Angiopoietin-like protein 8 differentially regulates ANGPTL3 and ANGPTL4 during postprandial partitioning of fatty acids.
adipose tissue
angiopoietin-like protein 3
angiopoietin-like protein 4
lipid metabolism
lipoprotein lipase
metabolic syndrome
muscle
obesity
postprandial condition
triglycerides
Journal
Journal of lipid research
ISSN: 1539-7262
Titre abrégé: J Lipid Res
Pays: United States
ID NLM: 0376606
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
25
03
2020
revised:
09
05
2020
pubmed:
4
6
2020
medline:
14
8
2021
entrez:
4
6
2020
Statut:
ppublish
Résumé
Angiopoietin-like protein (ANGPTL)8 has been implicated in metabolic syndrome and reported to regulate adipose FA uptake through unknown mechanisms. Here, we studied how complex formation of ANGPTL8 with ANGPTL3 or ANGPTL4 varies with feeding to regulate LPL. In human serum, ANGPTL3/8 and ANGPTL4/8 complexes both increased postprandially, correlated negatively with HDL, and correlated positively with all other metabolic syndrome markers. ANGPTL3/8 also correlated positively with LDL-C and blocked LPL-facilitated hepatocyte VLDL-C uptake. LPL-inhibitory activity of ANGPTL3/8 was >100-fold more potent than that of ANGPTL3, and LPL-inhibitory activity of ANGPTL4/8 was >100-fold less potent than that of ANGPTL4. Quantitative analyses of inhibitory activities and competition experiments among the complexes suggested a model in which localized ANGPTL4/8 blocks the LPL-inhibitory activity of both circulating ANGPTL3/8 and localized ANGPTL4, allowing lipid sequestration into fat rather than muscle during the fed state. Supporting this model, insulin increased ANGPTL3/8 secretion from hepatocytes and ANGPTL4/8 secretion from adipocytes. These results suggest that low ANGPTL8 levels during fasting enable ANGPTL4-mediated LPL inhibition in fat tissue to minimize adipose FA uptake. During feeding, increased ANGPTL8 increases ANGPTL3 inhibition of LPL in muscle via circulating ANGPTL3/8, while decreasing ANGPTL4 inhibition of LPL in adipose tissue through localized ANGPTL4/8, thereby increasing FA uptake into adipose tissue. Excessive caloric intake may shift this system toward the latter conditions, possibly predisposing to metabolic syndrome.
Identifiants
pubmed: 32487544
pii: S0022-2275(20)43489-3
doi: 10.1194/jlr.RA120000781
pmc: PMC7397750
doi:
Substances chimiques
ANGPTL3 protein, human
0
ANGPTL8 protein, human
0
Angiopoietin-Like Protein 3
0
Angiopoietin-Like Protein 4
0
Angiopoietin-Like Protein 8
0
Angiopoietin-like Proteins
0
Biomarkers
0
Fatty Acids
0
Peptide Hormones
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1203-1220Informations de copyright
Copyright © 2020 Chen et al. Published by The American Society for Biochemistry and Molecular Biology, Inc.
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