Key result
Overexpression of a human apoB transgene in the heart prevented the 48% increase in heart triglycerides and deterioration of heart function seen in diabetic wild type mice after 12 weeks.
Why the study?
Does overexpression of a human apoB transgene in the heart prevent cardiac triglyceride accumulation and cardiac dysfunction in streptozotocin-treated diabetic mice?
Does overexpression of a human apoB transgene in the heart prevent cardiac triglyceride accumulation and cardiac dysfunction in streptozotocin-treated diabetic mice?
Overexpression of apolipoprotein B in the heart prevents cardiac triglyceride accumulation and subsequent diabetic cardiomyopathy in a mouse model, highlighting the role of cardiomyocyte lipoprotein formation in cardiac lipid metabolism.
Answers are grounded in this paper and cite their sources.
May support cardiac apoB-mediated lipid export in diabetic mice; leaves open translation to human cardiomyopathy therapies.
The heart secretes apolipoprotein B (apoB) containing lipoproteins. Herein, we examined whether the overexpression of a human apoB transgene in the heart affects triglyceride accumulation and development of cardiac dysfunction in streptozotocin-treated diabetic mice. Blood glucose, plasma free fatty acids, and plasma triglycerides were similarly affected in diabetic wild type mice and diabetic apoB transgenic mice as compared with non-diabetic mice of the same genotype. After 12 weeks, heart triglycerides were increased by 48% in diabetic wild type mice. These mice displayed an increased expression of brain natriuretic peptide and deterioration of heart function on echocardiography. In diabetic apoB transgenic mice, heart triglyceride levels were identical to those in non-diabetic wild type and apoB transgenic mice, and brain natriuretic peptide expression as well as echocardiographic indexes of heart function were only marginally affected or unaffected. The findings suggest that triglyceride accumulation in the heart is important for development of diabetic cardiomyopathy in mice, and that lipoprotein formation by cardiomyocytes plays an integrated role in cardiac lipid metabolism.
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Nielsen et al. (2002) studied Diabetic cardiomyopathy. Overexpression of a human apoB transgene in the heart vs. Wild type mice was evaluated on Heart triglyceride accumulation and development of cardiac dysfunction. Overexpression of a human apoB transgene in the heart prevented the 48% increase in heart triglycerides and deterioration of heart function seen in diabetic wild type mice after 12 weeks.
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