Exposure to chronic stress leads to disturbances in glucose metabolism in the brain, and changes in the functioning of neurons coexisting with the development of depression. The detailed molecular mechanism and cerebral gluconeogenesis during depression are not conclusively established. The aim of the research was to assess the expression of selected genes involved in cerebral glucose metabolism of mice in the validated animal paradigm of chronic stress. To confirm the induction of depression-like disorders, we performed three behavioral tests: sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST). In order to study the cerebral glucose metabolism of the brain, mRNA levels of the following genes were determined in the prefrontal cortex of mice: , , , , and . It has been shown that exogenous, chronic administration of corticosterone developed a model of depression in behavioral tests. There were statistically significant changes in the mRNA level of the , , , and genes. The obtained results suggest changes in cerebral glucose metabolism as a process of adaptation to stressful conditions, and may provide the basis for introducing new therapeutic strategies for chronic stress-related depression.
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http://dx.doi.org/10.3390/brainsci12040498 | DOI Listing |
Pol J Vet Sci
June 2024
İstanbul University-Cerrahpaşa, Department of Industrial Engineering, Faculty of Engineering, Istanbul, 34320, Türkiye.
The aim of this study was to evaluate the changes in calcium, phosphorus and some biochemical parameters in dogs with open and closed cervix pyometra, which was then compared with a control group. A total of 62 bitches of age group 5-10 years old irrespective of breed were enrolled into the study. Control group consisted of 22 bitches which were clinically healthy and in luteal phase of the estrus cycle.
View Article and Find Full Text PDFJ Integr Neurosci
December 2024
Department of Neurology, Hainan West Central Hospital, 571799 Danzhou, Hainan, China.
Background: Ischemic stroke (IS) is the leading cause of mortality worldwide. Herein, we aimed to identify novel biomarkers and explore the role of C-type lectin domain family 7 member A () in IS.
Methods: Differentially expressed genes (DEGs) were screened using the GSE106680, GSE97537, and GSE61616 datasets, and hub genes were identified through construction of protein-protein interaction networks.
Oncol Res
December 2024
Department of Respiratory Medicine, Shandong Provincial Third Hospital, Jinan, 250010, China.
Background: To investigate SCL/TAL 1 interrupting locus ()'s role and prognostic significance in lung adenocarcinoma (LUAD) progression, we examined and E2 promoter binding factor 1 (E2F1) expression and their impacts on LUAD prognosis using Gene Expression Profiling Interactive Analysis (GEPIA).
Methods: Functional assays including CCK-8, wound-healing, 5-ethynyl-2-deoxyuridine (EdU), Transwell assays, and flow cytometry, elucidated and E2F1's effects on cell viability, proliferation, apoptosis, and migration. Gene set enrichment analysis (GSEA) identified potential pathways, while metabolic assays assessed glucose metabolism.
Front Endocrinol (Lausanne)
December 2024
Recordati Rare Diseases, Central and Eastern Europe, Warsaw, Poland.
Pasireotide is an effective treatment for both Cushing's disease (CD) and acromegaly due to its ability to suppress adrenocorticotropic hormone and growth hormone, and to normalize insulin-like growth factor-1 levels, resulting in tumor shrinkage. However, it may also cause hyperglycemia as a side effect in some patients. The aim of this study was to review previous recommendations regarding the management of pasireotide-induced hyperglycemia in patients with CD and acromegaly and to propose efficient monitoring and treatment algorithms based on recent evidence and current guidelines for type 2 diabetes treatment.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Department of Endocrinology and Metabolism, The First Affiliated Hospital of Ningbo University, Ningbo, Zhejiang, China.
Short stature, joint hyperextension, ocular hypotension, Rieger abnormalities, and delayed tooth eruption (SHORT) syndrom is a rare primary autosomal dominant genetic disorder mainly caused by pathogenic loss-of-function variants in the phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) gene. We report the case of a Chinese adult female patient with SHORT syndrome, carrying a PIK3R1 gene variant (c.1945C > T), who developed abnormal glucose metabolism and severe postprandial insulin resistance over 9 years.
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