Hormonal
Lipoprotein lipase (LPL) is not strictly necessary or sufficient for normal fat deposition in white adipose tissue; downstream regulation of fatty acid uptake and esterification (mediated by insulin and acylation-stimulating protein) is the primary determinant of fat storage.
Do not assume that strategies targeting Lipoprotein Lipase (LPL) activity alone will effectively change body fat levels. Fat storage in adipose tissue is primarily controlled by what happens *after* LPL releases fatty acids—specifically, how insulin and other factors drive those fatty acids back into fat cells (esterification). If you increase LPL activity without ensuring these downstream storage pathways are active, you may simply circulate more fatty acids rather than storing them.
Normal fat deposition in adipose tissue can occur in the complete absence of LPL, and conversely, if LPL activity is increased by pharmacological means, increased fat storage does not necessarily follow... In white adipose tissue, it is clear that there is a major locus of control of fatty acid disposition downstream from LPL.
Why this rating
Based on human case studies (LPL deficiency), transgenic mouse models, and in vivo human catheterization studies.
Source
Lipoprotein lipase and the disposition of dietary fatty acids
Barbara A. Fielding et al. · British Journal Of Nutrition · 1998
DOI 10.1017/s0007114598001585
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