scholarly journals Chrono-Nutrition Has Potential in Preventing Age-Related Muscle Loss and Dysfunction

2021 ◽  
Vol 15 ◽  
Author(s):  
Shinya Aoyama ◽  
Yasukazu Nakahata ◽  
Kazuyuki Shinohara
Keyword(s):  
Circadian Clock ◽  
Clock Gene ◽  
Gene Knockout ◽  
Core Body Temperature ◽  
Muscle Growth ◽  
Mutant Mice ◽  
Muscle Loss ◽  
Temperature Disturbance ◽  
Age Related ◽  
Core Body

The mammalian circadian clock systems regulate the day–night variation of several physiological functions such as the sleep/wake cycle and core body temperature. Disturbance in the circadian clock due to shiftwork and chronic jetlag is related to the risk of several disorders such as metabolic syndrome and cancer. Recently, it has been thought that shiftwork increases the risk of sarcopenia which is characterized by age-related decline of muscle mass and its dysfunctions including muscle strength and/or physical performance. First, we summarize the association between circadian rhythm and the occurrence of sarcopenia and discuss its mechanistic insight by focusing on the muscle function and molecular clock gene in knockout or mutant mice. The clock gene knockout or mutant mice showed early aging phenotypes, including low survival rate and muscle loss. It suggests that improvement in the disturbance of the circadian clock plays an important role in the aging process of healthy muscles. Nutritional intake has the potential to augment muscle growth and entrain the peripheral clock. Second, we discuss the potential of chrono-nutrition in preventing aging-related muscle loss and dysfunction. We also focus on the effects of time-restricted feeding (TRF) and the distribution of protein intake across three meals.

scholarly journals Skipping Breakfast for 6 Days Delayed the Circadian Rhythm of the Body Temperature without Altering Clock Gene Expression in Human Leukocytes

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2797 ◽  
Author(s):  
Hitomi Ogata ◽  
Masaki Horie ◽  
Momoko Kayaba ◽  
Yoshiaki Tanaka ◽  
Akira Ando ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Temperature ◽  
Clock Gene ◽  
Core Body Temperature ◽  
The Core ◽  
Clock Gene Expression ◽  
Meal Timing ◽  
Dim Light ◽  
Core Body ◽  
Skipping Breakfast

Breakfast is often described as “the most important meal of the day” and human studies have revealed that post-prandial responses are dependent on meal timing, but little is known of the effects of meal timing per se on human circadian rhythms. We evaluated the effects of skipping breakfast for 6 days on core body temperature, dim light melatonin onset, heart rate variability, and clock gene expression in 10 healthy young men, with a repeated-measures design. Subjects were provided an isocaloric diet three times daily (3M) or two times daily (2M, i.e., breakfast skipping condition) over 6 days. Compared with the 3M condition, the diurnal rhythm of the core body temperature in the 2M condition was delayed by 42.0 ± 16.2 min (p = 0.038). On the other hand, dim light melatonin onset, heart rate variability, and clock gene expression were not affected in the 2M condition. Skipping breakfast for 6 days caused a phase delay in the core body temperature in healthy young men, even though the sleep–wake cycle remained unchanged. Chronic effects of skipping breakfast on circadian rhythms remain to be studied.

scholarly journals Dysregulation of adipose ILC2 underlies thermogenic failure in aging

2020 ◽  
Author(s):  
Emily L. Goldberg ◽  
Irina Shchukina ◽  
Yun-Hee Youm ◽  
Christina D. Camell ◽  
Tamara Dlugos ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Core Body Temperature ◽  
Lymphoid Cells ◽  
Adipose Tissue Inflammation ◽  
Age Related ◽  
Core Body ◽  
Old Mice ◽  
Functional Defects ◽  
Age Related Changes

AbstractAging impairs the integrated immunometabolic responses which have evolved to maintain core body temperature in homeotherms to survive cold-stress, infections, and dietary restriction. Adipose tissue inflammation regulates the thermogenic stress response but how adipose tissue-resident cells instigate thermogenic failure in aged are unknown. Here, we define alterations in the adipose-resident immune system and identify that type 2 innate lymphoid cells (ILC2) are lost in aging. Restoration of ILC2 numbers in aged mice to levels seen in adults through IL-33 supplementation failed to rescue old mice from metabolic impairment and cold-induced lethality. Transcriptomic analyses revealed intrinsic defects in aged ILC2, and adoptive transfer of adult ILC2 are sufficient to protect old mice against cold. Thus, the functional defects in adipose ILC2 during aging drive thermogenic failure.One Sentence SummaryAge-related changes in adipose tissue drive reprogramming of ILC2 that leads to impaired cold tolerance

scholarly journals Age-related changes in core body temperature and activity in triple-transgenic Alzheimer's disease (3xTgAD) mice

