Alterations in hippocampal neurogenesis and hippocampal insulin signaling pathway in rat with metabolic syndrome
Özet
Objective(s): We aimed to examine the level of hippocampal neurogenesis, and assess learning and
anxiety and the level of some proteins involving insulin signaling pathways in rats with Metabolic
Syndrome (MetS); and to reveal the relationship among them.
Materials and Methods: Totally, 30 Wistar-albino rats were used. The rats were divided into three
groups: Control, MetS, and MetS+Ins. Immunohistochemical staining was performed to evaluate the
levels of neurogenesis markers; Doublecortin (DCX), Neuronal-Differentiation-1 (NeuroD1), Ki67,
and Neuronal nuclear protein (NeuN). Then, cleaved caspase-3 and TUNEL labeling were performed
to detect the level of apoptosis. Additionally, behavior tests were performed to evaluate the learningmemory levels and anxiety-like behaviors. Insulin, Insulin Receptor (IR), Insulin Receptor Substrate
(IRS2), glucose transporter (GLUT)-3, and GLUT4 protein expression levels were analyzed to evaluate
the possible changes in the insulin signaling pathway.
Results: An increase in anxiety with memory deficiency was observed in MetS. In the hippocampus
of MetS, an increase was detected in the level of apoptosis, whereas a decrease was detected in the
expression level of the neurogenesis marker. Insulin secretion and IR levels decreased in hippocampal
neurons. We observed that GLUT3 and GLUT4 levels increased because of the non-activated insulin
signaling pathway.
Conclusion: We think that the insulin signaling pathway may have an effect on the decreased
neurogenesis in the MetS group. So, the evaluation of the Mitogen-activated protein kinase (MAPK)
pathway and the investigation of the effect of endoplasmic reticulum stress on this pathway will be
among the targets of our future studies.
