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Native valve infective endocarditis (IE) is rare, with an incidence of 3–7 cases per 100,000 person-years.1,2 Cardiac structural complications from local infection extension include valvular destruction, peri-annular abscess and fistula formation. Left ventricular pseudoaneurysm (LVP) from IE is exceedingly rare, occurring in <1% of cases, and is associated with high morbidity and mortality. Diagnosis is challenging due to nonspecific symptoms […]

Role of the IRS-1 and/or -2 in the pathogenesis of insulin resistance in Dahl salt-sensitive (S) rats

Marlene F. Shehata
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Published Online: Jul 30th 2018 Heart International 2009;4(1):e6 DOI: https://doi.org/10.4081/hi.2009.e6
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Abstract

Overview

Insulin resistance is a common finding in
hypertensive humans and animal models. The
Dahl salt-sensitive (S) rat is an ideal model of
genetically predetermined insulin resistance
and salt-sensitive hypertension. Along the
insulin signaling pathway, the insulin receptor
substrates 1 and 2 (IRS-1 and -2) are important
mediators of insulin signaling. IRS-1
and/or IRS-2 genetic variant(s) and/or
enhanced serine phosphorylation correlate
with insulin resistance. The present commentary
was designed to highlight the significance
of IRS-1 and/or -2 in the pathogenesis of
insulin resistance. An emphasis will be given
to the putative role of IRS-1 and/or -2 genetic
variant(s) and serine phosphorylation in precipitating
insulin resistance.

Keywords

Dahl S rats, insulin resistance, saltsensitivity, insulin signaling pathway, genetic contributors, molecular contributors.

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Article Information

Correspondence

Marlene Shehata, 207-1140 Fisher Avenue, K1Z 8M5, Ottawa, ON, Canada. E-mail: marlenefouad@yahoo.com

Received

2009-05-12T00:00:00

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