Noh_2006_Cardiovasc.Drugs.Ther_20_441

Reference

Title : Cardiac metabolism and mechanics are altered by genetic loss of lipoprotein triglyceride lipolysis - Noh_2006_Cardiovasc.Drugs.Ther_20_441
Author(s) : Noh HL , Yamashita H , Goldberg IJ
Ref : Cardiovasc Drugs Ther , 20 :441 , 2006
Abstract :

INTRODUCTION: Most circulating fatty acids are contained in lipoprotein triglycerides. For the heart to acquire these lipids, they must be broken down into free fatty acids via the enzyme lipoprotein lipase (LpL). Although it has long been known that hearts primarily use esterified fatty acids as fuel, different sources of fatty acids were thought to be interchangeable. MATERIALS AND
METHODS: By creating mice with neonatal and acute LpL deletion we showed that lipoprotein-derived fatty acids could not be replaced by albumin-associated free fatty acids. Loss of cardiac LpL forces the heart to increase its uptake of glucose, reduce fatty acid oxidation, and eventually leads to cardiac dysfunction. In contrast, cardiomyocyte specific overexpression of an anchored form of LpL leads to excess lipid uptake, induction of fatty acid oxidation genes, and dilated cardiomyopathy. CONCLUSION: Increasing lipid secretion from the heart or redirecting lipids to adipose tissue can alleviate this lipotoxic situation.

PubMedSearch : Noh_2006_Cardiovasc.Drugs.Ther_20_441
PubMedID: 17139480

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Citations formats

Noh HL, Yamashita H, Goldberg IJ (2006)
Cardiac metabolism and mechanics are altered by genetic loss of lipoprotein triglyceride lipolysis
Cardiovasc Drugs Ther 20 :441

Noh HL, Yamashita H, Goldberg IJ (2006)
Cardiovasc Drugs Ther 20 :441