Alterations in cerebral perfusion and substrate metabolism in type 2 diabetes: interactions with APOE-ε4
Authors' conclusion
Type 2 diabetes was associated with decreased cerebral perfusion and glucose uptake but increased fatty acid uptake in white matter. The elevated fatty acid uptake observed both in individuals with type 2 diabetes and in APOE-ε4 carriers suggests a common metabolic dysfunction for these Alzheimer's disease risk factors and suggests that targeting cerebral metabolic dysfunction, particularly fatty acid metabolism, could be a potential strategy for reducing the risk for neurodegeneration in individuals with type 2 diabetes.
Study context
- Population
- Individuals with T2D, overweight individuals and lean controls
- Participants
- 38 individuals
- Exposure
- T2D vs overweight vs lean controls
- T2Dn = 10
- Overweightn = 13
- Leann = 15reference
- Outcome
- Cerebral metabolism: glucose and fatty acid uptake and cerebral blood flow
Methodological detailsmultimodal imaging (FDG and FTHA PET, arterial spin-labelling MRI, 1H-MRS), lumbar puncture neurodegeneration markers
- Multimodal imaging (FDG and FTHA PET, arterial spin-labelling MRI, 1H-MRS)
- Lumbar puncture neurodegeneration markers
Main finding
As reported in the abstract
- Glucose uptake and perfusion correlated negatively with HOMA-IR, insulin and HbA1c
- p<0.001-p<0.05
Observational data: associations, not effects.
Further findings
- Fatty acid uptake by APOE-ε4 status (post hoc) — In non-carriers, fatty acid uptake correlated positively with HOMA-IR, insulin and HbA1c · T2D vs Lean · post hoc analyses
- P < 0.05 · P < 0.01-p<0.05
- Fatty acid uptake by APOE-ε4 status (post hoc): APOE-ε4 non-carriers: higher fatty acid uptake with T2D than lean
Fatty acid uptake by APOE-ε4 status (post hoc)
- Lean APOE-ε4 carriers had increased fatty acid uptake in the entire brain vs lean non-carriers
Original publication
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