Insulin stimulates endogenous angiotensin II production via a mitogen-activated protein kinase pathway in vascular smooth muscle cells

Tuck, Michael L.; Bounoua, Farida; Eslami, Pirooz; Nyby, Michael D.; Eggena, Peter; Corry, Dalila B.

doi:10.1097/00004872-200409000-00023

Cited by 46 publications

(34 citation statements)

References 27 publications

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“…In the milieu of IR, the cardiovascular system is sensitized to the adverse trophic effects of RAS, which is evidenced by the frequent occurrence of diffuse vascular disease and left ventricular hypertrophy in diabetic patients, even when the lipid and BP levels are normal. High insulin levels stimulate the angiotensin II type 1 (AT1) receptor, which activates the RAS 28 and also the cardiac sympathetic nervous system. 29 In vessels, angiotensin II promotes superoxide anion generation and endothelial dysfunction.…”

Section: Effects Of Statin Therapy On Irmentioning

confidence: 99%

Statins and Renin-Angiotensin System Inhibitor Combination Treatment to Prevent Cardiovascular Disease

Lee

Sakuma

Ihm

et al. 2014

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp n the past, the goal of treating patients with hypertension or hypercholesterolemia was merely to control numerical factors such as blood pressure (BP) or serum cholesterol level alone; nowadays, it has changed. The updated guidelines target reductions in overall cardiovascular risk. 1,2 Hypercholesterolemia and hypertension are both associated with endothelial dysfunction and insulin resistance (IR) and their coexistence is a vicious cycle associated with an increased incidence of cardiovascular events. Moreover, both risk factors are frequently prevail together. 3,4 Indeed, more than 60% of hypertensive patients were consistently hypercholesterolemic in the United States National Health and Nutrition Examination Surveys 1988Surveys -2010 More importantly, the prevalence of dyslipidemia increased parallel to BP. In the prehypertensive range, prevalence was similar to that of the general population, approximately 26%; however, this prevalence doubles in the hypertensive population, reaching nearly 60%. 6 Although it is not possible to provide a definite pathogenesis of hypertensionhypercholesterolemia/dyslipidemia clustering, it is gaining consensus that IR and endothelial dysfunction might play major roles. 7, 8 From 1988-1994 to 2005-2010, control of concomitant hypertension and the low-density lipoprotein-cholesterol (LDL-C) level rose from 5.0% to 30.7%. By multivariable logistic regression, factors associated with concomitant hypertension, LDL-C, and non-high-density lipoprotein-cholesterol control were statin therapy (10.7) and antihypertensive (3.32) medications, and ≥2 healthcare visits/year (1.90), whereas age (0.77/10-year increase), black race (0.59), Hispanic ethnicity (0.62), cardiovascular disease (CVD) (0.44), and diabetes mel-

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Section: Effects Of Statin Therapy On Irmentioning

confidence: 99%

Statins and Renin-Angiotensin System Inhibitor Combination Treatment to Prevent Cardiovascular Disease

Lee

Sakuma

Ihm

et al. 2014

Circ J

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“…ANG II and mineralocorticoids, in contrast, cause vasoconstriction and enhance the expression of proinflammatory cytokines, adhesion molecules, growth, and inflammatory pathways (80,85,86,135,153,192,207,208). Furthermore, ANG II and aldosterone interfere with many of the metabolic signaling actions of insulin and IGF-1 in the CV system (9, 80, 85, 86, 102, 135, 153, 186, 188 -190, 207, 208, 230).…”

