Liver fatty acid binding protein gene-ablation exacerbates weight gain in high-fat fed female mice.
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Research Areas
- Ethics and Fundamental Issues of Law and Justice (Fundamental Issues and Purpose of Human Life)
- Evolution of Thought (Fundamental Issues and Purpose of Human Life)
- Humanities (Human and social sciences)
- Language, Knowledge, Significance and Thought Building (Fundamental Issues and Purpose of Human Life)
- Ontological and Metaphysical Matters (Fundamental Issues and Purpose of Human Life)
- Social Relations and Structures (Human and social sciences)
Publication Details
Output type: Journal article
Author list: McIntosh, Atshaves, Landrock, Landrock, Martin, Storey, Kier, Schroeder
Publisher: Springer Verlag (Germany)
Publication year: 2013
Volume number: 48
Issue number: 5
Start page: 435
End page: 48
Number of pages: -386
ISSN: 0024-4201
eISSN: 1558-9307
Languages: English-Great Britain (EN-GB)
Unpaywall Data
Open access status: green
Full text URL: https://europepmc.org/articles/pmc3640860?pdf=render
Abstract
Loss of liver fatty acid binding protein (L-FABP) decreases long chain fatty acid uptake and oxidation in primary hepatocytes and in vivo. On this basis, L-FABP gene ablation would potentiate high-fat diet-induced weight gain and weight gain/energy intake. While this was indeed the case when L-FABP null (-/-) mice on the C57BL/6NCr background were pair-fed a high-fat diet, whether this would also be observed under high-fat diet fed ad libitum was not known. Therefore, this possibility was examined in female L-FABP (-/-) mice on the same background. L-FABP (-/-) mice consumed equal amounts of defined high-fat or isocaloric control diets fed ad libitum. However, on the ad libitum-fed high-fat diet the L-FABP (-/-) mice exhibited: (1) decreased hepatic long chain fatty acid (LCFA) β-oxidation as indicated by lower serum β-hydroxybutyrate level; (2) decreased hepatic protein levels of key enzymes mitochondrial (rate limiting carnitine palmitoyl acyltransferase A1, CPT1A; HMG-CoA synthase) and peroxisomal (acyl CoA oxidase 1, ACOX1) LCFA β-oxidation; (3) increased fat tissue mass (FTM) and FTM/energy intake to the greatest extent; and (4) exacerbated body weight gain, weight gain/energy intake, liver weight, and liver weight/body weight to the greatest extent. Taken together, these findings showed that L-FABP gene-ablation exacerbated diet-induced weight gain and fat tissue mass gain in mice fed high-fat diet ad libitum--consistent with the known biochemistry and cell biology of L-FABP.
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