2012 ◽  
Vol 6 (1) ◽  
pp. 160-170 ◽  
Author(s):  
E. M. Knight ◽  
T. M. Brown ◽  
S. Gumusgoz ◽  
J. C. M. Smith ◽  
E. J. Waters ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Age Related ◽  
Core Body ◽  
Age Related Changes

γ-Aminobutyric Acid Type A Receptor β2 Subunit Mediates the Hypothermic Effect of Etomidate in Mice

2004 ◽  
Vol 100 (6) ◽  
pp. 1438-1445 ◽  
Author(s):  
Jennifer Cirone ◽  
Thomas W. Rosahl ◽  
David S. Reynolds ◽  
Richard J. Newman ◽  
Gillian F. O'Meara ◽  
...  
Keyword(s):  
Gabaa Receptor ◽  
Core Body Temperature ◽  
Mutant Mice ◽  
Aminobutyric Acid ◽  
Wild Type ◽  
Acid Type ◽  
Hypothermic Response ◽  
Beta 2 ◽  
Core Body ◽  
Receptor Beta

Background The authors have previously described that the gamma-aminobutyric acid type A (GABAA) receptor beta 2N265S mutation results in a knock-in mouse with reduced sensitivity to etomidate. After recovery from etomidate anesthesia, these mice have improved motor performance and less slow wave sleep. Because most clinically used anesthetics produce hypothermia, the effect of this mutation on core body temperature was investigated. Methods The effect of etomidate and propofol on core body temperature were measured using radiotelemetry in freely moving GABAA receptor beta 2N265S mutant mice and wild-type controls. Results beta 2N265S mutant mice have a reduced hypothermic response to anesthetic doses of etomidate compared with wild-type controls and after a transient loss of righting reflex regain normothermia more rapidly compared with wild-type controls. Subanesthetic doses of etomidate produce hypothermia, which was not observed in the mutant mice. Vehicle administration resulted in a stress-induced hyperthermic response in both genotypes. Propofol produced a hypothermic response that was similar in both genotypes. Conclusions The GABAA receptor beta 2 subunit mediates a significant proportion of the hypothermic effects of etomidate. As the beta 2 subunit mediates postrecovery ataxia and sedation, anesthetic agents that do not have in vivo potency at beta 2 subunit-containing receptors offer the potential for surgical anesthesia with improved recovery characteristics.

Abstract P199: Circadian Contributions To Blood Pressure Variation Under Constant Conditions

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Gabrielle F Gloston ◽  
Annie E Ensor ◽  
Samarth Patel ◽  
Rebecca Williams ◽  
Courtney M Peterson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Temperature ◽  
Circadian Clock ◽  
Environmental Changes ◽  
Core Body Temperature ◽  
Circadian System ◽  
External Factors ◽  
Future Research ◽  
Physiological Processes ◽  
Core Body

The circadian clock is an endogenous biological timekeeper that responds to environmental changes and governs various physiological processes over a 24-hour cycle. Blood pressure (BP) variation is thought to be controlled by the circadian clock, but few studies have examined circadian control of BP in humans. Moreover, it is unknown whether nighttime BP dipping is driven by the circadian system or by external factors. We investigated whether the circadian system drives 24-hour rhythms in BP, including nighttime BP dipping, using a 30-hour constant routine (CR) protocol. The CR protocol controls for external factors, allowing circadian rhythms to be isolated and measured, by having participants lie in a semi-recumbent posture in dim light (<10 lux) at a constant temperature, consume isocaloric snacks every 2 hours, and maintain wakefulness. To measure the BP rhythm, ambulatory BP was measured every 30 minutes (SpaceLabs 90227), and to measure the central circadian rhythm, core body temperature was measured every 10 seconds using an ingestible, wireless sensor (HQInc Core Body Temperature Wireless Data Record and Sensor). To date, 17 normotensive African American participants (13 females and 4 males), with a mean age of 37 (± 11.3) years and body mass index (BMI) of 32.5 kg/m 2 , have completed the study. Approximately 59% of participants (10 of 17) had non-dipping systolic BP at screening, defined as a <10% decrease in mean systolic BP from daytime to nighttime. Under constant conditions, 94% of participants (16 of 17) had a non-dipping BP phenotype. Median systolic BP dipping was 0.8% for females and 2.2% for males. There was a robust rhythm in participants’ core body temperature but not BP, suggesting that the circadian clock may not contribute substantially to a nighttime decrease in BP in normotensive African Americans. Instead, the non-dipping BP phenotype is likely more so a result of behavioral and/or physiological sleep-related processes. Future research and interventions for non-dipping BP may need to target these underlying behavioral and physiological processes.

scholarly journals Circadian clock regulation of skeletal muscle growth and repair

