Adipose Tissue Insulin Resistance Predicts the Severity of Liver Fibrosis in Patients With Type 2 Diabetes and Nonalcoholic Fatty Liver Disease (NAFLD)
Authors' conclusion
These findings pinpoint to the central role of dysfunctional, insulin-resistant adipose tissue to advanced fibrosis in T2D, beyond simply BMI or steatosis. The clinical implication is that targeting adipose tissue should be the priority of treatment in NAFLD.
Study context
- Population
- People with T2D screened by elastography for hepatic steatosis and fibrosis in outpatient clinics of a university ambulatory care practice
- Participants
- 483 people
- Exposure
- Adipose tissue insulin resistance (IR) (adipo-IR) vs hepatic IR (HOMA-IR) and other factors as predictors of liver fibrosis
- Outcome
- Liver steatosis (controlled attenuation parameter), fibrosis (liver stiffness measurement), and measurements of IR (adipo-IR, HOMA-IR) and fibrosis (cytokeratin-18)
Methodological detailselastography screening, university ambulatory care practice
- Elastography screening
- University ambulatory care practice
Main finding
As reported in the abstract
Prevalence of clinically significant liver fibrosis
11%
Model 1 (clinical variables): BMI strongest association with fibrosis, OR
2.56
CI 1.87–3.50P < 0.01
Model 3 (adjusted for BMI, AST, steatosis): only adipo-IR remained associated with fibrosis, OR (CI 1.05-2.16; P = 0.03); not BMI, hepatic IR or steatosis
1.51
Observational data: associations, not effects.
Further findings
Characteristics of those with significant fibrosis
- More metabolic syndrome features, lower adiponectin, higher AST, ALT, liver fat and cytokeratin-18 (P < 0.05-0.01)
Original publication
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