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Adiponectin improves cardiomyocyte contractile function in db/db diabetic obese mice
1Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, Wyoming, USA.
Obesity (Silver Spring, Md.)
|December 6, 2008
Summary
Adiponectin, a fat-derived hormone, improves cardiac function in diabetic obesity by enhancing cardiomyocyte contractility and calcium handling. This study suggests adiponectin may protect against diabetic cardiomyopathy via IRS-1 and c-Jun pathways.
Area of Science:
- Cardiovascular Biology
- Metabolic Disease Research
- Endocrinology
Background:
- Low adiponectin levels correlate with coronary heart disease, type 2 diabetes, obesity, and insulin resistance.
- High adiponectin levels predict reduced coronary risk in epidemiological studies.
- The specific role of adiponectin in cardiomyocyte function remains unclear.
Purpose of the Study:
- To investigate the role of adiponectin in cardiac contractile function.
- To examine adiponectin's effects in the db/db mouse model of diabetic obesity.
Main Methods:
- Cardiomyocytes from lean control and db/db mice were assessed for mechanical properties and intracellular Ca(2+) transients.
- Western blotting was used to evaluate protein expression and phosphorylation (IRS-1, Akt, c-Jun, JNK) and endoplasmic reticulum (ER) stress markers.
- Cardiomyocytes were treated with adiponectin (10 microg/ml).
Main Results:
- db/db mouse cardiomyocytes showed impaired contractile function (reduced peak shortening, maximal velocity, prolonged re-lengthening) and abnormal intracellular Ca(2+) handling.
- Adiponectin treatment abrogated these deficits in db/db mouse cardiomyocytes.
- Increased ratios of phosphorylated c-Jun/c-Jun and phosphorylated IRS-1/IRS-1 in db/db mice were attenuated by adiponectin.
- Elevated ER stress markers (PERK, IRE-1, eIF2alpha) in db/db mice were not affected by adiponectin.
Conclusions:
- Adiponectin treatment improves cardiomyocyte dysfunction in db/db diabetic obese mice.
- The protective mechanism may involve modulation of c-Jun and IRS-1 signaling pathways.
- Adiponectin's role in mitigating diabetic cardiomyopathy warrants further investigation.
