Insulin and myocardial blood flow

Sundell, Jan; Knuuti, Juhani

doi:10.1016/s0008-6363(02)00718-6

Cited by 56 publications

(45 citation statements)

References 94 publications

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“…Insulin-and IGF-1-induced increases in myocardial contractility result in increased oxygen consumption (198). Cardiac oxygen demand is a potent determinant of myocardial blood flow (MBF), and insulin and IGF-1 enhance MBF and promote capillary recruitment in the heart (84,198).…”

Section: Insulin and Ang II In The Heartmentioning

confidence: 99%

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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

262

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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Section: Insulin and Ang II In The Heartmentioning

confidence: 99%

“…Cardiac oxygen demand is a potent determinant of myocardial blood flow (MBF), and insulin and IGF-1 enhance MBF and promote capillary recruitment in the heart (84,198). Hyperinsulinemia Fig.…”

Section: Insulin and Ang II In The Heartmentioning

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

262

230

View full text Add to dashboard Cite

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“…Chronic hyperglycemia is capable, through the mechanism of glucotoxicity (99), of further worsening ␤-cell secretion. Chronic hyperinsulinemia may lead to ␤-cell exhaustion, may cause downregulation of the insulin receptor thus increasing insulin resistance (32), and may produce the well-known negative consequences on the vascular endothelium (106,111). This vicious cycle plays a significant role in the pathogenesis and evolution of type 2 diabetes [as thoroughly examined in some recent surveys (34,59,97)].…”

Section: Effects Of Early Insulin Response On Prandial Glucose Metabomentioning

confidence: 99%

First-phase insulin secretion: does it exist in real life? Considerations on shape and function

Caumo¹,

Luzi²

2004

American Journal of Physiology-Endocrinology and Metabolism

151

120

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To fulfill its preeminent function of regulating glucose metabolism, insulin secretion must not only be quantitatively appropriate but also have qualitative, dynamic properties that optimize insulin action on target tissues. This review focuses on the importance of the first-phase insulin secretion to glucose metabolism and attempts to illustrate the relationships between the first-phase insulin response to an intravenous glucose challenge and the early insulin response following glucose ingestion. A clear-cut first phase occurs only when the ␤-cell is exposed to a rapidly changing glucose stimulus, like the one induced by a brisk intravenous glucose administration. In contrast, peripheral insulin concentration following glucose ingestion does not bear any clear sign of biphasic shape. Coupling data from the literature with the results of a ␤-cell model simulation, a close relationship between the first-phase insulin response to intravenous glucose and the early insulin response to glucose ingestion emerges. It appears that the same ability of the ␤-cell to produce a pronounced first phase in response to an intravenous glucose challenge can generate a rapidly increasing early phase in response to the blood glucose profile following glucose ingestion. This early insulin response to glucose is enhanced by the concomitant action of incretins and neural responses to nutrient ingestion. Thus, under physiological circumstances, the key feature of the early insulin response seems to be the ability to generate a rapidly increasing insulin profile. This notion is corroborated by recent experimental evidence that the early insulin response, when assessed at the portal level with a frequent sampling, displays a pulsatile nature. Thus, even though the classical first phase does not exist under physiological conditions, the oscillatory behavior identified at the portal level does serve the purpose of rapidly exposing the liver to elevated insulin levels that, also in virtue of their up-and-down pattern, are particularly effective in restraining hepatic glucose production. insulin pulsatile secretion; mathematical models; early-phase insulin secretion IN THE PAST THREE DECADES, the relevance of insulin secretion abnormalities in the pathogenesis of type 2 diabetes mellitus have been extensively debated (32,43,86,93,97), and a consensus has been reached that, to fulfill its pivotal role in regulating glucose metabolism, insulin secretion must not only be quantitatively appropriate, but also possess qualitative, dynamic features that optimize insulin action on target tissues. In particular, increasing emphasis has been placed on the importance of the so-called first-phase insulin secretion to glucose homeostasis (27,35,55). The aim of this review is to address the following questions. Does a first-phase insulin secretion really exist in in vivo physiology? What is the relationship between the first-phase insulin response to a brisk intravenous glucose challenge and the early insulin response following glucose ingestion? What ar...

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“…Insulin may also be a coronary vasodilator through the nitric oxide pathway in healthy individuals, as well as in patients with type 1 diabetes, obesity, and coronary artery disease. 71 Reports of using GIK to support the failing heart after MI date back to the 1960s. 72, 73 Despite that long history, results from trials employing GIK in MI and cardiac surgery are often inconclusive due to small sample sizes and differences of study design and GIK infusions.…”

Section: Cardiovascularmentioning

confidence: 99%

Intensive Insulin Therapy in Critically Ill Patients

2002

N Engl J Med

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Insulin and myocardial blood flow

Cited by 56 publications

References 94 publications

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

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

First-phase insulin secretion: does it exist in real life? Considerations on shape and function

Intensive Insulin Therapy in Critically Ill Patients

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