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Purpose: Hyperglycemia affects FDG uptake in the brain, potentially emulating Alzheimer's disease in normal individuals. This study investigates global and regional cerebral FDG uptake as a function of plasma glucose in a cohort of patients.
Methods: 120 consecutive male patients with FDG PET/CT for initial oncologic staging (July-Dec 2015) were reviewed. Patients with dementia, cerebrovascular accident, structural brain lesion, prior oncology treatment or high metabolic tumor burden (recently shown affecting brain FDG uptake) were excluded. 53 (24 nondiabetic) eligible patients (age 65.7 ± 2.8 mean ± SE) were analyzed with parametric computer software, MIMneuro™. Regional Z-scores were evaluated as a function of plasma glucose and age using multi variable linear mixed effects models with false discovery analysis adjusting for multiple comparisons. If the regression slope was significantly (p < 0.05) different than zero, hyperglycemia effect was present.
Results: There was a negative inverse relationship (p < 0.001) between global brain FDG uptake and hyperglycemia. No regional hyperglycemia effect on uptake were present when subjects were normalized using pons or cerebellum. However, regional hyperglycemia effects were seen (p < 0.047-0.001) when normalizing by the whole brain. No obvious pattern was seen in the regions affected. Age had a significant effect using whole brain normalization (p < 0.04-0.01).
Conclusions: Cortical variation in FDG uptake were identified when subjects were hyperglycemic. However, these variations didn't fit a particular pattern of dementia and the severity of the affect is not likely to alter clinical interpretation.
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http://dx.doi.org/10.1016/j.biopha.2019.108628 | DOI Listing |
Curr Med Res Opin
September 2025
Department of Internal Medicine, Taksim Training and Research Hospital, Istanbul, Turkey.
Introduction: Diabetes Mellitus is a chronic disease characterised by elevated plasma glucose (PG) levels. HbA1c has been widely utilized for diabetes diagnosis. However, certain conditions restrict its use.
View Article and Find Full Text PDFJ Neurooncol
September 2025
Department of Neurology, Xiangya Hospital, Central South University, No.87 Xiangya Road, Kaifu District, Changsha, 410008, Hunan Province, China.
Background And Objective: Differentiating central nervous system infections (CNSIs) from brain tumors (BTs) is difficult due to overlapping features and the limited individual indicators, and cerebrospinal fluid (CSF) cytology remains underutilized. To improve differential diagnosis, we developed a model based on 9 early, cost-effective cerebrospinal fluid parameters, including CSF cytology.
Methods: Patients diagnosed with CNSIs or BTs at Xiangya Hospital of Central South University between October 1st, 2017 and March 31st, 2024 were enrolled and divided into the training set and the test set.
Int J Mol Med
November 2025
Department of Neurosciences 'Rita Levi Montalcini', University of Turin, I‑10125 Turin, Italy.
Kinases are activators of well‑known inflammatory cascades implicated in metabolic disorders, and abnormal activation of casein kinase II (CK2) is associated with several inflammatory disorders. However, thus far, its role in the low‑grade chronic inflammatory response known as 'metaflammation', which is a hallmark of obesity and type 2 diabetes, has not yet been elucidated. The present study aimed to evaluate the role of CK2 in diet‑induced metaflammation and the effects of the CK2 inhibitor 4,5,6,7‑tetrabromobenzotriazole (TBB) on a murine model fed a high‑fat‑high‑sugar (HFHS) diet.
View Article and Find Full Text PDFMol Nutr Food Res
September 2025
Facultat De Medicina i Ciències De La Salut, Universitat Rovira i Virgili, Reus, Spain.
High-fat (HF) diets contribute to obesity, insulin resistance, fatty liver, gut microbiota dysbiosis, oxidative stress, and low-grade chronic inflammation. This study evaluated the preventive effects of dietary Type 2 resistant starch (RS2) from high-amylose maize and low-dose d-fagomine (FG) from buckwheat on these metabolic disturbances. Male Wistar-Kyoto rats (9-10 weeks old) were assigned to four diet groups for 10 weeks: standard (STD) diet, HF diet (45% kcal from fat), HF + RS diet (15% RS2), and HF + FG diet (0.
View Article and Find Full Text PDFEMBO J
September 2025
School of Life and Environmental Sciences, Faculty of Science, The University of Sydney, Sydney, NSW, Australia.
Insulin resistance is a heritable risk factor for many chronic diseases; however, the genetic drivers remain elusive. In seeking these, we performed genetic mapping of insulin sensitivity in 670 chow-fed Diversity Outbred in Australia (DOz) mice and identified a genome-wide significant locus (QTL) on chromosome 8 encompassing 17 defensin genes. By taking a systems genetics approach, we identified alpha-defensin 26 (Defa26) as the causal gene in this region.
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