Impaired Adipocyte SLC7A10 Promotes Lipid Storage in Association With Insulin Resistance and Altered Branched-chain Amino Acid (BCAA) Metabolism
Authors' conclusion
Reduced SLC7A10 activity strongly affects flux of BCAAs in adipocytes, which may fuel continued lipogenesis during insulin resistance, and be reflected in increased circulating levels of the valine-derived catabolite 3-HIB.
Study context
- Population
- Human and mouse adipose cultures (3T3-L1 adipocytes, human subcutaneous adipose tissue (SAT) cultures); human SAT in 2 independent cohorts2 independent cohorts
- Comparison
- Impaired SLC7A10 vs normal SLC7A10 activity in adipocytes
- Outcome
- Effects of SLC7A10 impairment in adipocytes and correlations in human cohorts
Methodological detailsadipocyte cultures, RNA sequencing, targeted metabolite analyses (GC-MS/MS), 2 independent human cohorts
- Adipocyte cultures
- RNA sequencing
- Targeted metabolite analyses (GC-MS/MS)
- 2 independent human cohorts
Main finding
As reported in the abstract
- SLC7A10 impairment altered expression of genes related to metabolic processes, including BCAA catabolism, lipogenesis and glyceroneogenesis
- In 3T3-L1 adipocytes, SLC7A10 inhibition increased fatty acid uptake and cellular content of glycerol and cholesterol
- In SAT cultures, SLC7A10 impairment altered uptake of aspartate and glutamate, increased net uptake of BCAAs and increased net release of 3-HIB
- In human cohorts, SLC7A10 mRNA correlated inversely with total fat mass, circulating triacylglycerols, BCAAs and 3-HIB
Original publication
Impaired Adipocyte SLC7A10 Promotes Lipid Storage in Association With Insulin Resistance and Altered BCAA Metabolism. J Clin Endocrinol Metab. Published 14 March 2023. doi:10.
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