Role of aldosterone and angiotensin II in insulin resistance: an update

Lastra-Lastra, Guido; Sowers, James R.; Restrepo-Erazo, Katherine; Manrique‐Acevedo, Camila; Lastra-González, Guido

doi:10.1111/j.1365-2265.2008.03498.x

Cited by 83 publications

(66 citation statements)

References 47 publications

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“…Both experimental and clinical studies implicate also aldosterone in the development of insulin resistance, hypertension, endothelial dysfunction, cardiovascular tissue fibrosis, inflammation, and oxidative stress. Blockade of renin-angiotensin-aldosterone system (RAAS) components, in particular aldosterone receptor, results in attenuation of insulin resistance, glucose homeostasis, as well as decreased cardiovascular disease morbidity and mortality (Lastra-Lastra et al 2009;McGuire et al 2008). In agreement with our study, E2/DRSP therapy induced an improvement in insulin sensitivity, as suggested by the decrease in HOMA index.…”

Section: Discussionsupporting

confidence: 88%

Short-term effects of low-dose estrogen/drospirenone vs low-dose estrogen/dydrogesterone on glycemic fluctuations in postmenopausal women with metabolic syndrome

Rizzo

Leo

Franciscis

et al. 2013

AGE

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This study aims to compare the effects of low-dose emidrate estradiol/drospirenone (E2/DRSP) vs low-dose emidrate estradiol/dydrogesterone (E2/DG) combination on the mean amplitude of glycemic excursions (MAGE) value in postmenopausal women affected by metabolic syndrome (MS). One hundred sixty postmenopausal women were recruited to receive a treatment with oral doses of E2/1 mg plus drospirenone/2 mg (E2/DRSP group) or oral dose of E2/1 mg plus dydrogesterone/5 mg (E2/DG group) for 6 months. At enrollment and after 6 months, anthropometric, metabolic, and inflammatory parameters have been assessed. MAGE, evaluated during 48-h continuous subcutaneous glucose monitoring (CSGM), allowed us to assess daily glucose fluctuations at baseline and after 6 months. After hormone therapy, both groups showed a significant decline in fasting plasma glucose levels (p<0.05), while only E2/DRSP group showed a statistically significant decline in waist circumferences, post-prandial glycemia, LDL, plasma triglycerides, MAGE, HOMA index, and plasma IL-6 (p<0.05) levels. In the whole population (n=160), after 6 months of indicated therapy, changes in fasting plasma glucose and PAI-1 levels correlated with the changes in MAGE values, while only in E2/DRSP group that MAGE reduction was positively associated with a stronger decrease in waist circumferences, triglycerides, and TNF-α plasma levels. The independent effect of hormone therapy (HT) on reduction in MAGE value has been tested in three different multiple linear regression models. HT resulted to be associated with MAGE, independent of other confounding variables. Although both groups had a decline in fasting plasma glucose, only drospirenone treatment revealed positive effects on glycemic excursions and insulin sensitivity, induced favorable changes in lipid profile, and showed an improvement of inflammatory indices in postmenopausal women with MS.

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Section: Discussionsupporting

confidence: 88%

Short-term effects of low-dose estrogen/drospirenone vs low-dose estrogen/dydrogesterone on glycemic fluctuations in postmenopausal women with metabolic syndrome

Rizzo

Leo

Franciscis

et al. 2013

AGE

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“…24,25 Potassium can regulate insulin receptor function and glucosestimulated insulin secretion by b-cells. 26 A positive correlation between adiponectine with insulinsensitizing properties and potassium was recently noted in PA and low renin hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%

The prevalence of metabolic syndrome and its components in two main types of primary aldosteronism

et al. 2010

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Metabolic syndrome (MS) is frequent clinical condition in patients with hypertension. Primary aldosteronism (PA) is a common form of secondary hypertension. This study was aimed at investigating the prevalence of the MS and its components in the two major forms of PA, in unilateral aldosterone-producing adenoma (APA) and bilateral aldosterone overproduction because of idiopathic hyperaldosteronism (IHA). The diagnosis of the particular form of PA was based on adrenal venous sampling and/or successful surgery confirmed by histopathological examination. We analyzed clinical and laboratory data from 100 patients with PA (50 patients with IHA and 50 patients with APA) and from 90 patients with essential hypertension (EH). Metabolic profiles of patients with bilateral form of PA (because of IHA) were similar to EH, but differed from those in patients with unilateral form of PA (APA). The prevalence of the MS (62% in IHA, 34% in APA and 56% in EH), the body mass index value (30 ± 4 kg m -2 in IHA, 27±5 kg m -2 in APA and 29±5 kg m -2 in EH) and triglycerides levels (1.9±0.9 mmol l -1 in IHA,1.4± 0.8 mmol l -1 in APA and 2.01 ± 1.39 mmol l -1 in EH) were all significantly (Po0.05) higher in IHA compared with APA patients. Metabolic profile of patients with bilateral form of PA (because of IHA) is similar to EH in contrast to unilateral form of PA (APA).

