Time‐restricted feeding alleviates cardiac dysfunction induced by simulated microgravity via restoring cardiac FGF21 signaling

Wang, Xinpei; Xing, Changyang; Zhang, Jiaxin; Zhou, Jiaheng; Li, Yunchu; Yang, Hongyan; Zhang, Peng-Fei; Zhang, Wei; Huang, Yin; Jiang, Long; Gao, Feng; Xing, Zhen; Li, Jia

doi:10.1096/fj.202001246rr

Cited by 15 publications

(12 citation statements)

References 65 publications

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“…Transthoracic echocardiography was performed using a VisualSonics Vevo 2100 high-resolution in vivo imaging system (VisualSonics Inc., Toronto, Canada) as described previously [ 21 ]. Mice were anesthetized by isoflurane (1%) with maintenance of stable heart rate and body temperature.…”

Section: Methodsmentioning

confidence: 99%

Alternate-Day Ketogenic Diet Feeding Protects against Heart Failure through Preservation of Ketogenesis in the Liver

Guo¹,

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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As heart failure develops, the heart utilizes ketone bodies at increased rates, indicating an adaptive stress response. Thus, increasing ketone body availability exerts protective effects against heart failure. However, although it is the widely used approach for increasing ketone body availability, the ketogenic diet shows limited cardioprotective effects against heart failure. This study was aimed at examining the effects of the ketogenic diet on heart failure and the underlying mechanisms. Pressure overload-induced heart failure was established by transverse aortic constriction (TAC) in mice. Continuous ketogenic diet feeding for 8 weeks failed to protect the heart against heart failure. It showed no significant effects on cardiac systolic function and fibrosis but aggravated cardiac diastolic function in TAC mice. Specifically, it induced systemic lipid metabolic disorder and hepatic dysfunction in TAC mice. It decreased the content of 3-hydroxy-3-methylglutaryl-CoA lyase (HMGCL), a key enzyme in ketogenesis, and impaired the capacity of hepatic ketogenesis in TAC mice. It preserved the capacity of hepatic ketogenesis and exerted cardioprotective effects against heart failure, increasing cardiac function and decreasing cardiac fibrosis, in liver-specific HMGCL-overexpressed TAC mice. Importantly, we found that alternate-day ketogenic diet feeding did not impair the capacity of hepatic ketogenesis and exerted potent cardioprotective effects against heart failure. These results suggested that alternate-day but not continuous ketogenic diet protects against heart failure through preservation of ketogenesis in the liver.

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Section: Methodsmentioning

confidence: 99%

Alternate-Day Ketogenic Diet Feeding Protects against Heart Failure through Preservation of Ketogenesis in the Liver

Guo¹,

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…The combination of dietary defenses and endogenous antioxidants production, seems to play a significant protective role against oxidative damages (Gao and Chilibeck, 2020). Protection from cardiovascular problems may be obtained with low-glycemic index diets because bed rest reportedly induces glucose intolerance (Wang X. P. et al, 2020). As regards to bone damages, particular attention was paid to vitamin D3.…”

Section: Nutrients To Counteract Spaceflight Damagesmentioning

confidence: 99%

Spaceflight Induced Disorders: Potential Nutritional Countermeasures

Costa

Ambesi-Impiombato

Beccari

et al. 2021

Front. Bioeng. Biotechnol.

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Space travel is an extreme experience even for the astronaut who has received extensive basic training in various fields, from aeronautics to engineering, from medicine to physics and biology. Microgravity puts a strain on members of space crews, both physically and mentally: short-term or long-term travel in orbit the International Space Station may have serious repercussions on the human body, which may undergo physiological changes affecting almost all organs and systems, particularly at the muscular, cardiovascular and bone compartments. This review aims to highlight recent studies describing damages of human body induced by the space environment for microgravity, and radiation. All novel conditions, to ally unknown to the Darwinian selection strategies on Earth, to which we should add the psychological stress that astronauts suffer due to the inevitable forced cohabitation in claustrophobic environments, the deprivation from their affections and the need to adapt to a new lifestyle with molecular changes due to the confinement. In this context, significant nutritional deficiencies with consequent molecular mechanism changes in the cells that induce to the onset of physiological and cognitive impairment have been considered.

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“…In contrast, spaceflight for one week did not affect cardiac mass [13], although it is possible that this period is too short to cause demonstrable cardiac atrophy. Hindlimb unloading (HU), a ground-based rodent model for simulating weightlessness, is reported to cause cardiac atrophy in some studies [14,15], but not in others [13], thus further work in this area is needed.…”

Section: Introductionmentioning

confidence: 99%

Spaceflight Modulates the Expression of Key Oxidative Stress and Cell Cycle Related Genes in Heart

Kumar

Tahimic

Almeida

et al. 2021

IJMS

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Spaceflight causes cardiovascular changes due to microgravity-induced redistribution of body fluids and musculoskeletal unloading. Cardiac deconditioning and atrophy on Earth are associated with altered Trp53 and oxidative stress-related pathways, but the effects of spaceflight on cardiac changes at the molecular level are less understood. We tested the hypothesis that spaceflight alters the expression of key genes related to stress response pathways, which may contribute to cardiovascular deconditioning during extended spaceflight. Mice were exposed to spaceflight for 15 days or maintained on Earth (ground control). Ventricle tissue was harvested starting ~3 h post-landing. We measured expression of select genes implicated in oxidative stress pathways and Trp53 signaling by quantitative PCR. Cardiac expression levels of 37 of 168 genes tested were altered after spaceflight. Spaceflight downregulated transcription factor, Nfe2l2 (Nrf2), upregulated Nox1 and downregulated Ptgs2, suggesting a persistent increase in oxidative stress-related target genes. Spaceflight also substantially upregulated Cdkn1a (p21) and cell cycle/apoptosis-related gene Myc, and downregulated the inflammatory response gene Tnf. There were no changes in apoptosis-related genes such as Trp53. Spaceflight altered the expression of genes regulating redox balance, cell cycle and senescence in cardiac tissue of mice. Thus, spaceflight may contribute to cardiac dysfunction due to oxidative stress.

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Time‐restricted feeding alleviates cardiac dysfunction induced by simulated microgravity via restoring cardiac FGF21 signaling

Cited by 15 publications

References 65 publications

Alternate-Day Ketogenic Diet Feeding Protects against Heart Failure through Preservation of Ketogenesis in the Liver

Alternate-Day Ketogenic Diet Feeding Protects against Heart Failure through Preservation of Ketogenesis in the Liver

Spaceflight Induced Disorders: Potential Nutritional Countermeasures

Spaceflight Modulates the Expression of Key Oxidative Stress and Cell Cycle Related Genes in Heart

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