Key result
ANGPTL8/betatrophin improved glucose tolerance in older mice without altering insulin concentration, and its knockout in insulin-resistant HepG2 cells altered 83 metabolites.
Why the study?
ANGPTL8/betatrophin is associated with glucose homeostasis and lipid metabolism, but its mechanism in glucose metabolism remains unclear.
Population
Kunming mice of different ages and high insulin-induced insulin-resistant HepG2 cells
Comparison
ANGPTL8/betatrophin knockout vs wild-type HepG2 cells
Design
Preclinical animal and in vitro study
Authors
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Hypothesis-generating for ANGPTL8 in age-related glucose intolerance; human studies required before any therapeutic consideration.
ANGPTL8/betatrophin plays a role in glucose metabolism and insulin resistance, affecting multiple metabolic pathways in HepG2 cells and improving glucose tolerance in older mice.
Xu et al. (2021) studied Insulin resistance. ANGPTL8/betatrophin knockout vs. Wild type cells / control mice was evaluated on Glucose tolerance and metabolomic changes. ANGPTL8/betatrophin improved glucose tolerance in older mice without altering insulin concentration, and its knockout in insulin-resistant HepG2 cells altered 83 metabolites.
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