ArticlePhysiological reports2022
Acute effects of euglycemic-hyperinsulinemia on myocardial contractility in male mice.
Article in Physiological reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Refining the assessment of cardiac dysfunction in MAFLD and MASLD: a commentary on study limitations.Hepatology international · 2026Article
- Acute effects of euglycemic-hyperinsulinemia on myocardial contractility in male mice.Physiological reports · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
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