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Introduction: Abdominal adipose tissue (AT) mass has adverse effects on the brain. This study aimed to investigate the effect of glucose uptake by abdominal AT on brain aging.
Methods: Three-hundred twenty-five participants underwent total-body positron emission tomography scan. Brain age was estimated in an independent test set (n = 98) using a support vector regression model that was built using a training set (n = 227). Effects of abdominal subcutaneous and visceral AT (SAT/VAT) glucose uptake on brain age delta were evaluated using linear regression.
Results: Higher VAT glucose uptake was linked to negative brain age delta across all subgroups. Higher SAT glucose uptake was associated with negative brain age delta in lean individuals. In contrast, increased SAT glucose uptake demonstrated positive trends with brain age delta in female and overweight/obese participants.
Discussion: Increased glucose uptake of the abdominal VAT has positive influences on the brain, while SAT may not have such influences, except for lean individuals.
Highlights: Higher glucose uptake of the visceral adipose tissue was linked to decelerated brain aging. Higher glucose uptake of the subcutaneous adipose tissue (SAT) was associated with negative brain age delta in lean individuals. Faster brain aging was associated with increased glucose uptake of the SAT in female and overweight and obese individuals.
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http://dx.doi.org/10.1002/alz.14193 | DOI Listing |
Diabetes
September 2025
Institute for Physical Activity and Nutrition, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, Victoria, Australia.
Unlabelled: Despite stimulating glucagon secretion, the mechanisms by which protein ingestion lowers glucose excursions remain unclear. We investigated this using the triple stable isotope glucose tracer technique to measure postprandial glucose fluxes. Eleven healthy adults completed three trials, ingesting 25 g glucose (25G; 100 kcal), 50 g glucose (50G; 200 kcal), or 25 g glucose plus 25 g whey protein (25WG; 200 kcal).
View Article and Find Full Text PDFExp Ther Med
November 2025
Department of Obstetrics and Gynecology, Affiliated Maternity and Child Health Care Hospital of Nantong University, Nantong, Jiangsu 226007, P.R. China.
Gestational diabetes mellitus (GDM), a type of diabetes mellitus occurring in pregnant women, increases the risk of birth trauma. Solute carrier family 2 member 4 (SLC2A4) polymorphism is notably associated with GDM susceptibility; however, the mechanism is unknown. In the present study, HTR-8/SVneo cells were treated with high glucose concentrations and transfected with SLC2A4 and Forkhead box O (FoxO)1 to investigate their roles in the insulin (INS) resistance of GDM trophoblast cells.
View Article and Find Full Text PDFFEBS Lett
September 2025
Kusuma School of Biological Sciences, Indian Institute of Technology-Delhi, Hauz Khas, New Delhi, India.
Neuronal insulin signaling is essential for regulating glucose metabolism and cognitive functions in the brain. Disruptions cause neuronal insulin resistance, potentially causing type 2 diabetes (T2D) and Alzheimer's disease (AD). Therefore, we investigated alternative pathways that maintain glucose homeostasis beyond traditional insulin signaling.
View Article and Find Full Text PDFDiabetes Obes Metab
September 2025
Turku PET Centre, University of Turku, Turku, Finland.
Aims: Obesity is associated with increased insulin-stimulated brain glucose uptake (BGU) which is opposite to decreased GU observed in peripheral tissues. Increased BGU was shown to be reversed by weight loss and exercise training, but the mechanisms remain unknown. We investigated whether neuroinflammation (TSPO availability) and brain activity drive the obesity-associated increase in BGU and whether this increase is reversed by exercise training.
View Article and Find Full Text PDFNucl Med Biol
August 2025
Department of Radiology, University of Pennsylvania, Philadelphia, PA, USA.
Background: Glutamine is an important metabolic substrate in many aggressive tumors, with comparable importance to glucose metabolism. Utilizing human breast cancer mouse xenograft models, we studied the kinetics of the PET imaging agent, L-5-[C]-glutamine ([C]glutamine or [C]GLN) a biochemical authentic substrate for glutamine metabolism, to further characterize the metabolism of glutamine and downstream labeled metabolites. Studies were performed with and without inhibition of the enzyme, glutaminase (GLS), the first step in glutamine catabolism that generates glutamate, and key target for therapy directed to glutamine-metabolizing cancers.
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