Altered Concentrations in Dyslipidemia Evidence a Role for ANGPTL8/Betatrophin in Lipid Metabolism in Humans.

Altered Concentrations in Dyslipidemia Evidence a Role for ANGPTL8/Betatrophin in Lipid Metabolism in Humans.

J Clin Endocrinol Metab. 2016 Jul 29;:jc20162084

Authors: Gómez-Ambrosi J, Pascual-Corrales E, Catalán V, Rodríguez A, Ramírez B, Romero S, Vila N, Ibáñez P, Margall MA, Silva C, Gil MJ, Salvador J, Frühbeck G

Abstract
CONTEXT: ANGPTL8/betatrophin is a secreted protein initially involved in β-cell replication. Recent data in humans and mice models suggest that ANGPTL8/betatrophin is more related to lipid metabolism.
OBJECTIVE: The aim of the present study was to compare the circulating concentrations of ANGPTL8/betatrophin in individuals with dyslipidemia defined as having high or low levels of HDL-cholesterol or triglycerides, respectively.
DESIGN, SETTING, AND PARTICIPANTS: Serum concentrations of ANGPTL8/betatrophin were measured by ELISA in 177 subjects. We studied two different selected case-control dyslipidemic cohorts including individuals with high (n=43) or low (n=46) circulating concentrations of HDL-cholesterol or with low (n=48) or high (n=40) levels of triglycerides.
RESULTS: Circulating concentrations of ANGPTL8/betatrophin were significantly lower in individuals with dyslipidemia P<0.001 in both males (C 27.8 ± 15.2 vs DL 17.0 ± 11.2 ng/mL) and females (C 50.0 ± 22.2 vs DL 27.0 ± 16.5 ng/mL). The magnitude of the differences was higher in dyslipidemic patients with low HDL-cholesterol than in those with high TG concentrations. ANGPTL8/betatrophin levels were lower in subjects with T2D (P<0.001) but the impact of T2D vanished (P=0.257) when the effect of dyslipidemia was included in the analysis.
CONCLUSIONS: We conclude that serum ANGPTL8/betatrophin concentrations are altered in human dyslipidemia. ANGPTL8/betatrophin emerges as a potential player in dyslipidemia with a strong association with HDL-C and a potential therapeutic tool for the treatment of dyslipidemia.

PMID: 27472196 [PubMed - as supplied by publisher]

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