Clock regulation of dietary lipid absorption

Hussain, M. Mahmood; Pan, Xiaoyue

doi:10.1097/mco.0b013e3283548629

Cited by 26 publications

(16 citation statements)

References 25 publications

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“…Rhythmic triglyceride content was shown to be increased in Clock mutant mice via decreased interaction of Clock with small heterodimer partner ( Shp ), a nuclear receptor that represses Cyp7a1 gene expression, which resulted in sustained microsomal triglyceride transfer protein expression. 31 , 32 Liver gene expression of both Shp and microsomal triglyceride transfer protein were reduced after sleep disruption (data not shown), indicating differential gene expression changes in response to distinct types of circadian disruption (genetic or behavioral). Interestingly, Shp − / − mice are protected against fatty liver disease, and knockdown of the clock gene neuronal PAS domain protein 2 ( Npas2 ) reversed this phenotype and resulted in steatosis.…”

Section: Discussionmentioning

confidence: 94%

Short-Term Circadian Disruption Impairs Bile Acid and Lipid Homeostasis in Mice

Ferrell

Chiang

2015

Cellular and Molecular Gastroenterology and Hepatology

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Background & AimsBile acids are physiologic detergents that also activate nuclear receptors to regulate glucose and lipid homeostasis. Cholesterol 7α-hydroxylase (Cyp7a1), the rate-limiting enzyme that converts cholesterol to bile acids, is transcriptionally regulated by bile acids and circadian rhythms. Fasting, nutrients, and the circadian clock critically control hepatic bile acid and lipid homeostasis, and circadian misalignment is associated with the metabolic syndrome in humans. To delineate these interactions, we employed a sleep disruption model to induce circadian disruption and examined hepatic metabolism with respect to bile acids, lipids, and clock gene expression.MethodsB6xC57 mice were maintained on chow or Western diet and were sleep disrupted for 6 hours/day for 5 days. Mice were sacrificed at 4-hour intervals over 24 hours. Hepatic metabolic genes were examined, and bile acid pool and lipid profiles were measured over 24 hours.ResultsSleep disruption significantly suppressed circadian expression of core clock genes, genes involved in lipid metabolism, and key regulators of Cyp7a1 as well as Cyp7a1 expression itself. Sleep disruption abolished the peak in serum cholesterol and increased liver and serum free fatty acids. Bile acid pool size was increased while liver bile acids were decreased. Chromatin immunoprecipitation assay revealed that hepatocyte nuclear factor 4α (HNF4α) and D-site binding protein (Dbp) occupancies were suppressed at the Cyp7a1 promoter in sleep-disrupted mice. When coupled with Western diet, sleep disruption abolished liver clock rhythms and elevated free fatty acids.ConclusionsEven short-term circadian disruption dramatically alters hepatic clock gene expression, bile acid metabolism, and lipid homeostasis to contribute to dyslipidemia.

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Section: Discussionmentioning

confidence: 94%

Short-Term Circadian Disruption Impairs Bile Acid and Lipid Homeostasis in Mice

Ferrell

Chiang

2015

Cellular and Molecular Gastroenterology and Hepatology

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“…Night shift work is associated with both sleep deprivation and disrupted melatonin production (Burch JB et al, 2005) [40] and melatonin plays a key role in the circadian rhythms [41] . Two proteins involved in circadian regulation, CLOCK (which stands for circadian locomotor output cycles kaput) and nocturnin, play an important role in the regulation of dietary lipid absorption [42] . CLOCK plays a role in turning off the genes involved in lipid absorption at the onset of the day, and CLOCK deficiency increases lipid absorption.…”

Section: Discussionmentioning

confidence: 99%

Separate and Joint Associations of Shift Work and Sleep Quality with Lipids

Charles

Tinney-Zara

et al. 2016

Safety and Health at Work

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BackgroundShift work and/or sleep quality may affect health. We investigated whether shift work and sleep quality, separately and jointly, were associated with abnormal levels of triglycerides, total cholesterol (TC), and low-and high-density lipoprotein cholesterol in 360 police officers (27.5% women).MethodsTriglycerides, TC, and high-density lipoprotein were analyzed on the Abbott Architect; low-density lipoprotein was calculated. Shift work was assessed using City of Buffalo payroll work history records. Sleep quality (good, ≤ 5; intermediate, 6–8; poor, ≥ 9) was assessed using the Pittsburgh Sleep Quality Index questionnaire. A shift work + sleep quality variable was created: day plus good sleep; day plus poor sleep; afternoon/night plus good; and poor sleep quality. Mean values of lipid biomarkers were compared across categories of the exposures using analysis of variance/analysis of covariance.ResultsShift work was not significantly associated with lipids. However, as sleep quality worsened, mean levels of triglycerides and TC gradually increased but only among female officers (age- and race-adjusted p = 0.013 and 0.030, respectively). Age significantly modified the association between sleep quality and TC. Among officers ≥ 40 years old, those reporting poor sleep quality had a significantly higher mean level of TC (202.9 ± 3.7 mg/dL) compared with those reporting good sleep quality (190.6 ± 4.0 mg/dL) (gender- and race-adjusted p = 0.010). Female officers who worked the day shift and also reported good sleep quality had the lowest mean level of TC compared with women in the other three categories (p = 0.014).ConclusionSleep quality and its combined influence with shift work may play a role in the alteration of some lipid measures.

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“…The promoter region of Noc harbors an E-box, a cyclic AMP response element (CRE) and a photoreceptor-conserved element II (PCE II), all of which are under circadian control [52,56,57]. Noc is an important mediator of lipid metabolism, adipogenesis, glucose homeostasis, inflammation and osteogenesis [53,58]. In the sponge Suberites domuncula , Nocturnin regulates the deadenylation of the glycogenin mRNA, which encodes a key metabolic enzyme for carbohydrate/glycogen metabolism.…”

Section: Control Of Mrna Polyadenylationmentioning

confidence: 99%

Ribonucleoprotein Complexes That Control Circadian Clocks

Wang

Liang

Chen

et al. 2013

IJMS

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Circadian clocks are internal molecular time-keeping mechanisms that enable organisms to adjust their physiology and behavior to the daily surroundings. Misalignment of circadian clocks leads to both physiological and health impairment. Post-transcriptional regulation and translational regulation of circadian clocks have been extensively investigated. In addition, accumulating evidence has shed new light on the involvement of ribonucleoprotein complexes (RNPs) in the post-transcriptional regulation of circadian clocks. Numerous RNA-binding proteins (RBPs) and RNPs have been implicated in the post-transcriptional modification of circadian clock proteins in different model organisms. Herein, we summarize the advances in the current knowledge on the role of RNP complexes in circadian clock regulation.

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Clock regulation of dietary lipid absorption

Cited by 26 publications

References 25 publications

Short-Term Circadian Disruption Impairs Bile Acid and Lipid Homeostasis in Mice

Short-Term Circadian Disruption Impairs Bile Acid and Lipid Homeostasis in Mice

Separate and Joint Associations of Shift Work and Sleep Quality with Lipids

Ribonucleoprotein Complexes That Control Circadian Clocks

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