Biochemical effect of a ketogenic diet on the brains of obese adult rats

Mohamed, H. E.; Elswefy, Sahar E; Rashed, Leila A.; Ellatif, Sally K Abd

doi:10.1016/j.jocn.2009.11.005

Cited by 19 publications

(16 citation statements)

References 32 publications

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“…Prior studies have demonstrated that up-regulation of adiponectin suppressed inflammatory mediators (e.g., TNF-α, IL-1, IL-6, and IL-10) and led to weight loss [44], whereas increased leptin expression correlated with a pro-inflammatory action [45]. Additionally, KD-treated obese rats showed increases in adiponectin expression, weight-loss and down-regulation of TNF-α levels [37]. Thus, it appears that a metabolic treatment such as the KD or calorie restriction induces changes in specific hormones that positively modulate neuroinflammation.…”

Section: Discussionmentioning

confidence: 98%

“…Many metabolic substrates [e.g., polyunsaturated fatty acids (PUFAs) and ketones] and hormones [e.g., leptin and adiponectin] [35]–[37] are both elaborated and altered by KD treatment. Interestingly, dietary supplementation with omega-3 PUFAs – which mirrors one important facet of the KD – led to decreased pro-inflammatory and enhanced anti-inflammatory changes in models of MS [38].…”

Section: Discussionmentioning

confidence: 99%

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Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis

et al. 2012

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A prominent clinical symptom in multiple sclerosis (MS), a progressive disorder of the central nervous system (CNS) due to heightened neuro-inflammation, is learning and memory dysfunction. Here, we investigated the effects of a ketogenic diet (KD) on memory impairment and CNS-inflammation in a murine model of experimental autoimmune encephalomyelitis (EAE), using electrophysiological, behavioral, biochemical and in vivo imaging approaches. Behavioral spatial learning deficits were associated with motor disability in EAE mice, and were observed concurrently with brain inflammation. The KD improved motor disability in the EAE model, as well as CA1 hippocampal synaptic plasticity (long-term potentiation) and spatial learning and memory (assessed with the Morris Water Maze). Moreover, hippocampal atrophy and periventricular lesions in EAE mice were reversed in KD-treated EAE mice. Finally, we found that the increased expression of inflammatory cytokines and chemokines, as well as the production of reactive oxygen species (ROS), in our EAE model were both suppressed by the KD. Collectively, our findings indicate that brain inflammation in EAE mice is associated with impaired spatial learning and memory function, and that KD treatment can exert protective effects, likely via attenuation of the robust immune response and increased oxidative stress seen in these animals.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis

et al. 2012

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“…Statistical analysis was performed using SPSS program (version 16; SPSS Inc., Chicago, Illinois, USA) . Student “t” test and the analysis of variance (one way ANOVA) were used for comparison between groups [35] . …”

Section: Methodsmentioning

confidence: 99%

Neuroprotective effect of resveratrol in diabetic cerebral ischemic-reperfused rats through regulation of inflammatory and apoptotic events

