Deficits in brain glucose transport among younger adults with obesity
Authors' conclusion
We conclude that CMRglucose is unlikely to differ between groups due to similar VTCA, and, therefore, the glucose transport Tmax is lower in individuals with obesity. These human findings suggest that obesity is associated with reduced cerebral glucose transport capacity even at a young age and in the absence of other cardiometabolic comorbidities, which may have implications for long-term brain function and health.
Study context
- Population
- Young healthy adults, lean or with obesity (mean age, 27 years)
- Participants
- 7 vs 11
- Exposure
- Young adults with obesity vs lean participants
- Obesityn = 7
- Leann = 11reference
- Outcome
- Ratio of brain glucose uptake to cerebral glucose metabolic rate (Tmax/CMRglucose)
Methodological detailsMR spectroscopy with hyperglycemic clamp, [1-13C] glucose
- MR spectroscopy with hyperglycemic clamp
- [1-13C] glucose
Main finding
As reported in the abstract
Obesity
2.12
± 0.51
Lean
2.67
± 0.51
P = 0.04
Observational data: associations, not effects.
Further findings
| Outcome | P value |
|---|---|
| Cerebral tricarboxylic acid cycle flux (VTCA)Similar between groups | P = 0.64 |
Cerebral tricarboxylic acid cycle flux (VTCA)
- VTCA similar between the two groups
Correlation of total nonesterified fatty acids with Tmax/CMRglucose
- Negative correlation (r; p = 0.045)
- r = −0.477
Original publication
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