scholarly journals Lateralization of the central circadian pacemaker output: a test of neural control of peripheral oscillator phase

2010 ◽  
Vol 299 (3) ◽  
pp. R751-R761 ◽  
Author(s):  
Carrie E. Mahoney ◽  
Daniel Brewer ◽  
Mary K. Costello ◽  
Judy McKinley Brewer ◽  
Eric L. Bittman
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Adrenal Medulla ◽  
Neural Control ◽  
Clock Gene ◽  
Neural Pathways ◽  
Peripheral Organs ◽  
Peripheral Oscillators ◽  
Clock Gene Expression ◽  
Oscillator Phase

To evaluate the contribution of neural pathways to the determination of the circadian oscillator phase in peripheral organs, we assessed lateralization of clock gene expression in Syrian hamsters induced to split rhythms of locomotor activity by exposure to constant light. We measured the ratio of haPer1, haPer2, and haBmal1 mRNA on the high vs. low (H/L) side at 3-h intervals prior to the predicted activity onset (pAO). We also calculated expression on the sides ipsilateral vs. contralateral (I/C) to the side of the suprachiasmatic nucleus (SCN) expressing higher haPer1. The extent of asymmetry in split hamsters varied between specific genes, phases, and organs. Although the magnitude of asymmetry in peripheral organs was never as great as that in the SCN, we observed significantly greater lateralization of clock gene expression in the adrenal medulla and cortex, lung, and skeletal muscle, but not in liver or kidney, of split hamsters than of unsplit controls. We observed fivefold lateralization of expression of the clock-controlled gene, albumin site D-element binding protein ( Dbp), in skeletal muscle (H/L: 10.7 ± 3.7 at 3 h vs. 2.2 ± 0.3 at 0 h pAO; P = 0.03). Furthermore, tyrosine hydroxylase expression was asymmetrical in the adrenal medulla of split (H/L: 1.9 ± 0.5 at 0 h) vs. unsplit hamsters (1.2 ± 0.04; P < 0.05). Consistent with a model of neurally controlled gene expression, we found significant correlations between the phase angle between morning and evening components (ψme) and the level of asymmetry (H/L or I/C). Our results indicate that neural pathways contribute to, but cannot completely account for, SCN regulation of the phase of peripheral oscillators.

Hormonal regulation of core clock gene expression in skeletal muscle following acute aerobic exercise

2019 ◽  
Vol 508 (3) ◽  
pp. 871-876 ◽  
Author(s):  
Patrick G. Saracino ◽  
Michael L. Rossetti ◽  
Jennifer L. Steiner ◽  
Bradley S. Gordon
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Hormonal Regulation ◽  
Clock Gene ◽  
Clock Gene Expression ◽  
Core Clock Gene

scholarly journals Effects of Nocturnal Light on (Clock) Gene Expression in Peripheral Organs: A Role for the Autonomic Innervation of the Liver

PLoS ONE ◽  
2009 ◽  
Vol 4 (5) ◽  
pp. e5650 ◽  
Author(s):  
Cathy Cailotto ◽  
Jun Lei ◽  
Jan van der Vliet ◽  
Caroline van Heijningen ◽  
Corbert G. van Eden ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Autonomic Innervation ◽  
Peripheral Organs ◽  
Clock Gene Expression

scholarly journals Influence of obesity, weight loss, and free fatty acids on skeletal muscle clock gene expression

2020 ◽  
Vol 318 (1) ◽  
pp. E1-E10 ◽  
Author(s):  
Laura Sardon Puig ◽  
Nicolas J. Pillon ◽  
Erik Näslund ◽  
Anna Krook ◽  
Juleen R. Zierath
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Weight Loss ◽  
Circadian Clock ◽  
Clock Gene ◽  
Clock Genes ◽  
Expression Profiles ◽  
Normal Weight ◽  
Nonesterified Fatty Acid ◽  
Clock Gene Expression

