Ketogenic diet delays the phase of circadian rhythms and does not affect AMP-activated protein kinase (AMPK) in mouse liver

Genzer, Yoni; Dadon, Maayan; Burg, Chen; Chapnik, Nava; Froy, Oren

doi:10.1016/j.mce.2015.09.012

Cited by 28 publications

(22 citation statements)

References 39 publications

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“…The pathway Z scores, indicating the relative degree of activation (positive Z score) or inhibition (negative Z score) of the total of 17 coherently-regulated pathways are represented in Figure 8B. Corroborating our multiple observations of an aberrant aging process in the GIT2KO mice we found consistent and significant GIT2KO-specific alterations in aging-related pathways linked to clock gene disruption: ‘ Mitochondrial dysfunction’ [90]; ‘ AMPK Signaling’ [91]; ‘ P2Y Purinergic Receptor Signaling pathway’ [92]; ‘ P70S6K Signaling’ [93]; ‘ Telomerase Signaling pathway’ [94]; ‘ Superpathway of Cholesterol Biosynthesis’ [95]; ‘ PI3K/AKT Signaling pathway’ [96]. In the context of these multiple interconnected pathways there are also a group of inter-related pathways linking immune cell function (‘ PKCθ Signaling in T Lymphocytes’ , ‘ CD28 Signaling in T Helper Cells’ , ‘ iCOS-iCOSL Signaling in T Helper Cells ’) with Ephrin receptor signaling and clathrin-mediated endocytic subcellular trafficking [97].…”

Section: Resultssupporting

confidence: 59%

“…Nearly all of the coherent and commonly-controlled signaling pathways were strongly linked to cellular clock control mechanisms, e.g. ‘ Mitochondrial Dysfunction’ [90], ‘ AMPK Signaling’ [91], ‘ P70S6K Signaling’ [93], ‘Telomerase Signaling ’ [94], ‘ Superpathway of Cholesterol Biosynthesis’ [95] and ‘ PI3K/AKT Signaling’ [96]. Additional GIT2KO multi-immune tissue signaling pathways also demonstrated multiple functional data corpi links as ‘ P2Y Purinergic Receptor Signaling’ has been shown to strongly control the AMPK signaling pathway [92].…”

Section: Discussionmentioning

confidence: 99%

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Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption

Siddiqui

Lustig²,

Carter³

et al. 2017

Aging

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Recent research has proposed that GIT2 (G protein-coupled receptor kinase interacting protein 2) acts as an integrator of the aging process through regulation of ‘neurometabolic’ integrity. One of the commonly accepted hallmarks of the aging process is thymic involution. At a relatively young age, 12 months old, GIT2−/− mice present a prematurely distorted thymic structure and dysfunction compared to age-matched 12 month-old wild-type control (C57BL/6) mice. Disruption of thymic structure in GIT2−/− (GIT2KO) mice was associated with a significant reduction in the expression of the cortical thymic marker, Troma-I (cytokeratin 8). Double positive (CD4+CD8+) and single positive CD4+ T cells were also markedly reduced in 12 month-old GIT2KO mice compared to age-matched control wild-type mice. Coincident with this premature thymic disruption in GIT2KO mice was the unique generation of a novel cervical ‘organ’, i.e. ‘parathymic lobes’. These novel organs did not exhibit classical peripheral lymph node-like characteristics but expressed high levels of T cell progenitors that were reflexively reduced in GIT2KO thymi. Using signaling pathway analysis of GIT2KO thymus and parathymic lobe transcriptomic data we found that the molecular signaling functions lost in the dysfunctional GIT2KO thymus were selectively reinstated in the novel parathymic lobe – suggestive of a compensatory effect for the premature thymic disruption. Broader inspection of high-dimensionality transcriptomic data from GIT2KO lymph nodes, spleen, thymus and parathymic lobes revealed a systemic alteration of multiple proteins (Dbp, Tef, Per1, Per2, Fbxl3, Ddit4, Sin3a) involved in the multidimensional control of cell cycle clock regulation, cell senescence, cellular metabolism and DNA damage. Altered cell clock regulation across both immune and non-immune tissues therefore may be responsible for the premature ‘aging’ phenotype of GIT2KO mice.

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Section: Resultssupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption

Siddiqui

Lustig²,

Carter³

et al. 2017

Aging

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“…Enhancing SIRT1 function has further demonstrated its utility in restoring circadian rhythms in conditions where SIRT1 expression is diminished, such as aging . A prior study showed that KD can rescue entrainment of diurnal rest‐activity patterns in Kcna1 ‐null mice, although the role of SIRT1 has not been directly investigated . Enhancement of SIRT1 activity may constitute part of the therapeutic effectiveness of KD, complementing its antiseizure effects by assisting recovery of normal circadian rhythms.…”

Section: Discussionmentioning

confidence: 99%

Altered circadian rhythms and oscillation of clock genes and sirtuin 1 in a model of sudden unexpected death in epilepsy

et al. 2018

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Attenuated oscillation of several core clock genes correlates with, and may underlie, aberrant diurnal and circadian rest-activity and sleep-wake patterns observed in Kcna1-null mice. This could contribute to late complications in epilepsy, such as sudden unexpected death in epilepsy. Sirt1 may represent a useful therapeutic target for rescuing circadian clock gene rhythmicity and sleep patterns in epilepsy.

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“…Hypoglycemia induces the release of adrenalin and alters circulating insulin levels, both of which modulate the phase of peripheral clock gene rhythms (Terazono et al, 2003). Inducing hyperglycemia without increasing body mass -by feeding mice a diet with a very high fat content -was shown to delay the clock in peripheral tissues and to phase-delay rest-activity rhythms (Genzer et al, 2015;Honma et al, 2016). Furthermore, recently it was reported that liver-derived ketone bodies (resulting from conversion of endogenous fat reserves to supply energy) play an important role in the rhythmicity of food anticipation (see Glossary; Chavan et al, 2016).…”

Section: Homeostatic Feedback On Peripheral Circadian Phasementioning

confidence: 99%

The flexible clock: predictive and reactive homeostasis, energy balance and the circadian regulation of sleep–wake timing

Riede

Vinne

Hut

2017

Journal of Experimental Biology

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The Darwinian fitness of mammals living in a rhythmic environment depends on endogenous daily (circadian) rhythms in behavior and physiology. Here, we discuss the mechanisms underlying the circadian regulation of physiology and behavior in mammals. We also review recent efforts to understand circadian flexibility, such as how the phase of activity and rest is altered depending on the encountered environment. We explain why shifting activity to the day is an adaptive strategy to cope with energetic challenges and show how this can reduce thermoregulatory costs. A framework is provided to make predictions about the optimal timing of activity and rest of non-model species for a wide range of habitats. This Review illustrates how the timing of daily rhythms is reciprocally linked to energy homeostasis, and it highlights the importance of this link in understanding daily rhythms in physiology and behavior.

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Ketogenic diet delays the phase of circadian rhythms and does not affect AMP-activated protein kinase (AMPK) in mouse liver

Cited by 28 publications

References 39 publications

Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption

Genomic deletion of GIT2 induces a premature age-related thymic dysfunction and systemic immune system disruption

Altered circadian rhythms and oscillation of clock genes and sirtuin 1 in a model of sudden unexpected death in epilepsy

The flexible clock: predictive and reactive homeostasis, energy balance and the circadian regulation of sleep–wake timing

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