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Publication
ApoA-IV improves insulin sensitivity and glucose uptake in mouse adipocytes via
PI3K-Akt Signaling.
Authors Li X, Wang F, Xu M, Howles P, Tso P
Submitted By Submitted Externally on 2/1/2017
Status Published
Journal Scientific reports
Year 2017
Date Published
Volume : Pages 7 : 41289
PubMed Reference 28117404
Abstract Insulin resistance is a risk factor for type 2 diabetes mellitus. We
investigated the effect of ApoA-IV on glucose uptake in the adipose and muscle
tissues of mice and cultured 3T3-L1 adipocytes. We found that treatment with
ApoA-IV lowered fasting blood glucose in both WT and diabetic KKAy mice by
increasing glucose uptake in cardiac muscle, white adipose tissue, and brown
adipose tissue through a mechanism that was partially insulin independent. Cell
culture experiments showed that ApoA-IV improved glucose uptake in adipocytes in
the absence of insulin by upregulating GLUT4 translocation by PI3K mediated
activation of Akt signaling pathways. Considering our previous finding that
ApoA-IV treatment enhanced pancreatic insulin secretion, these results suggests
that ApoA-IV acts directly upon adipose tissue to improve glucose uptake and
indirectly via insulin signaling. Our findings warrant future studies to
identify the receptor for ApoA-IV and the downstream targets of PI3K-Akt
signaling that regulate glucose uptake in adipocytes as potential therapeutic
targets for treating insulin resistance.






Genes
SymbolDescription
Apoa4apolipoprotein A-IV
anonagouti

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