Insulin, renin-aldosterone system and blood pressure in obese people

Andronico, Giuseppe; Cottone, Santina; Mangano, M T; Ferraro-Mortellaro, R.; Baiardi, Gustavo; Grassi, Nello; Ferrara, L.; Mulè, Giuseppe; Cerasola, Giovanni

doi:10.1038/sj.ijo.0801483

Cited by 34 publications

(21 citation statements)

References 24 publications

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“…The association between primary hyperaldosteronism and glucose intolerance and insulin resistance has been reported in some studies [32,33] but not all [34,35]. Plasma aldosterone correlates positively with insulin in both normotensive and hypertensive humans [36,37]; it also correlates with insulin resistance measured with the homeostasis model assessment in subjects with primary hyperaldosteronism [32,38]. Fallo et al [39] found a signifi cantly higher prevalence of hyperglycemia in patients with primary hyperaldosteronism than in patients with essential hypertension (27% vs 15%).…”

Section: Aldosterone In Obesity and Metabolic Syndromementioning

confidence: 93%

Aldosterone and cardiovascular risk

Vogt¹,

Burnier

2009

Current Science Inc

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Through its classic effects on sodium and potassium homeostasis, aldosterone, when produced in excess, is associated with the development of hypertension and hence with higher cardiovascular and renal risk. In recent years, experimental and epidemiologic data have suggested that aldosterone also may be linked to high cardiovascular risk independently of its effects on blood pressure. Thus, aldosterone has been associated with obesity and metabolic syndrome in selected populations, and these associations may further contribute to the higher cardiovascular risk of subjects with elevated aldosterone levels. Moreover, aldosterone has been reported to promote inflammation, oxidative stress, and fibrosis in a number of tissues. Clinical evidence indicates that patients with primary hyperaldosteronism have a higher risk of developing cardiovascular and renal complications than patients with essential hypertension who have the same level of blood pressure. Aldosterone receptor blockade has been shown to lower cardiovascular mortality after myocardial infarction and in patients with congestive heart failure. Some studies have also demonstrated that aldosterone blockade could have a favorable impact on the progression of renal disease. However, prospective interventional trials are needed to further evaluate the impact of blockade of aldosterone on cardiovascular risk.

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Section: Aldosterone In Obesity and Metabolic Syndromementioning

confidence: 93%

Aldosterone and cardiovascular risk

Vogt¹,

Burnier

2009

Current Science Inc

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“…27 Epidemiological studies have shown that metabolic syndrome increases the risk of microalbuminuria, 28 and some investigators have reported clearly increased plasma aldosterone levels in severely obese subjects. 29 In obese spontaneously hypertensive rats (SHRs), a model of metabolic syndrome manifested by a cluster of visceral obesity, hypertension, insulin resistance, and dyslipidemia, urinary protein excretion was found to markedly increase in an age-dependent manner that was associated with foot process effacement, suggesting podocyte injury, whereas in nonobese SHRs the urinary protein levels remained low and there were no changes in the podocytes. Interestingly, the serum aldosterone level was clearly higher in the obese SHRs than in the nonobese SHRs.…”

