Differential Fasting Plasma Glucose and Ketone Body Levels in GHRKO versus 3xTg-AD Mice: A Potential Contributor to Aging-Related Cognitive Status?

Griffith, Chelsea M.; Macklin, Lauren N; Bartke, Andrzej; Patrylo, Peter R.

doi:10.1155/2017/9684061

Cited by 3 publications

(3 citation statements)

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“…This supports past ndings showing an elevation in SIRT1 levels 1 day prior to ischemia that gradually decreased over a period of 7 days(46). Our study's results align with prior studies of intermittent fasting and caloric restriction for 30 days post-injury( 41) and with research involving KD and SIRT1 in health-enhancing, aging, longevity, and neurodegeneration in animal models (33,34).…”

Section: Discussionsupporting

confidence: 88%

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Ketogenic Diet as a Potential Treatment for Traumatic Brain Injury in Mice

Har-Even

Rubovitch

Ratliff

et al. 2021

Preprint

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Background: Traumatic brain injury (TBI) is a brain dysfunction without present treatment. Previous studies have shown that animals fed a ketogenic diet (KD) perform better in learning tasks than those fed a standard diet (SD) following brain injury. The goal of this study was to examine whether KD is neuroprotective in a TBI mouse model. Methods: We utilized a closed head injury model to induce mild TBI (mTBI) in mice. Mice were fed KD or SD starting immediately following the trauma and throughout the following 30 days. Tail blood ketone bodies levels were checked at 0, 3, 7 and 30 days post injury. Behavioral tests took place at 7 and 30days post injury, visual and spatial memory impairments were assessed using the Novel object recognition (NOR) paradigm and the Y-maze test, respectively, and anxiety-like behavior was assessed using the elevated plus maze test. Primary mouse SIRT1 levels antibodies were used to detect changes in protein levels following TBI induction and treatments 7 and 30 days post injury and Immunohistochemical sections were stained with, NeuN (for mature neurons), Iba-1 (for microglia) and GFAP (for astrocyte). Results: Elevated levels of ketone bodies were confirmed in the blood following KD. Cognitive and behavioral performance was assessed post injury and molecular and cellular changes were assessed within the temporal cortex and hippocampus. Y‑maze and NOR tasks indicated that mTBI mice maintained on KD displayed better cognitive abilities than mTBI mice maintained on SD. Mice maintained on SD post-injury demonstrated SIRT1 reduction when compared with uninjured and KD groups. In addition, KD management attenuated mTBI-induced microglia activation and astrocyte reactivity in the dentate gyrus and decreased degeneration of neurons in the dentate gyrus and in the cortex. Conclusion: These results support accumulating evidence that KD may be an effective approach to increase the brain’s resistance to damage and suggest a potential new therapeutic strategy for treating mTBI.

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Section: Discussionsupporting

confidence: 88%

“…Ketone bodies in the blood were measured using the Precision Xtra Blood Glucose and Ketone Monitoring System (Abbott, Columbus, OH) (34). Mice were anesthetized with iso urane and tails were cut approximately 0.2mm from the end, a drop of blood was squeezed directly into a testing strip attached to the measuring instrument.…”

Section: Measurement Of Ketone Bodiesmentioning

confidence: 99%

Ketogenic Diet as a Potential Treatment for Traumatic Brain Injury in Mice

Har-Even

Rubovitch

Ratliff

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Ketone bodies in the blood were measured using the Precision Xtra Blood Glucose and Ketone Monitoring System (Abbott, Columbus, OH) 60 . Mice were anesthetized with isoflurane and tails were cut approximately 0.2 mm from the end, a drop of blood was squeezed directly into a testing strip attached to the measuring instrument.…”

Section: Methodsmentioning

confidence: 99%

Ketogenic Diet as a potential treatment for traumatic brain injury in mice

Har-Even

Rubovitch

Ratliff

et al. 2021

Sci Rep

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Traumatic brain injury (TBI) is a brain dysfunction without present treatment. Previous studies have shown that animals fed ketogenic diet (KD) perform better in learning tasks than those fed standard diet (SD) following brain injury. The goal of this study was to examine whether KD is a neuroprotective in TBI mouse model. We utilized a closed head injury model to induce TBI in mice, followed by up to 30 days of KD/SD. Elevated levels of ketone bodies were confirmed in the blood following KD. Cognitive and behavioral performance was assessed post injury and molecular and cellular changes were assessed within the temporal cortex and hippocampus. Y-maze and Novel Object Recognition tasks indicated that mTBI mice maintained on KD displayed better cognitive abilities than mTBI mice maintained on SD. Mice maintained on SD post-injury demonstrated SIRT1 reduction when compared with uninjured and KD groups. In addition, KD management attenuated mTBI-induced astrocyte reactivity in the dentate gyrus and decreased degeneration of neurons in the dentate gyrus and in the cortex. These results support accumulating evidence that KD may be an effective approach to increase the brain’s resistance to damage and suggest a potential new therapeutic strategy for treating TBI.

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