The molecular circadian clock plays a role in metabolic homeostasis. We tested the hypothesis obesity and systemic factors associated with insulin resistance affect skeletal muscle clock gene expression. We determined clock gene expression in skeletal muscle of obese women ( n = 5) and men ( n = 18) before and 6 mo after Roux-en-Y gastric bypass (RYGB) surgery and normal-weight controls (women n = 6, men n = 8). Skeletal muscle clock gene expression was affected by obesity and weight loss. CRY1 mRNA ( P = 0.05) was increased and DBP mRNA ( P < 0.05) was decreased in obese vs. normal weight women and restored to control levels after RYGB-induced weight loss. CLOCK, CRY1, CRY2, and DBP mRNA ( P < 0.05) was decreased in obese men compared with normal weight men. Expression of all other clock genes was unaltered by obesity or weight loss in both cohorts. We correlated clock gene expression with clinical characteristics of the participants. Among the genes studied, DBP and PER3 expression was inversely correlated with plasma lipids in both cohorts. Circadian time-course studies revealed that core clock genes oscillate over time ( P < 0.05), with BMAL1, CIART, CRY2, DBP, PER1, and PER3 expression profiles altered by palmitate treatment. In conclusion, skeletal muscle clock gene expression and function is altered by obesity, coincident with changes in plasma lipid levels. Palmitate exposure disrupts clock gene expression in myotubes, indicating that dyslipidemia directly alters the circadian program. Strategies to reduce lipid overload and prevent elevations in nonesterified fatty acid and cholesterol levels may sustain circadian clock signals in skeletal muscle.

Metabolic homeostasis in mice with disrupted Clock gene expression in peripheral tissues

2007 ◽  
Vol 293 (4) ◽  
pp. R1528-R1537 ◽  
Author(s):  
David J. Kennaway ◽  
Julie A. Owens ◽  
Athena Voultsios ◽  
Michael J. Boden ◽  
Tamara J. Varcoe
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Circadian Rhythms ◽  
Glucose Tolerance ◽  
Gene Disruption ◽  
Plasma Insulin ◽  
Clock Gene ◽  
Metabolic Homeostasis ◽  
Peripheral Tissues ◽  
Clock Gene Expression

The role of peripheral vs. central circadian rhythms and Clock in the maintenance of metabolic homeostasis and with aging was examined by using ClockΔ19 +MEL mice. These have preserved suprachiasmatic nucleus and pineal gland rhythmicity but arrhythmic Clock gene expression in the liver and skeletal muscle. ClockΔ19 +MEL mice showed fasting hypoglycemia in young-adult males, fasting hyperglycemia in older females, and substantially impaired glucose tolerance overall. ClockΔ19 +MEL mice had substantially reduced plasma insulin and plasma insulin/glucose nocturnally in males and during a glucose tolerance test in females, suggesting impaired insulin secretion. ClockΔ19 +MEL mice had reduced hepatic expression and loss of rhythmicity of gck, pfkfb3, and pepck mRNA, which is likely to impair glycolysis and gluconeogenesis. ClockΔ19 +MEL mice also had reduced glut4 mRNA in skeletal muscle, and this may contribute to poor glucose tolerance. Whole body insulin tolerance was enhanced in ClockΔ19 +MEL mice, however, suggesting enhanced insulin sensitivity. These responses occurred although the ClockΔ19 mutation did not cause obesity and reduced plasma free fatty acids while increasing plasma adiponectin. These studies on clock-gene disruption in peripheral tissues and metabolic homeostasis provide compelling evidence of a relationship between circadian rhythms and the glucose/insulin and adipoinsular axes. It is, however, premature to declare that clock-gene disruption causes the full metabolic syndrome.

Role of non-neural signals in regulation of circadian rhythms of core clock gene expression in mouse peripheral organs

2006 ◽  
Vol 27 (1) ◽  
pp. 18-19
Author(s):  
Eric L. Bittman ◽  
Anastasia Nikiforov ◽  
Ruth Harris ◽  
Judy McKinley Brewer
Keyword(s):  
Gene Expression ◽  
Circadian Rhythms ◽  
Clock Gene ◽  
Neural Signals ◽  
Peripheral Organs ◽  
Clock Gene Expression ◽  
Core Clock Gene

scholarly journals Time of Day Dependent Effects of Contractile Activity on the Phase of the Skeletal Muscle Clock

2020 ◽  
Author(s):  
Denise Kemler ◽  
Christopher A. Wolff ◽  
Karyn A. Esser
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Circadian Clock ◽  
Clock Gene ◽  
Treadmill Exercise ◽  
Contractile Activity ◽  
Phase Changes ◽  
Phase Advance ◽  
Clock Gene Expression ◽  
Core Clock Gene

ABSTRACTExercise has been proposed to be a zeitgeber for the muscle circadian clock mechanism. However, this is not well defined and it is unknown if exercise timing induces directional shifts of the muscle clock. Our purpose herein was to assess the effect of one bout of treadmill exercise on skeletal muscle clock phase changes. We subjected PERIOD2::LUCIFERASE mice (n=30F) to one 60-minute treadmill exercise bout at three times of day. Exercise at ZT5, 5h after lights on, induced a phase advance (1.4±0.53h; p=0.038), whereas exercise at ZT11, 1h before lights off, induced a phase delay (−0.95±0.43h; p=0.0315). Exercise at ZT17, middle of the dark phase, did not alter muscle clock phase. Exercise induces diverse systemic changes so we developed an in-vitro model system to examine effects of contractile activity on muscle clock phase. Contractions applied at peak or trough Bmal1 expression induced significant phase delays (applied at peak: 1.3±0.02h; p=0.0425; applied at trough: 1.8±0.02h, p=0.0074). Contractions applied during the transition from peak to trough Bmal1 expression induced a phase advance (1.8±0.03h; p=0.0265). Lastly, contractions at different times of day resulted in differential changes of core-clock gene expression demonstrating an exercise and clock interaction, providing insight into potential mechanisms exercise-induced phase shifts. These data demonstrate that muscle contractions, as part of exercise, are sufficient to shift muscle circadian clock phase, likely through changes in core-clock gene expression. Additionally, our findings that exercise induces directional muscle clock phase changes confirms exercise is a bone fide environmental time cue for skeletal muscle.

Daily rhythm and regulation of clock gene expression in the rat pineal gland

2004 ◽  
Vol 120 (2) ◽  
pp. 164-172 ◽  
Author(s):  
V Simonneaux ◽  
V.-J Poirel ◽  
M.-L Garidou ◽  
D Nguyen ◽  
E Diaz-Rodriguez ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pineal Gland ◽  
Clock Gene ◽  
Daily Rhythm ◽  
Clock Gene Expression ◽  
Rat Pineal Gland

A genetic CLOCK variant associated with cluster headache causing increased mRNA levels

Cephalalgia ◽  
2017 ◽  
Vol 38 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Carmen Fourier ◽  
Caroline Ran ◽  
Margret Zinnegger ◽  
Anne-Sofie Johansson ◽  
Christina Sjöstrand ◽  
...  
Keyword(s):  
Gene Expression ◽  
Circadian Rhythm ◽  
Cluster Headache ◽  
Clock Gene ◽  
Control Sample ◽  
Mrna Levels ◽  
Nucleotide Polymorphisms ◽  
Primary Fibroblast ◽  
Clock Gene Expression ◽  
Diurnal Preference

Background Cluster headache is characterized by recurrent unilateral headache attacks of severe intensity. One of the main features in a majority of patients is a striking rhythmicity of attacks. The CLOCK ( Circadian Locomotor Output Cycles Kaput) gene encodes a transcription factor that serves as a basic driving force for circadian rhythm in humans and is therefore particularly interesting as a candidate gene for cluster headache. Methods We performed an association study on a large Swedish cluster headache case-control sample (449 patients and 677 controls) screening for three single nucleotide polymorphisms (SNPs) in the CLOCK gene implicated in diurnal preference (rs1801260) or sleep duration (rs11932595 and rs12649507), respectively. We further wanted to investigate the effect of identified associated SNPs on CLOCK gene expression. Results We found a significant association with rs12649507 and cluster headache ( p = 0.0069) and this data was strengthened when stratifying for reported diurnal rhythmicity of attacks ( p = 0.0009). We investigated the effect of rs12649507 on CLOCK gene expression in human primary fibroblast cultures and identified a significant increase in CLOCK mRNA expression ( p = 0.0232). Conclusions Our results strengthen the hypothesis of the involvement of circadian rhythm in cluster headache.

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