Section: Involvement Of Aldosterone Excess In Obesity-induced Proteinmentioning

confidence: 99%

Mineralocorticoid Receptors, Salt-Sensitive Hypertension, and Metabolic Syndrome

Fujita

2010

Hypertension

110

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Abstract-Obese persons with metabolic syndrome often have associated with salt-sensitive hypertension, microalbuminuria, and cardiac dysfunction, and the plasma aldosterone level in one-third of metabolic syndrome patients is clearly elevated. Hyperaldosteronism, which may be caused at least partially by certain adipocyte-derived factors, contributes to the development of proteinuria in obese hypertensive rats, and salt loading aggravates the proteinuria and induces cardiac diastolic dysfunction because of inadequate suppression of plasma aldosterone level. However, mineralocorticoid receptor (MR) antagonists prevent salt-induced renal and cardiac damage, suggesting that aldosterone excess and a high-salt diet exert an unfavorable synergistic action on the kidney and heart. In Dahl salt-sensitive rats, however, despite appropriate suppression of plasma aldosterone with a high-salt diet, salt loading paradoxically activated renal MR signaling, and the renal injury was markedly prevented by MR antagonists. Accordingly, we discovered an alternative pathway of MR activation in which Rac1, a small GTP-binding protein, activates MRs. Salt loading activates renal Rac1 in Dahl salt-sensitive rats, and Rac1 in turn induces MR activation, which results in renal injury, and the renal injury has been found to be prevented by Rac1 inhibitors. Moreover, several metabolic syndrome-related factors induce Rac1 activation, and one of them, hyperglycemia, activates MRs via Rac1 activation. Consistent with this, Rac1 inhibitors attenuated the proteinuria and renal injury in obese hypertensive animals. Thus, both salt and obesity activate Rac1 and cause MR activation. Abnormal activation of the aldosterone/MR pathway plays a key role in the development of salt-sensitive hypertension and renal injury in metabolic syndrome. (Hypertension. 2010;55:813-818.)Key Words: salt Ⅲ aldosterone Ⅲ mineralocorticoid receptor Ⅲ Rac1 Ⅲ obesity I t is well known that populations with a high dietary salt intake have higher incidences of hypertension, and salt loading not only increases blood pressure (BP) but causes cardiovascular damage in animals and humans. [1][2][3] We showed recently that salt exerted a more injurious effect on the kidneys and heart of obese hypertensive rats with metabolic syndrome than in lean hypertensive rats. 4 -6 In a recent investigation to identify the mechanism of the salt-induced cardiovascular damage, we discovered signaling cross-talk between Rac1 and mineralocorticoid receptor (MR), an alternative pathway that modulates MR activity, 7 and we obtained evidence suggesting that abnormal activation of the aldosterone/MR pathway is involved in the development of salt-induced hypertension and cardiovascular damage in metabolic syndrome. 8,9 Mechanism of Salt-Sensitive Hypertension in Metabolic SyndromeThe BP of individual hypertensive patients responds differently to salt loading, 1-4 and environmental factors and genetic factors may be involved in the salt sensitivity of BP. Recent clinical studies have demonstrated tha...

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“…It has been shown that plasma renin activity is significantly increased in obese individuals. 131,132 This increase is associated with higher levels of angiotensin II, which increase tubular absorption of sodium and contribute to systemic hypertension. 133,134 Although the pathophysiological mechanisms explaining the lowering of blood pressure with weight loss are not clear, numerous factors are probably involved.…”

Section: Systemic Hypertensionmentioning

confidence: 99%

Bariatric Surgery and Cardiovascular Risk Factors

Poirier¹,

Cornier²,

Mazzone³

et al. 2011

Circulation

299

134

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T he rate of obesity is rising logarithmically, especially in those with severe obesity (body mass index [BMI] Ͼ40 kg/m 2 ). Cardiologists, endocrinologists, internists, family practitioners, and most healthcare professionals are increasingly confronted with the severely obese patient and with postoperative bariatric patients because obesity is associated with significant morbidity and increased mortality. In addition, more adolescents these days are severely obese. Substantial long-term successes of lifestyle modifications and drug therapy have been disappointing in this population. The National Institutes of Health has suggested that surgical therapy be proposed to those patients with BMI Ͼ40 kg/m 2 or Ͼ35 kg/m 2 with serious obesity-related comorbidities such as systemic hypertension, type 2 diabetes mellitus, and obstructive sleep apnea. When indicated, surgical intervention leads to significant improvements in decreasing excess weight and comorbidities that can be maintained over time. These include diabetes mellitus, dyslipidemia, liver disease, systemic hypertension, obstructive sleep apnea, and cardiovascular dysfunction. Recent prospective, nonrandomized, observational, or case-control population studies have also shown bariatric surgery to prolong survival in the severely obese. Different types of bariatric procedures are being performed. Historically, operative mortality was between 0.1% and 2.0% with more recent data not exceeding 1%. Early complications include pulmonary embolus (0.5%), anastomotic leaks (1.0% to 2.5%), and bleeding (1.0%). Late complications include anastomotic stricture, anastomotic ulcers, hernias, band slippage, and behavioral maladaptation. The number of bariatric operations being performed is increasing tremendously as a result of increasing medical need and the evolution of safer surgical techniques and guidelines. Currently, bariatric surgery should be reserved for patients who have severe obesity in whom efforts at medical therapy have failed and an acceptable operative risk is present.

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Insulin, renin-aldosterone system and blood pressure in obese people

Cited by 34 publications

References 24 publications

Aldosterone and cardiovascular risk

Aldosterone and cardiovascular risk

Mineralocorticoid Receptors, Salt-Sensitive Hypertension, and Metabolic Syndrome

Bariatric Surgery and Cardiovascular Risk Factors

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