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1549 ◽  
Author(s):  
Somik Chatterjee ◽  
Ke Ma
Keyword(s):  
Skeletal Muscle ◽  
Circadian Clock ◽  
Muscle Growth ◽  
Muscle Metabolism ◽  
Muscle Physiology ◽  
Skeletal Muscle Growth ◽  
Age Related ◽  
Evolutionarily Conserved ◽  
Key Aspects ◽  
And Function

Accumulating evidence indicates that the circadian clock, a transcriptional/translational feedback circuit that generates ~24-hour oscillations in behavior and physiology, is a key temporal regulatory mechanism involved in many important aspects of muscle physiology. Given the clock as an evolutionarily-conserved time-keeping mechanism that synchronizes internal physiology to environmental cues, locomotor activities initiated by skeletal muscle enable entrainment to the light-dark cycles on earth, thus ensuring organismal survival and fitness. Despite the current understanding of the role of molecular clock in preventing age-related sarcopenia, investigations into the underlying molecular pathways that transmit clock signals to the maintenance of skeletal muscle growth and function are only emerging. In the current review, the importance of the muscle clock in maintaining muscle mass during development, repair and aging, together with its contribution to muscle metabolism, will be discussed. Based on our current understandings of how tissue-intrinsic muscle clock functions in the key aspects muscle physiology, interventions targeting the myogenic-modulatory activities of the clock circuit may offer new avenues for prevention and treatment of muscular diseases. Studies of mechanisms underlying circadian clock function and regulation in skeletal muscle warrant continued efforts.

scholarly journals Epigenetic regulation of the circadian genePer1in the hippocampus mediates age-related changes in memory and synaptic plasticity

2018 ◽  
Author(s):  
Janine L. Kwapis ◽  
Yasaman Alaghband ◽  
Enikö A. Kramár ◽  
Alberto J. López ◽  
Annie Vogel Ciernia ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Circadian Clock ◽  
Clock Gene ◽  
Memory Performance ◽  
Activity Patterns ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Age Related

AbstractAging is accompanied by impairments in both circadian rhythmicity and long-term memory. Although it is clear that memory performance is affected by circadian cycling, it is unknown whether age-related disruption of the circadian clock causes impaired hippocampal memory. Here, we show that the repressive histone deacetylase HDAC3 restricts long-term memory, synaptic plasticity, and learning-induced expression of the circadian genePer1in the aging hippocampus without affecting rhythmic circadian activity patterns. We also demonstrate that hippocampalPer1is critical for long-term memory formation. Together, our data challenge the traditional idea that alterations in the core circadian clock drive circadian-related changes in memory formation and instead argue for a more autonomous role for circadian clock gene function in hippocampal cells to gate the likelihood of long-term memory formation.

scholarly journals Pregnancy Suppresses the Daily Rhythmicity of Core Body Temperature and Adipose Metabolic Gene Expression in the Mouse

Endocrinology ◽  
2016 ◽  
Vol 157 (9) ◽  
pp. 3320-3331 ◽  
Author(s):  
Michaela D. Wharfe ◽  
Caitlin S. Wyrwoll ◽  
Brendan J. Waddell ◽  
Peter J. Mark
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Clock Gene ◽  
Clock Genes ◽  
Core Body Temperature ◽  
Rhythmic Expression ◽  
Clock Gene Expression ◽  
Metabolic Genes ◽  
Core Body

Maternal adaptations in lipid metabolism are crucial for pregnancy success due to the role of white adipose tissue as an energy store and the dynamic nature of energy needs across gestation. Because lipid metabolism is regulated by the rhythmic expression of clock genes, it was hypothesized that maternal metabolic adaptations involve changes in both adipose clock gene expression and the rhythmic expression of downstream metabolic genes. Maternal core body temperature (Tc) was investigated as a possible mechanism driving pregnancy-induced changes in clock gene expression. Gonadal adipose tissue and plasma were collected from C57BL/6J mice before and on days 6, 10, 14, and 18 of pregnancy (term 19 d) at 4-hour intervals across a 24-hour period. Adipose expression of clock genes and downstream metabolic genes were determined by quantitative RT-PCR, and Tc was measured by intraperitoneal temperature loggers. Adipose clock gene expression showed robust rhythmicity throughout pregnancy, but absolute levels varied substantially across gestation. Rhythmic expression of the metabolic genes Lipe, Pnpla2, and Lpl was clearly evident before pregnancy; however, this rhythmicity was lost with the onset of pregnancy. Tc rhythm was significantly altered by pregnancy, with a 65% decrease in amplitude by term and a 0.61°C decrease in mesor between days 6 and 18. These changes in Tc, however, did not appear to be linked to adipose clock gene expression across pregnancy. Overall, our data show marked adaptations in the adipose clock in pregnancy, with an apparent decoupling of adipose clock and lipolytic/lipogenic gene rhythms from early in gestation.

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