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Inhibiting phosphatidylcholine remodeling in adipose tissue increases insulin sensitivity
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Jiang, Xian-Cheng
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Spring 2023
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2023-08-24
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He_Mulin_thesis.pdf
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Abstract
Cell membrane phosphatidylcholine composition is regulated by lysophosphatidylcholine
acyltransferase (LPCAT); changes in membrane phosphatidylcholine saturation are implicated in
metabolic disorders. Here, we identified LPCAT3 as the major isoform of LPCAT in adipose
tissues and created adipocyte-specific Lpcat3-knockout mice to study adipose tissue lipid
metabolism. Transcriptome sequencing and plasma adipokine profiling were used to investigate
how LPCAT3 regulates adipose tissue insulin signaling. LPCAT3 deficiency reduced
polyunsaturated phosphatidylcholines in adipocyte plasma membranes, increasing insulin
sensitivity. LPCAT3 deficiency influenced membrane lipid rafts, which activated insulin receptors
and AKT in adipose tissue, and attenuated diet-induced insulin resistance. Conversely, higher
LPCAT3 activity in adipose tissues from ob/ob, db/db, and high-fat diet-fed mice reduced insulin
signaling. Adding polyunsaturated phosphatidylcholines to mature human or mouse adipocytes
in vitro worsened insulin signaling. We suggest that targeting LPCAT3 in adipose tissues to
manipulate membrane phospholipid saturation is a new strategy to treat insulin resistance.
Citation
He, M (2023). Inhibiting phosphatidylcholine remodeling in adipose tissue increases insulin sensitivity [Doctoral Dissertation, SUNY Downstate Health Sciences University]. SUNY Open Access Repository. https://soar.suny.edu/handle/20.500.12648/14757