August 1, 2005DiabetesOpen Access

Insulin and Inositol 1,4,5-Trisphosphate Trigger Abnormal Cytosolic Ca2+ Transients and Reveal Mitochondrial Ca2+ Handling Defects in Cardiomyocytes of ob/ob Mice

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Population

Freshly isolated ventricular cardiomyocytes from normal and ob/ob mice

Comparison

Application of insulin or membrane-permeant… vs Wild-type cardiomyocytes and baseline conditions…

Design

Preclinical

Authors

JFJérémy FauconnierCentre National de la Recherche Scientifique JLJohanna T. LannerKarolinska Institutet SZShi‐Jin ZhangNorth Sichuan Medical University

Discussion

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Implication

May predispose obese diabetic hearts to arrhythmias; hypothesis-generating for Ca2+ mechanisms in human type 2 diabetes.

Structured PICO

Population

Freshly isolated ventricular cardiomyocytes from normal (wild-type) and ob/ob mice (an animal model of obesity and type 2 diabetes)

Intervention

Application of insulin (6 or 60 nmol/l) or membrane-permeant inositol trisphosphate (IP3) analog

Comparator

Wild-type cardiomyocytes and baseline conditions without insulin

Outcome

Electrically evoked Ca2+ transients and mitochondrial Ca2+ handlingsurrogate

Insulin triggers abnormal Ca2+ transients in ob/ob mouse cardiomyocytes via increased IP3 and impaired mitochondrial Ca2+ handling, which may predispose to arrhythmias in obesity and type 2 diabetes.

Cite This Study

Fauconnier et al. (2005) studied this question.

synapsesocial.com/papers/6a91b66076d7fdaedb5ce189 https://doi.org/10.2337/diabetes.54.8.2375

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Insulin and Inositol 1,4,5-Trisphosphate Trigger Abnormal Cytosolic Ca2+ Transients and Reveal Mitochondrial Ca2+ Handling Defects in Cardiomyocytes of ob/ob Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Insulin and Inositol 1,4,5-Trisphosphate Trigger Abnormal Cytosolic Ca2+ Transients and Reveal Mitochondrial Ca2+ Handling Defects in Cardiomyocytes of ob/ob Mice

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider