The effect of ketogenic diets on neurogenesis and apoptosis in the dentate gyrus of the male rat hippocampus

Irfannuddin, Irfannuddin; Sarahdeaz, Siti Fazzaura Putri; Murti, Krisna; Santoso, Budi; Koibuchi, Noriyuki

doi:10.1186/s12576-020-00786-7

Cited by 7 publications

(4 citation statements)

References 24 publications

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“…It has been found, however, that when using levodopa together with a ketogenic diet, the results can be far more favourable than those of the treatment with the drug alone (through an improvement of its bioavailability) [ 187 , 188 , 189 ]. Studies on PD animal models have clearly demonstrated that ketone bodies reduce dopaminergic neuronal death (BHB administered in vitro to cortical neurons and subcutaneously infused in mice) [ 38 , 190 ], decrease the number of proinflammatory cells in the brain and improve motor functions [ 62 ]. Another potentially possible mechanism of the ketogenic diet’s influence on PD is the indirect effect mediated by changes in the intestinal microbiome.…”

Section: The Role Of the Ketogenic Diet In The Therapy Of Parkinson’s...mentioning

confidence: 99%

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

2022

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Over a hundred years of study on the favourable effect of ketogenic diets in the treatment of epilepsy have contributed to a long-lasting discussion on its potential influence on other neurological diseases. A significant increase in the number of scientific studies in that field has been currently observed. The aim of this paper is a widespread, thorough analysis of the available scientific evidence in respect of the role of the ketogenic diet in the therapy of neurological diseases such as: epilepsy, Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS) and migraine. A wide range of the mechanisms of action of the ketogenic diet has been demonstrated in neurological diseases, including, among other effects, its influence on the reduction in inflammatory conditions and the amount of reactive oxygen species (ROS), the restoration of the myelin sheath of the neurons, the formation and regeneration of mitochondria, neuronal metabolism, the provision of an alternative source of energy for neurons (ketone bodies), the reduction in glucose and insulin concentrations, the reduction in amyloid plaques, the induction of autophagy, the alleviation of microglia activation, the reduction in excessive neuronal activation, the modulation of intestinal microbiota, the expression of genes, dopamine production and the increase in glutamine conversion into GABA. The studies discussed (including randomised controlled studies), conducted in neurological patients, have stressed the effectiveness of the ketogenic diet in the treatment of epilepsy and have demonstrated its promising therapeutic potential in Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS) and migraine. A frequent advantage of the diet was demonstrated over non-ketogenic diets (in the control groups) in the therapy of neurological diseases, with simultaneous safety and feasibility when conducting the nutritional model.

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Section: The Role Of the Ketogenic Diet In The Therapy Of Parkinson’s...mentioning

confidence: 99%

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

2022

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“…Ki67 is a commonly used marker for assessing cell proliferation ( 34 ). It has been indicated that Ki67 immunoexpression is significantly reduced in the DG of STZ-induced DM rats ( 35 , 36 ).…”

Section: Discussionmentioning

confidence: 99%

Insulin and liraglutide attenuate brain pathology in diabetic mice by enhancing the Wnt/β‑catenin signaling pathway

Zhao

Ping

et al. 2022

Exp Ther Med

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Insulin and liraglutide have been demonstrated to control blood glucose and exert neuroprotective effects. However, the impact of liraglutide or insulin alone or in combination on brain pathology in type 1 diabetes mellitus (T1DM) and their underlying mechanisms are unclear. In the present study, diabetes mellitus (DM) was induced via intraperitoneal injection of streptozotocin in mice and subsequently mice were treated with insulin, liraglutide, a combination of the two drugs or saline. Changes in body weight and blood glucose were assessed weekly. The pathological changes in the brain tissue and the apoptosis of neurons were assessed using H&E staining and TUNEL staining. The mRNA and protein expression levels of apoptosis-related proteins were detected using reverse transcription-quantitative PCR (RT-qPCR) and western blotting, respectively. Moreover, Ki67 protein expression was analyzed using immunohistochemistry and the mRNA and protein expression levels of Wnt/β-catenin signaling pathway-related proteins were examined using RT-qPCR and western blotting, respectively. The results of the present study suggested that DM mice developed hyperglycemia and weight loss and also exhibited significantly increased neural cell apoptosis and significantly reduced numbers of Ki67-positive cells. Liraglutide significantly decreased blood glucose levels in DM mice, whereas both insulin and the combination of the two drugs failed to control blood glucose well. Insulin, liraglutide and their combination also failed to control body weight well, but significantly attenuated brain pathological changes and activation of the pro-apoptotic proteins Caspase-3 and Bax, which may have resulted in the significant increase in the expression levels of Wnt/β-catenin signaling pathway-associated molecules such as Wnt3a and S9-pGSK-3β. Liraglutide also promoted the protein expression of the neurogenesis marker of Ki67 and the antiapoptotic factor Bcl-2. These results suggested that insulin and liraglutide may improve brain damage via upregulation of the Wnt/β-catenin signaling pathway and could be of therapeutic relevance for improvement of cognitive impairment in patients with DM.

