Insulin resistance in adipose tissue and fatty liver, but not fat mass, are involved in worsening glycaemic status: The Hiroshima study on glucose metabolism and cardiovascular diseases
Authors' conclusion
Adipose tissue insulin resistance, rather than fat mass, is crucial in all stages of deterioration of glycaemic status. Fatty liver plays a decisive role in the eventual development of type 2 diabetes.
Study context
- Population
- Individuals who underwent two 75-g OGTTs at baseline and follow-up (Hiroshima study on glucose metabolism and CVD)
- Participants
- 3,644 individuals
- Exposure
- Highest vs lowest quartiles of Adipo-IR, lipid accumulation product (LAP) and fatty liver index (FLI)
- Outcome
- Progression from normoglycaemia to prediabetes and from prediabetes to T2D
- Follow-up
- mean 2.9-year follow-up
Methodological detailslongitudinal, two 75-g OGTTs at baseline and follow-up
- Longitudinal
- Two 75-g OGTTs at baseline and follow-up
Main finding
As reported in the abstract
Progression of impaired glucose metabolism by Adipo-IR quartile
Highest quartile vs Lowest quartileOdds ratio (95% CI)
Baseline Adipo-IR; normoglycaemia to prediabetes
2.22(1.36–3.65)
Change in Adipo-IR; normoglycaemia to prediabetes
2.70(1.83–3.98)
Baseline Adipo-IR; prediabetes to T2D
2.02(1.04–3.92)
Change in Adipo-IR; prediabetes to T2D
3.09(1.84–4.19)
- Progressed from normoglycaemia to prediabetes
- 463 (32.4%)
- Developed T2D from prediabetes
- 198 (10.6%)
Observational data: associations, not effects.
Further findings
FLI
- Changes in FLI were associated with progression from prediabetes to T2D
LAP
- LAP did not affect progression of impaired glucose metabolism
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
Insulin resistance in adipose tissue and fatty liver, but not fat mass, are involved in worsening glycaemic status: The Hiroshima study on glucose metabolism and cardiovascular diseases. Diabetes Obes Metab. Published 5 March 2025. doi:10. 1111/ dom. 16307
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