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Endocrine Abstracts (2022) 83 DOMNP2 | DOI: 10.1530/endoabs.83.DOMNP2

1Center for Diabetes, Endocrinology and Cardiometabolism, Thalassotherapia Opatija, Opatija; 2Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka; 3Radiology Department, Thalassotherapia Opatija, Opatija; 4Clinic for Heart and Blood Vessels, Thalassotherapia Opatija, Opatija; 5Department of Rehabilitation and Sports Medicine, Faculty of Medicine, University of Rijeka, Rijeka; 6Department of Internal Medicine, Faculty of Medicine, University of Rijeka, Rijeka; 7Department of Endocrinology, Diabetes and Metabolic Diseases, Clinical Hospital Center Rijeka, Rijeka


Background: Emerging evidence shows that diabetes mellitus causes structural and functional alterations in the brain. Recent studies have shown that diabetes may induce reductions in N-acetyl aspartate (NAA) and glutamate concentrations in the cortical grey matter, but few studies have performed the neurochemical profiling of other brain regions in patients with diabetes. Hence, the aim was to investigate brain metabolites in other brain regions of adults with diabetes.

Case presentation: Brain metabolites, including NAA, creatine (Cr) and choline (Cho), were compared between 2 adult patients with type 1 diabetes (T1D) and 2 adult patients with type 2 diabetes (T2D) using single-voxel magnetic resonance (MR) spectroscopy in the following regions: the lentiform nucleus, centrum semiovale, thalamus and cerebellum. The results of MR spectroscopy were converted to standardized ratios: NAA/Cho, NAA/Cr and Cho/Cr; and were considered abnormal if <1.6, <1.2 and >1.5, respectively. All patients had diabetes for more than 7 years and reached their glycemic targets (A1c or time in range) before the scan. Almost 40% of analyzed brain metabolite ratios were considered abnormal, with fewer ratios considered abnormal in patients with T1D than those with T2D. Interestingly, one patient with T2D had an increased Cho/Cr ratio in all brain regions except the lentiform nucleus where decreased NAA/Cho ratio was noted. Similar changes in brain metabolites typically localised unilaterally in only one brain region were found in patients with T1D. The only unaffected parameter in all patients was the NAA/Cr ratio in centrum semiovale.

Conclusions: Distinct metabolic signatures of different brain regions may indicate subclinical region-specific diabetes-induced brain damage. Future large-scale studies should challenge the role of brain metabolites as biomarkers and potentially reveal the underlying mechanism involved in the pathogenesis of comorbid brain disorders in patients with diabetes.

Volume 83

ESE Young Endocrinologists and Scientists (EYES) 2022

Zagreb, Croatia
02 Sep 2022 - 04 Sep 2022

European Society of Endocrinology 

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