Mohamed

Elswefy

Hasan

et al. 2014

Diabetol Metab Syndr

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BackgroundDiabetes and cerebral ischemic-reperfusion are among the most common causes of neurological complications in Egypt. The prevalence of diabetes in Egypt is high and it can be considered as a major clinical and public health problem.MethodsBlood glucose, lipid profile, oxidative stress makers (cerebral MDA & GSH), cerebral interleukin-4 (IL-4) level and cerebral cyclooxygenase-2 (COX-2) gene expression were measured in male albino rats weighing 200 ± 20 g. The rats were divided into five groups, normal control group, diabetic group (diabetes was induced by single dose of streptozotocin [STZ]), diabetic cerebral ischemic-reperfused group, two treated groups (diabetic and diabetic ischemic-reperfused), both groups treated with resveratrol. Histological study was done using H&E, AgNOR and cresyl violet stains. Immunohistochemistry for Bax and COX-2 was done with morphometric study.ResultsDiabetic and diabetic cerebral ischemic- reperfused rats showed significant increase in serum glucose level, serum TAG, serum LDL-C, atherogenic index, cerebral MDA and upregulation of COX-2 gene expression. These groups showed significant decrease in serum HDL, cerebral IL-4 and depletion of cerebral GSH when compared to normal control rats. Treating these groups with resveratrol resulted in significant decrease in serum glucose level, serum TAG, TC, serum LDL-C, atherogenic index, cerebral MDA and downregulation of COX-2 gene expression. The results of COX-2 gene expression were confirmed by COX-2 immunohistochemistry. Also, significant increase in serum HDL, cerebral IL-4 and cerebral GSH contents could be observed in these treated groups as compared to normal control group. Cerebral apoptotic index and optical density of Bax reaction revealed significant increase in diabetic and diabetic cerebral ischemic-reperfused rats while treatment of these groups with resveratrol resulted in significant decrease in cerebral apoptotic index and optical density of Bax reaction. These apoptotic results were confirmed with AgNOR and cresyl violet stains.ConclusionThe results of this research suggest that upregulation of cerebral COX-2 gene along with the decrease in cerebral IL-4 and enhanced cerebral apoptosis is critically involved in cerebral damage associated with diabetes and cerebral ischemic-reperfusion. Resveratrol can ameliorate these effects and has promising neuroprotective effect in diabetic-induced cerebral complications.

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“…Positive effects of KD feeding have been found in models of amyotrophic lateral sclerosis (Zhao et al, 2006), Parkinson’s disease (Cheng et al, 2009; Yang and Cheng, 2010), and Alzheimer’s disease (Van der Auwera et al, 2005; Mohamed et al, 2010). In addition, KD feeding reverses aging-related impairments in brain biochemistry in animals (Studzinski et al, 2008; Balietti et al, 2010).…”

Section: Attenuating Brain Injury and Neurodegenerationmentioning

confidence: 99%

The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

Ruskin¹,

Masino²

2012

Front. Neurosci.

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A link between metabolism and brain function is clear. Since ancient times, epileptic seizures were noted as treatable with fasting, and historical observations of the therapeutic benefits of fasting on epilepsy were confirmed nearly 100 years ago. Shortly thereafter a high fat, low-carbohydrate ketogenic diet (KD) debuted as a therapy to reduce seizures. This strict regimen could mimic the metabolic effects of fasting while allowing adequate caloric intake for ongoing energy demands. Today, KD therapy, which forces predominantly ketone-based rather than glucose-based metabolism, is now well-established as highly successful in reducing seizures. Cellular metabolic dysfunction in the nervous system has been recognized as existing side-by-side with nervous system disorders – although often with much less obvious cause-and-effect as the relationship between fasting and seizures. Rekindled interest in metabolic and dietary therapies for brain disorders complements new insight into their mechanisms and broader implications. Here we describe the emerging relationship between a KD and adenosine as a way to reset brain metabolism and neuronal activity and disrupt a cycle of dysfunction. We also provide an overview of the effects of a KD on cognition and recent data on the effects of a KD on pain, and explore the relative time course quantified among hallmark metabolic changes, altered neuron function and altered animal behavior assessed after diet administration. We predict continued applications of metabolic therapies in treating dysfunction including and beyond the nervous system.

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Biochemical effect of a ketogenic diet on the brains of obese adult rats

Cited by 19 publications

References 32 publications

Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis

Inflammation-Mediated Memory Dysfunction and Effects of a Ketogenic Diet in a Murine Model of Multiple Sclerosis

Neuroprotective effect of resveratrol in diabetic cerebral ischemic-reperfused rats through regulation of inflammatory and apoptotic events

The Nervous System and Metabolic Dysregulation: Emerging Evidence Converges on Ketogenic Diet Therapy

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