Open AccessAcute effects of euglycemic‐hyperinsulinemia on myocardial contractility in male mice
Author(s) -
Tadinada Satya Murthy,
Grzesik Wojciech J.,
Kutschke William,
Weiss Robert M.,
Abel E. Dale
Publication year - 2022
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.15388
Subject(s) - hyperinsulinemia , medicine , endocrinology , contractility , inotrope , insulin , insulin resistance
Type 2 diabetes and obesity are associated with increased risk of cardiovascular disease, including heart failure. A hallmark of these dysmetabolic states is hyperinsulinemia and decreased cardiac reserve. However, the direct effects of hyperinsulinemia 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 β‐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 β‐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 β‐adrenergic stimulation remained intact in animals subject to euglycemic hyperinsulinemic clamps. β‐adrenergic activation of phospholamban phosphorylation was not impaired by hyperinsulinemia. These results suggest that short‐term hyperinsulinemia does not impair cardiac inotropic response to β‐adrenergic stimulation in vivo.