Journal article
Acute effects of euglycemic-hyperinsulinemia on myocardial contractility in male mice
Physiological reports, Vol.10(17), pp.e15388-n/a
09/01/2022
DOI: 10.14814/phy2.15388
PMCID: PMC9453172
PMID: 36073057
Abstract
Type 2 diabetes and obesity are associated with increased risk of cardiovascular disease, including heart failure. A hallmark of these dysmetabolic states is hyper-insulinemia and decreased cardiac reserve. However, the direct effects of hyper-insulinemia on myocardial function are incompletely understood. In this study, using invasive hemodynamics in mice, we studied the effects of short-term euglycemic hyperinsulinemia on basal myocardial function and subsequent responses of the myocardium to beta-adrenergic stimulation. We found that cardiac function as measured by left ventricular (LV) invasive hemodynamics is not influenced by acute exposure to hyperinsulinemia, induced by an intravenous insulin injection with concurrent inotropic stimulation induced by beta-adrenergic stimulation secondary to isoproterenol administration. When animals were exposed to 120-min of hyperinsulinemia by euglycemic-hyperinsulinemic clamps, there was a significant decrease in LV developed pressure, perhaps secondary to the systemic vasodilatory effects of insulin. Despite the baseline reduction, the contractile response to beta-adrenergic stimulation remained intact in animals subject to euglycemic hyperinsulinemic clamps. beta-adrenergic activation of phospholamban phosphorylation was not impaired by hyperinsulinemia. These results suggest that short-term hyperinsulinemia does not impair cardiac inotropic response to beta-adrenergic stimulation in vivo.
Details
- Title: Subtitle
- Acute effects of euglycemic-hyperinsulinemia on myocardial contractility in male mice
- Creators
- Satya Murthy Tadinada - University of IowaWojciech J. Grzesik - University of IowaWilliam Kutschke - University of IowaRobert M. Weiss - University of IowaE. Dale Abel - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Physiological reports, Vol.10(17), pp.e15388-n/a
- DOI
- 10.14814/phy2.15388
- PMID
- 36073057
- PMCID
- PMC9453172
- NLM abbreviation
- Physiol Rep
- ISSN
- 2051-817X
- eISSN
- 2051-817X
- Publisher
- Wiley
- Number of pages
- 9
- Grant note
- 20SFRN35120123 / American Heart Association RO1HL112413; RO1HL127764; RO1HL142935 / National Heart, Lung and Blood Institute; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) S10OD019941 / National Institutes of Health Office of Research Infrastructure Programs
- Language
- English
- Date published
- 09/01/2022
- Academic Unit
- Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Endocrinology and Metabolism; Internal Medicine
- Record Identifier
- 9984359571802771
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