from Mexico City concluded that IR in FHϩ subjects was more closely related to obesity than FH. 29 In general, most of these family studies offer strong evidence that young normotensive subjects who are FHϩ are at increased risk for BPE. These data also imply that hyperinsulinemia and IR precede the changes in BP.…”

Section: Discussionmentioning

confidence: 99%

Familial Hypertension, Insulin, Sympathetic Activity, and Blood Pressure Elevation

et al. 1998

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“…15,27 Previous studies have shown elevated fasting insulin and insulin-to- Early abnormalities in family hypertension EG Ciolac et al glucose levels, as well as reduced sensitivity of insulin-mediated cellular glucose disposal, in normotensive offspring of hypertensive parents; however, data have not been analysed separately by neither gender nor parental burden. 7,[24][25][26] The only study we have known that assayed fasting insulin and insulin resistance in normotensive with three different parental hypertension burden showed that normotensive offspring of two hypertensive parents had elevated plasma insulin levels and were more likely to show greater insulin resistance than normotensive individuals having either one hypertensive parent or normotensive parents; however, the data were also not analysed separately by gender.…”

Section: Lipids Glucose and Insulinmentioning

confidence: 99%

Haemodynamic, metabolic and neuro-humoral abnormalities in young normotensive women at high familial risk for hypertension

Ciolac

Bocchi²,

Bortolotto³

et al. 2010

J Hum Hypertens

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We analysed the haemodynamic, metabolic and hormonal status at rest and in response to exercise, in young normotensive women with two hypertensive parents (FH þ þ ; n ¼ 17; 25.1±4.8 years), one hypertensive parent (FH þ ; n ¼ 18; 24.9 ± 4.1 years) and normotensive parents (FHÀ; n ¼ 15; 25.3 ± 3.8 years). Casual and ambulatorial blood pressure (BP), carotid-femoral pulse wave velocity (PWV) and biochemistry were analysed. BP, nor-epinephrine (NE), epinephrine (EPI), endothelin-1 (ET-1) and nitrite/nitrate (NOx) levels were also analysed during a graded exercise test (GXT). Casual and ambulatorial BP were not different between groups, but PWV was 7.5 and 12.6% higher in FH þ þ than FH þ and FHÀ, respectively, and 4.8% higher in FH þ than FHÀ (Pp0.01). Insulin and insulin-to-glucose ratio were increased in FH þ þ and FH þ (Po0.05), and lowdensity lipoprotein (LDL)-cholesterol tended to be higher only in FH þ þ (P ¼ 0.07). FH þ þ showed higher exercise and recovery diastolic BP and EPI levels, and increased resting, exercise and recovery NE, and ET-1 levels than FHÀ (Po0.05). FH þ showed only greater resting, exercise and recovery NE, and rest ET-1 (Po0.05). Resting, exercise and recovery NOx were lower in FH þ þ and FH þ than FHÀ (Po0.01). Haemodynamic, metabolic and hormonal abnormalities were presented in nonhypertensive young women offspring of hypertensive parents before any increase in BP. Greater abnormalities were observed in women with a strong family history of hypertension (FH þ þ ). These results suggest that there is an early vascular, metabolic and hormonal involvement in a familial hypertensive disorder.

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“…We propose that increased [Ca2+]i in platelets could be a genetic marker of abnormal calcium homeostasis in the subjects with a positive family history of essential hypertension. In the logistic regression analysis of the offspring of individuals with essential hypertension, Mino et al reported glucose to insulin ratio and on serum insulin levels after oral glucose loading (26). They suggested that insulin resistance was more closely related to obesity, but not to a family history of hypertension.…”

Section: Relationship Between Insulin Sensitivity and Calcium Homeostmentioning

confidence: 99%

Insulin Sensitivity and Calcium Homeostasis in Young, Lean, Normotensive Male Subjects.

et al. 2000

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Insulin resistance is known to be closely related to essential hypertension. It has been hypothesized that abnormal calcium homeostasis both at the cellular level and in the whole body plays a substantial role in hypertension associated with insulin resistance. We attempted to determine the relationships among insulin sensitivity, blood pressure (BP), body mass index (BMI), and calcium-related parameters in young, lean, normotensive male subjects with extreme susceptibilities to hypertension, and to investigate the effects of euglycemic hyperinsulinemia on calcium-related parameters. Seven young, lean, normotensive male subjects with family histories of essential hypertension and 10 age-matched controls without any parental cardiovascular events were enrolled. Insulin sensitivity measurement by the euglycemic hyperinsulinemic clamp technique and a 75-g oral glucose tolerance test were performed. Calcium-related parameters, including intracellular Ca2+ levels in platelets, were measured simultaneously.Diastolic BP was inversely correlated with insulin sensitivity in vivo (M-value). Insulin sensitivity was inversely correlated with BMI and with intracellular Ca2+ in platelets. In the multivariate stepwise regression analysis using both diastolic BP and insulin sensitivity as dependent variables, BMI was found to be a determinant independent variable. Euglycemic hyperinsulinemia decreased intact parathyroid hormone levels and increased fractional excretion of calcium. In conclusion, BMI rather than a family history of hypertension plays a determinant role on the regulation of diastolic BP and insulin sensitivity even in young, lean, normotensive male subjects with extreme predispositions for the development of hypertension. Hyperinsulinemia decreased intact parathyroid hormone levels and increased fractional excretion of calcium. (Hypertens Res 2000; 23: 433-440)

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Insulin resistance in offspring of hypertensive subjects

Cited by 13 publications

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Familial Hypertension, Insulin, Sympathetic Activity, and Blood Pressure Elevation

Familial Hypertension, Insulin, Sympathetic Activity, and Blood Pressure Elevation

Haemodynamic, metabolic and neuro-humoral abnormalities in young normotensive women at high familial risk for hypertension

Insulin Sensitivity and Calcium Homeostasis in Young, Lean, Normotensive Male Subjects.

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