Brain glucose hypometabolism and hippocampal inflammation in Goto-Kakizaki rats

Brain glucose hypometabolism and hippocampal inflammation in Goto-Kakizaki rats

Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the h...

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Bibliographic Details
Published in:Brazilian journal of medical and biological research Vol. 56; no. 1; p. e12742
Main Authors: Borges, J C O, Oliveira, V A B, Serdan, T D A, Silva, F L R, Santos, C S, Pauferro, J R B, Ribas, A S F, Manoel, R, Pereira, A C G, Correa, I S, Pereira, J N B, Bazotte, R B, Levada-Pires, A C, Pithon-Curi, T C, Gorjão, R, Curi, R, Hirabara, S M, Masi, L N
Format: Journal Article
Language:English
Published: Brazil Associacao Brasileira de Divulgacao Cientifica (ABDC) 01-01-2023
Revista Brasileira de Pesquisas Medicas
Associação Brasileira de Divulgação Científica
Subjects:
Analysis
Animal experimentation
Animal models
BIOLOGY
Cognitive disorders
Dextrose
Diabetes
Diabetes mellitus (non-insulin dependent)
Diagnosis
Distribution
Energy balance
Evaluation
Gene expression
Genetic transcription
Glucose
Goto-Kakizaki rats
Health aspects
High fat diet
Hippocampus
Hyperglycemia
Hypothalamus
IL-1β
Inflammation
Insulin resistance
Leptin
MEDICINE, RESEARCH & EXPERIMENTAL
Molecular modelling
Neurological diseases
Neuroprotection
NF-κB protein
Obesity
Type 2 diabetes
Brazil
Insulin resistance
Hyperglycemia
Cognitive disorders
Leptin
Hippocampus
Goto-Kakizaki rats
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Summary:Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the hippocampus. The Goto-Kakizaki (GK) rat is a non-obese type 2 diabetes mellitus (T2DM) animal model used to investigate diabetes-associated molecular mechanisms without obesity jeopardizing effects. Wistar and GK rats received the maintenance adult rodent diet. Also, an additional control group of Wistar rats received a high-fat and high-sugar diet (HFHS) provided by free consumption of condensed milk. All diets and water were provided ad libitum for eight weeks. Brain glucose uptake was evaluated by 2-deoxy-2-[fluorine-18] fluoro-D-glucose under basal (saline administration) or stimulated (CL316,243, a selective β3-AR agonist) conditions. The animals were fasted for 10-12 h, anesthetized, and euthanized. The brain was quickly dissected, and the hippocampal area was sectioned and stored at -80°C in different tubes for protein and RNA analyses on the same animal. GK rats exhibited attenuated brain glucose uptake compared to Wistar animals and the HFHS group under basal conditions. Also, the hippocampus of GK rats displayed upregulated leptin receptor, IL-1β, and IL-6 gene expression and IL-1β and the subunit of the transcription factor NF-κB (p-p65) protein expression. No significant alterations were detected in the hippocampus of HFHS rats. Our data indicated that a genetic predisposition to T2DM has significant brain deteriorating features, including brain glucose hypometabolism, neuroinflammation, and leptin signaling disruption in the hippocampal area.
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content type line 23
ISSN:0100-879X
1414-431X
1414-431X
1678-4510
DOI:10.1590/1414-431X2023e12742