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“…Ki-67 is an excellent marker for determining cellular proliferation ( Irfannuddin et al, 2021 ). Hence, neuronal proliferation in the hippocampal DG was assessed using ki-67 immunoexpression.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Anti-inflammatory and Neuroprotective Effects of Cinnamomum cassia and Zingiber officinale Alleviate Diabetes-Induced Hippocampal Changes in Male Albino Rats: Structural and Molecular Evidence

Almohaimeed

Mohammedsaleh

Batawi

et al. 2021

Front. Cell Dev. Biol.

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Background: Depression has been reported as a common comorbidity in diabetes mellitus although the underlying mechanism responsible for this is not well known. Although both ginger and cinnamon has anti-diabetic, antioxidant, and neuroprotective properties, their efficacy in inhibiting neuroinflammation, when simultaneously administrated, has not been investigated yet.Objectives: The study was designed to assess the synergistic effect of Cinnamomum cassia and Zingiber officinale on regulating blood glucose, improve hippocampal structural changes and depressive-like alternations in diabetic rats, and try to identify the mechanism behind this effect.Materials and Methods: Thirty male Sprague–Dawley rats were divided into five equal groups (n = 6): the normal control, untreated streptozotocin (STZ)-diabetic, cinnamon-treated diabetic [100 mg/kg of body weight (BW)/day for 6 weeks], ginger-treated diabetic (0.5 g/kg BW/day for 6 weeks), and ginger plus cinnamon-treated diabetic groups. Forced swim test and elevated plus maze behavioral tests were performed at the end of the experiment. HOMA-IR, HOMA β-cells, blood glucose, insulin, corticosterone, pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and IL-6), and total anti-oxidant capacity (TAC) were assessed in the serum. BDNF mRNA level was assessed in hippocampus using qRT-PCR. Hippocampal histopathological changes were also assessed, and immunoexpression of glial fibrillary acidic protein (GFAP), caspase-3, and Ki-67 was measured.Results: Diabetes-induced depressive-like changes in the STZ group were biochemically confirmed by assessing serum corticosterone level, as well as behaviorally using FST and EPM tests. Diabetes also induced degenerative changes in the hippocampus. Treatment of diabetic rats with ginger, cinnamon, or the combination of these alleviated the degenerative structural changes and significantly up-regulated serum insulin, TAC, hippocampal BDNF mRNA, and hippocampal immunoexpression of ki67, while they significantly reduced serum blood glucose, IL-6, TNF-α, IL1β, as well as hippocampal immunoexpression of GFAP and Caspase-3 compared to the untreated diabetic group. Improvement induced by the combination of ginger and cinnamon was superior to the single administration of either of these.Conclusion:Cinnamomum cassia and Zingiber officinale have synergistic anti-diabetic, antioxidant, anti-inflammatory, antidepressant-like, and neuroprotective effects. The use of a combination of these plants could be beneficial as alternative or complementary supplements in managing DM and decreasing its neuronal and psychiatric complications.

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The effect of ketogenic diets on neurogenesis and apoptosis in the dentate gyrus of the male rat hippocampus

Cited by 7 publications

References 24 publications

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

The Role of Ketogenic Diet in the Treatment of Neurological Diseases

Insulin and liraglutide attenuate brain pathology in diabetic mice by enhancing the Wnt/β‑catenin signaling pathway

Synergistic Anti-inflammatory and Neuroprotective Effects of Cinnamomum cassia and Zingiber officinale Alleviate Diabetes-Induced Hippocampal Changes in Male Albino Rats: Structural and Molecular Evidence

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