Insulin resistance, cardiovascular stiffening and cardiovascular disease.


Journal

Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267

Informations de publication

Date de publication:
06 2021
Historique:
received: 22 12 2020
revised: 10 03 2021
accepted: 17 03 2021
pubmed: 27 3 2021
medline: 25 6 2021
entrez: 26 3 2021
Statut: ppublish

Résumé

The cardiometabolic syndrome (CMS) and obesity are typically characterized by a state of metabolic insulin resistance. As global and US rates of obesity increase there is an acceleration of the incidence and prevalence of insulin resistance along with associated cardiovascular disease (CVD). Under physiological conditions insulin regulates glucose homeostasis by enhancing glucose disposal in insulin sensitive tissues while also regulating delivery of nutrients through its vasodilation actions on small feed arteries. Specifically, insulin-mediated production of nitric oxide (NO) from the vascular endothelium leads to increased blood flow enhancing disposal of glucose. Typically, insulin resistance is considered as a decrease in sensitivity or responsiveness to the metabolic actions of insulin including insulin-mediated glucose disposal. However, a decreased sensitivity to the normal vascular actions of insulin, especially diminished nitric oxide production, plays an additional important role in the development of CVD in states of insulin resistance. One mechanism by which insulin resistance and attendant hyperinsulinemia promote CVD is via increases in vascular stiffness. Although obesity and insulin resistance are known to be associated with substantial increases in the prevalence of vascular fibrosis and stiffness the mechanisms and mediators that underlie vascular stiffening in insulin resistant states are complex and have only recently begun to be addressed. Current evidence supports the role of increased plasma levels of aldosterone and insulin and attendant reductions in bioavailable NO in the pathogenesis of impaired vascular relaxation and vascular stiffness in the CMS and obesity. Aldosterone and insulin both increase the activity of serum and glucocorticoid kinase 1 (SGK-1) which in turn is a major regulator of vascular and renal sodium (Na

Identifiants

pubmed: 33766485
pii: S0026-0495(21)00066-4
doi: 10.1016/j.metabol.2021.154766
pii:
doi:

Substances chimiques

Immediate-Early Proteins 0
Nitric Oxide 31C4KY9ESH
Protein Serine-Threonine Kinases EC 2.7.11.1
serum-glucocorticoid regulated kinase EC 2.7.11.1

Types de publication

Journal Article Research Support, N.I.H., Extramural Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

154766

Informations de copyright

Copyright © 2021 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The Authors have no conflicts of interest in regard to this manuscript.

Auteurs

Michael A Hill (MA)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA. Electronic address: hillmi@missouri.edu.

Yan Yang (Y)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA.

Liping Zhang (L)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA.

Zhe Sun (Z)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA.

Guanghong Jia (G)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Diabetes and Cardiovascular Center, University of Missouri School of Medicine, Columbia, MO 65212, USA; Department of Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA.

Alan R Parrish (AR)

Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA.

James R Sowers (JR)

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA; Diabetes and Cardiovascular Center, University of Missouri School of Medicine, Columbia, MO 65212, USA; Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO 65212, USA; Department of Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA. Electronic address: sowersj@health.missouri.edu.

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Classifications MeSH