Key result
Mice deficient in adipose tissue lipoprotein lipase maintained normal fat mass via massive upregulation of endogenous fatty acid synthesis, though this compensation was insufficient to maintain maximal fat mass on an ob/ob background.
Population
LPL knockout mice mated to transgenics expressing LPL under the control of a muscle-specific promoter to…
Comparison
Absolute adipose tissue LPL deficiency or… vs Wild-type mice or L2-MCK mice
Design
Preclinical, Semiquantitative analysis of intramuscular lipid was performed…
Follow-up
up to 7-12 months
Authors
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Findings remain preclinical and should not change practice; leaves open translational relevance of compensatory fatty acid synthesis.
Adipose tissue lipoprotein lipase deficiency in mice is compensated by massive upregulation of endogenous fatty acid synthesis, preserving fat mass on a normal diet but limiting fat accumulation in genetic obesity.
Weinstock et al. (1997) studied Lipoprotein lipase deficiency and obesity. Adipose tissue lipoprotein lipase deficiency (L0-MCK) vs. Wild-type (L2) or relative deficiency (L2-MCK) was evaluated on Body mass composition and adipose tissue fatty acid composition. Mice deficient in adipose tissue lipoprotein lipase maintained normal fat mass via massive upregulation of endogenous fatty acid synthesis, though this compensation was insufficient to maintain maximal fat mass on an ob/ob background.
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