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“…2 There is growing interest in the role of aldosterone and its receptor, mineralocorticoid receptor (MR), in the pathogenesis of insulin resistance. 3 For instance, clinical studies have shown that patients with primary aldosteronism exhibit impaired glucose tolerance. 4 Some possible mechanisms of insulin resistance induced by aldosterone have been considered, such as a low serum potassium concentration, and direct effects of aldosterone on insulin signaling.…”

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confidence: 99%

Aldosterone Induces Vascular Insulin Resistance by Increasing Insulin-Like Growth Factor-1 Receptor and Hybrid Receptor

Sherajee

Fujita

Rafiq

et al. 2012

ATVB

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Objective-We previously showed that aldosterone induces insulin resistance in rat vascular smooth muscle cells (VSMCs).Because insulin-like growth factor-1 receptor (IGF1R) affects insulin signaling, we hypothesized that aldosterone induces vascular insulin resistance and remodeling via upregulation of IGF1R and its hybrid insulin/insulin-like growth factor-1 receptor. Methods and Results-Hybrid receptor expression was measured by immunoprecipitation. Hypertrophy of VSMCs was evaluated by 3 H-labeled leucine incorporation. Aldosterone (10 nmol/L) significantly increased protein and mRNA expression of IGF1R and hybrid receptor in VSMCs but did not affect insulin receptor expression. Mineralocorticoid receptor blockade with eplerenone inhibited aldosterone-induced increases in IGF1R and hybrid receptor. Aldosterone augmented insulin (100 nmol/L)-induced extracellular signal-regulated kinase 1/2 phosphorylation. Insulin-induced leucine incorporation and ␣-smooth muscle actin expression were also augmented by aldosterone in VSMCs. These aldosterone-induced changes were significantly attenuated by eplerenone or picropodophyllin, an IGF1R inhibitor. Chronic infusion of aldosterone (0.75 g/hour) increased blood pressure and aggravated glucose metabolism in rats. Expression of hybrid receptor, azan-positive area, and oxidative stress in aorta was increased in aldosterone-infused rats. Spironolactone and tempol prevented these aldosterone-induced changes. Key Words: insulin resistance Ⅲ reactive oxygen species Ⅲ receptors Ⅲ signal transduction Ⅲ aldosterone I nsulin resistance is a major attribute of type 2 diabetes mellitus and metabolic syndrome. 1 Cardiovascular complications are often seen in these patients, and vascular insulin resistance is considered to be involved in proatherogenic changes and subsequent cardiovascular events. 2 There is growing interest in the role of aldosterone and its receptor, mineralocorticoid receptor (MR), in the pathogenesis of insulin resistance. 3 For instance, clinical studies have shown that patients with primary aldosteronism exhibit impaired glucose tolerance. 4 Some possible mechanisms of insulin resistance induced by aldosterone have been considered, such as a low serum potassium concentration, and direct effects of aldosterone on insulin signaling. 5,6 Previously, we have demonstrated that aldosterone induces insulin resistance in rat vascular smooth muscle cells (VSMCs) via the downregulation of insulin receptor substrate-1, a key molecule of insulin signaling pathway. 7 Our data also clearly showed that aldosterone attenuates glucose metabolism in VSMCs. However, the precise molecular mechanisms responsible for aldosterone-induced VSMC insulin resistance and proatherogenic changes have not been identified. Conclusion-AldosteroneInsulin induces various actions, such as glucose metabolism and normal cell physiology, by binding to the insulin receptor (IR). 8 The VSMCs express not only IR but also insulin-like growth factor-1 receptor (IGF1R). 8 Compared with IR, IGF1R is more ab...

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Role of aldosterone and angiotensin II in insulin resistance: an update

Cited by 83 publications

References 47 publications

Short-term effects of low-dose estrogen/drospirenone vs low-dose estrogen/dydrogesterone on glycemic fluctuations in postmenopausal women with metabolic syndrome

Short-term effects of low-dose estrogen/drospirenone vs low-dose estrogen/dydrogesterone on glycemic fluctuations in postmenopausal women with metabolic syndrome

The prevalence of metabolic syndrome and its components in two main types of primary aldosteronism

Aldosterone Induces Vascular Insulin Resistance by Increasing Insulin-Like Growth Factor-1 Receptor and Hybrid Receptor

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