Osteopontin‐driven T‐cell accumulation and function in adipose tissue and liver promoted insulin resistance and metabolic-associated fatty liver disease (MAFLD)
Authors' conclusion
Current findings highlight a critical role of SPP1 in the initiation of obesity-driven chronic inflammation by regulating accumulation and/or polarization of T cells. Early targeting of SPP1 could be beneficial for IR and MAFLD treatment.
Study context
- Population
- Human individuals with obesity (adipose tissue (AT) and liver, by T2D and MAFLD status); Spp1-knockout mice challenged with a high-fat diet
- Comparison
- Spp1 deficiency vs wild type; SPP1 expression by T2D and MAFLD status
- Outcome
- SPP1 and T-cell regulation in obesity-driven AT inflammation, IR and MAFLD
Methodological detailshuman tissue expression analysis, Spp1-knockout mice on high-fat diet
- Human tissue expression analysis
- Spp1-knockout mice on high-fat diet
Main finding
As reported in the abstract
- In humans with obesity, elevated AT SPP1 expression paralleled T-cell marker expression (CD4, CD8A) and insulin resistance (IR)
- Weight loss reversed AT inflammation with decreased SPP1 and CD8A expression
- In liver, elevated SPP1 expression correlated with MAFLD severity and hepatic T-cell markers
- In mice, Spp1 deficiency did not impact obesity but improved AT IR, with prevention of proinflammatory T-cell accumulation at the expense of regulatory T cells
- Spp1 deficiency decreased ex vivo Th1 polarization of AT CD4+ and CD8+ T cells
- Spp1 deficiency significantly reduced obesity-associated liver steatosis and inflammation
Original publication
Osteopontin‐driven T‐cell accumulation and function in adipose tissue and liver promoted insulin resistance and MAFLD. Obesity (Silver Spring). Published 19 September 2023. doi:10.
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