Section: Role Of Raas In Vascular Insulin Resistancementioning

confidence: 99%

Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance

Cooper

Whaley‐Connell²,

Habibi³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

266

230

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JR. Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance. Am J Physiol Heart Circ Physiol 293: H2009 -H2023, 2007. First published June 22, 2007; doi:10.1152/ajpheart.00522.2007.-Hypertension commonly occurs in conjunction with insulin resistance and other components of the cardiometabolic syndrome. Insulin resistance plays a significant role in the relationship between hypertension, Type 2 diabetes mellitus, chronic kidney disease, and cardiovascular disease. There is accumulating evidence that insulin resistance occurs in cardiovascular and renal tissue as well as in classical metabolic tissues (i.e., skeletal muscle, liver, and adipose tissue). Activation of the renin-angiotensin-aldosterone system and subsequent elevations in angiotensin II and aldosterone, as seen in cardiometabolic syndrome, contribute to altered insulin/ IGF-1 signaling pathways and reactive oxygen species formation to induce endothelial dysfunction and cardiovascular disease. This review examines currently understood mechanisms underlying the development of resistance to the metabolic actions of insulin in cardiovascular as well as skeletal muscle tissue.HYPERTENSION is present in ϳ30% of the adult United States population and often occurs in conjunction with insulin resistance and other components of the cardiometabolic syndrome (CMS) (29,115,163,186,190). According to recent data, up to 70 million Americans have insulin resistance, which plays a significant role in the relationship between hypertension, Type 2 diabetes mellitus, chronic kidney disease (CKD), and cardiovascular (CV) disease (CVD) (69). There is accumulating evidence that insulin resistance occurs in CV and renal tissue as well as in classical metabolic tissues (i.e., skeletal muscle, liver, and adipose tissue) (125,186,190). This review focuses on currently accepted mechanisms underlying the development of resistance to the metabolic actions of insulin in CV tissue (see Figs. 1 and 2) as well as skeletal muscle tissues (27,190) (see Fig. 3). Normal Actions of Insulin in CV TissueBoth insulin and IGF-1 receptors exist in CV tissue (186). Upon binding to specific receptors, they activate a number of downstream signaling systems that result in vasorelaxation (125, 188 -191) and myocardial glucose uptake and alteration of cardiac energy homeostasis (125,186,190). Activation of the insulin receptor (IR) and IGF-1 receptor, ligand-activated transmembrane receptors with tyrosine kinase activity, phosphorylates intracellular substrates including IR substrate (IRS) family members and Shc, which, in turn, serve as docking proteins for downstream signaling molecules (27,125). IRS phosphorylation of tyrosine moieties results in the engagement of Src homology 2 (SH2) domain-binding motifs for SH2 domain signaling molecules, including phosphatidyl 3-kinase (PI3K) and Grb-2. When SH2 domains of the p85 regulatory subunit bind to tyrosine-phosphorylated motifs on IRS-1, this activates the preassociated p110 catalytic subunit to generate phosph...

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“…Insulin resistance is always accompanied by hyperinsulinemia. Hyperinsulinemia enhances the action of Ang II by promoting Ang II secretion and upregulating the Ang II receptor expression (18,19), thereby propagating a vicious circle.…”

Section: Discussionmentioning

confidence: 99%

An Increased Circulating Angiotensin II Concentration is Associated with Hypoadiponectinemia and Postprandial Hyperglycemia in Men with Nonalcoholic Fatty Liver Disease

Xia

Wang

et al. 2013

Intern. Med.

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Objective Nonalcoholic fatty liver disease (NAFLD) is a condition associated with type 2 diabetes (T2D). Insulin resistance, a common pathogenesis of NAFLD and T2D, is partially caused by alterations in angiotensin II (Ang II) and is accompanied by hypoadiponectinemia. We aimed to investigate whether the circulating Ang II and adiponectin concentrations are related to hyperglycemia in male NAFLD patients. Methods Thirty-five controls and 85 NAFLD patients without prior known T2D were enrolled. All participants were non-smoking men who performed 75-g oral glucose tolerance tests. According to the American Diabetes Association (ADA) criteria, the NAFLD patients were divided into the euglycemia and hyperglycemia groups. The NAFLD patients with hyperglycemia were further divided into the isolated impaired fasting glucose (I-IFG) and postprandial hyperglycemia subgroups. The fasting serum Ang II and adiponectin concentrations were measured. Results Among the 85 NAFLD patients, 40 (47%) had hyperglycemia, including I-IFG (18%) and postprandial hyperglycemia (29%). The serum Ang II concentrations in the euglycemia and hyperglycemia groups were significantly higher than those observed in the control and euglycemia groups, respectively; whereas the serum adiponectin concentrations were significantly lower. The serum Ang II concentrations were significantly higher in the postprandial hyperglycemia subgroup than in the I-IFG subgroup. The serum Ang II and adiponectin concentrations were found to be independent predictors of hyperglycemia in the NAFLD patients. The serum Ang II concentration was significantly associated with the serum adiponectin and 2-hour postprandial glucose concentrations in the NAFLD patients. Conclusion An increased circulating Ang II concentration is associated with hypoadiponectinemia and postprandial hyperglycemia in male NAFLD patients and may be involved in the pathogenesis of T2D in NAFLD patients.

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Insulin stimulates endogenous angiotensin II production via a mitogen-activated protein kinase pathway in vascular smooth muscle cells

Cited by 46 publications

References 27 publications

Statins and Renin-Angiotensin System Inhibitor Combination Treatment to Prevent Cardiovascular Disease

Statins and Renin-Angiotensin System Inhibitor Combination Treatment to Prevent Cardiovascular Disease

Renin-angiotensin-aldosterone system and oxidative stress in cardiovascular insulin resistance

An Increased Circulating Angiotensin II Concentration is Associated with Hypoadiponectinemia and Postprandial Hyperglycemia in Men with Nonalcoholic Fatty Liver Disease

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