Streptozotocin induced hyperglycemia stimulates molecular signaling that promotes cell cycle reentry in mouse hippocampus

Yang, Euitaek; Gavini, Kartheek; Bhakta, Ami; Dhanasekaran, Muralikrishnan; Khan, Izhar Ahmad; Parameshwaran, Kodeeswaran

doi:10.1016/j.lfs.2018.05.019

Cited by 10 publications

(3 citation statements)

References 71 publications

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“…However, the pathogenesis of hippocampal impairment in diabetes remains unclear and debatable 22. In previous studies, impaired insulin sensitivity and induced long‐term hyperglycemia, oxidative stress, change in mitochondria bioenergetics, and neuronal apoptosis has been reported closely relating to changes in hippocampus 23–26. To date, there is no study focus on the relationship between postprandial GF and hippocampus impairment.…”

Section: Discussionmentioning

confidence: 99%

“…22 In previous studies, impaired insulin sensitivity and induced long-term hyperglycemia, oxidative stress, change in mitochondria bioenergetics, and neuronal apoptosis has been reported closely relating to changes in hippocampus. [23][24][25][26] To date, there is no study focus on the relationship between postprandial GF and hippocampus impairment. In our study, we established a postprandial GF state in diabetic rats and evaluated the impact on the hippocampus on neuroethology, inflammation, and neuronal apoptosis aspects.…”

Section: Discussionmentioning

confidence: 99%

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Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

Wang

Deng

Chen

et al. 2019

J of Cellular Biochemistry

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It is well‐recognized that glycemic disorders are leading causes of diabetic complications and acute fluctuation of blood glucose and reported more likely being related to oxidative stress, vasculopathy, and other diabetic complications than continuous hyperglycemia in patients with diabetic and animal models. To explore the hypothesis that acute glucose fluctuation (GF) aggravates inflammatory lesions and neuron apoptosis in the hippocampus of diabetic rats. Twenty female GK rats were randomly allocated into a glucose fluctuating group (GK‐GF) and a continuous hyperglycemia group (GK‐CHG) and 10 age‐matched female Wistar rats served as controls. GF was induced in the GK‐GF group by injection with glucose and insulin at different periods of time per day for 6 weeks. Body weight was determined weekly. At the end of the study, blood hemoglobin A1c (HbA1c) and serum lipids were measured. Serum and hippocampus interleukin 1β (IL‐1β), IL‐6, IL‐8, and tumor necrosis factor‐α (TNF‐α) were measured by enzyme‐linked immunosorbent assay and real‐time quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR). Hippocampus Bcl‐2, Bax, Pten, fas, and myc were quantified by qRT‐PCR and Western blot analysis and Mirror Water Maze (MWM) test was performed. We successfully established an animal model with daily GF and a control model with CHG using GK diabetic rats. The GF and CHG rats showed lower weight gain during the 6‐week experimental period with no significant difference in the levels of serum lipids such as total triglyceride, total cholesterol, high‐density lipoprotein cholesterol, and low‐density lipoprotein cholesterol compared with the control rats at the end of the study. Meanwhile, the GF and CHG rats showed higher blood HbA1c levels than that of control rats. MWM trainings tests detected that glucose disorders in GF and CHG rats tend to present longer latencies, more cross times and longer path length compared with those of the control rats, indicating impaired the hippocampus‐regulated behavioral function such as spatial orientating and memory. Importantly, it was found that GF promoted the expression of TNF‐α and IL‐1β in the hippocampus of the GF rats while continuous hyperglycemia in CHG rats had little effect on that. Furthermore, both GF and CHG diabetic rats had abnormal expression of apoptosis‐associated genes in the hippocampus compared with control Wistar rats and neurons apoptosis in GF rats appears to be more severe than CHG rats. Overall, this study confirmed that GF is a more critical factor that would promote the neuron apoptosis and induce inflammation in the hippocampus than continuous hyperglycemia in diabetic animals, which shed new light on the importance of monitoring and administration of blood glucose in the prevention and therapy for diabetes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

Wang

Deng

Chen

et al. 2019

J of Cellular Biochemistry

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“…When ERK1/2 is knocked down in Olig2 + oligodendroglial lineage cells, OPC proliferation diminishes [94] . Echoing ndings from Yang et al in hippocampal neurons [95] , OPCs in a high fat-high glucose environment display reduced ERK phosphorylation, proliferative capability, and cell viability. Ruiz-Palacios et al [96] also found a decline in OPC proliferative capacity in pups exposed to GDM in vivo.…”

Section: Discussionmentioning

confidence: 85%

Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring

Zhou,

Li,

Qiao

et al. 2024

Preprint

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Gestational diabetes mellitus (GDM) and prenatal exposure to valproic acid (VPA) are both constitute risk factors for autism in progeny. Notably, dysmyelination in the corpus callosum serves as a prominent element connecting GDM and autism in the white matter lesions. Objective: the cumulative effects of GDM and prenatal VPA on both autistic behavior and dysmyelination in progeny have been researched in this study. Methods: In vivo, female mice exhibiting leptin receptor deficiencies and maintained on a high-fat diet were utilized to create GDM models, to which prenatal VPA was administered. In vitro, oligodendrocyte precursor cells (OPCs) was treated with VPA in the high-fat and high-glucose culture. Results: the offspring subjected to both GDM and prenatal VPA demonstrated comparable declines in social interaction, myelination, and OPC maturation, akin to those exclusively exposed to VPA. Remarkably, the application of clemastine facilitated remyelination, ameliorated autistic behaviors, and promoted the OPCs progression. Furthermore, the compromised myelination and OPC maturation instigated by the combination of GDM and prenatal VPA were found to be less severe compared to those precipitated by VPA alone. This differential impact can be attributed to the opposing influences of GDM and VPA on gamma-aminobutyric acid receptor activation in OPCs, extracellular regulated protein kinases (ERK) phosphorylation in OPCs, and the modulation of histone deacetylase 3 and dual specificity phosphatase 5 expression. Conclusions: we delineate the antagonistic effects of GDM and prenatal VPA on ERK phosphorylation in fetal OPCs, consequently altering its proliferation and differentiation, thereby culminating in milder dysmyelination and autistic behaviors.

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Volumetric investigation of the hippocampus in rat offspring due to diabetes in pregnancy–A stereological study

Sadeghi

Asghari

Hami

et al. 2019

Journal of Chemical Neuroanatomy

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Streptozotocin induced hyperglycemia stimulates molecular signaling that promotes cell cycle reentry in mouse hippocampus

Cited by 10 publications

References 71 publications

Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

Acute glucose fluctuation induces inflammation and neurons apoptosis in hippocampal tissues of diabetic rats

Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring

Volumetric investigation of the hippocampus in rat offspring due to diabetes in pregnancy–A stereological study

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