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      Circadian rhythms in liver metabolism and disease

      review-article
      Author(s): , *
      Publication date (Electronic):
      Journal: Acta Pharmaceutica Sinica. B
      Publisher: Elsevier
      Keywords: Circadian rhythm, Liver, Metabolic syndrome, Type 2 diabetes, ARC, arcuate nucleus, BMAL1, brain and muscle ARNT-like 1, CAR, constitutive androstane receptor, CLOCK, circadian locomotor output cycles kaput, CRY, cryptochrome, CYP7A1, cholesterol 7α-hydroxylase, CYPs, cytochrome P450 enzymes, DBP, D-site binding protein, E-box, enhance box, EMT, emergency medical technician, FAA, food anticipatory activity, FASPS, familial advanced sleep-phase syndrome, FEO, food entrainable oscillator, FOXO3, forkhead box O3, FXR, farnesoid-X receptor, GLUT2, glucose transporter 2, HDAC3, histone deacetylase 3, HIP, hypoxia inducing protein, HLF, hepatic leukemia factor, LDL, low-density lipoprotein, LRH1, liver receptor homolog 1, NAD+, nicotinamide adenine dinucleotide, PER, period, RHT, retinohypothalamic tract, RORα, retinoid-related orphan receptor α, RORE, ROR-response element, SCN, suprachiasmatic nucleus, SHP, small heterodimer partner, SIRT1, sirtuin 1, TEF, thyrotroph embryonic factor, TGR5, G protein-coupled bile acid receptor, TTFL, transcriptional translational feedback loop

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          Abstract

          Mounting research evidence demonstrates a significant negative impact of circadian disruption on human health. Shift work, chronic jet lag and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.

          Graphical abstract

          Shift work, chronic jet lag, and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, Type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.

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          Disruption of the Clock Components CLOCK and BMAL1 Leads to Hypoinsulinemia and Diabetes

          Biliana Marcheva, Kathryn Moynihan Ramsey, Ethan D Buhr … (2010)
          The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night1–3. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and while rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes4, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism, and insulin signaling is delayed in circadian mutant mice, and both Clock 5,6 and Bmal1 7 mutants exhibit impaired glucose tolerance, reduced insulin secretion, and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival, and synaptic vesicle assembly. Remarkably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective β-cell function at the very latest stage of stimulus-secretion coupling. These results demonstrate a role for the β-cell clock in coordinating insulin secretion with the sleep-wake cycle, and reveal that ablation of the pancreatic clock can trigger onset of diabetes mellitus.
          Article 0 comments Cited 501 times – based on 0 reviews     Review now
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            Regulation of Circadian Behavior and Metabolism by Rev-erbα and Rev-erbβ

            Han-keun Cho, Xuan Zhao, Megumi Hatori … (2012)
            The circadian clock acts at the genomic level to coordinate internal behavioral and physiologic rhythms via the CLOCK-BMAL transcriptional heterodimer. Although the nuclear receptors REV-ERBα and β have been proposed to form an accessory feedback loop that contributes to clock function 1,2 , their precise roles and importance remain unresolved. To establish their regulatory potential we generated comparative cistromes of both REV-ERB isoforms, which revealed shared recognition at over 50% of their total sites and extensive overlap with the master circadian regulator BMAL1. While Rev-erbα has been shown to directly regulate Bmal1 expression 1,2 , the cistromic analysis reveals a direct connection between Bmal1 and Rev-erbα and β regulatory circuits than previously suspected. Genes within the intersection of the BMAL1, REV-ERBα and REV-ERBβ cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erbα/β function by creating double-knockout mice (DKOs) profoundly disrupted circadian expression of core circadian clock and lipid homeostatic gene networks. As a result, DKOs show strikingly altered circadian wheel-running behavior and deregulated lipid metabolism. These data now ally Rev-erbα/β with Per, Cry and other components of the principal feedback loop that drives circadian expression and suggest a more integral mechanism for the coordination of circadian rhythm and metabolism.
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              Circadian timing of food intake contributes to weight gain.

              Deanna Arble, Joseph Bass, Aaron D. Laposky … (2009)
              Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.
              Article 0 comments Cited 291 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                John Y.L. Chiang
                Journal
                Journal ID (nlm-ta): Acta Pharm Sin B
                Journal ID (iso-abbrev): Acta Pharm Sin B
                Title: Acta Pharmaceutica Sinica. B
                Publisher: Elsevier
                ISSN (Print): 2211-3835
                ISSN (Electronic): 2211-3843
                Publication date PMC-release: 02 February 2015
                Publication date (Print): March 2015
                Publication date (Electronic): 02 February 2015
                Volume: 5
                Issue: 2
                Pages: 113-122
                Affiliations
                [0005]Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown OH 44272, USA
                Author notes
                [* ]Corresponding author. Tel.: +1 330 3256694; fax: +1 330 3255910. jchiang@ 123456neomed.edu
                Article
                Publisher ID: S2211-3835(15)00005-2
                DOI: 10.1016/j.apsb.2015.01.003
                PMC ID: 4629216
                PubMed ID: 26579436
                SO-VID: bf81affd-3c9b-4aad-b63c-2a4035687db6
                Copyright © © 2015 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 21 November 2014
                Date revision received : 24 December 2014
                Date accepted : 4 January 2015
                Categories
                Subject: Review

                Keywords: circadian rhythm,liver,metabolic syndrome,type 2 diabetes,arc, arcuate nucleus,bmal1, brain and muscle arnt-like 1,car, constitutive androstane receptor,clock, circadian locomotor output cycles kaput,cry, cryptochrome,cyp7a1, cholesterol 7α-hydroxylase,cyps, cytochrome p450 enzymes,dbp, d-site binding protein,e-box, enhance box,emt, emergency medical technician,faa, food anticipatory activity,fasps, familial advanced sleep-phase syndrome,feo, food entrainable oscillator,foxo3, forkhead box o3,fxr, farnesoid-x receptor,glut2, glucose transporter 2,hdac3, histone deacetylase 3,hip, hypoxia inducing protein,hlf, hepatic leukemia factor,ldl, low-density lipoprotein,lrh1, liver receptor homolog 1,nad+, nicotinamide adenine dinucleotide,per, period,rht, retinohypothalamic tract,rorα, retinoid-related orphan receptor α,rore, ror-response element,scn, suprachiasmatic nucleus,shp, small heterodimer partner,sirt1, sirtuin 1,tef, thyrotroph embryonic factor,tgr5, g protein-coupled bile acid receptor,ttfl, transcriptional translational feedback loop
                Data availability:
                Keywords: circadian rhythm, liver, metabolic syndrome, type 2 diabetes, arc, arcuate nucleus, bmal1, brain and muscle arnt-like 1, car, constitutive androstane receptor, clock, circadian locomotor output cycles kaput, cry, cryptochrome, cyp7a1, cholesterol 7α-hydroxylase, cyps, cytochrome p450 enzymes, dbp, d-site binding protein, e-box, enhance box, emt, emergency medical technician, faa, food anticipatory activity, fasps, familial advanced sleep-phase syndrome, feo, food entrainable oscillator, foxo3, forkhead box o3, fxr, farnesoid-x receptor, glut2, glucose transporter 2, hdac3, histone deacetylase 3, hip, hypoxia inducing protein, hlf, hepatic leukemia factor, ldl, low-density lipoprotein, lrh1, liver receptor homolog 1, nad+, nicotinamide adenine dinucleotide, per, period, rht, retinohypothalamic tract, rorα, retinoid-related orphan receptor α, rore, ror-response element, scn, suprachiasmatic nucleus, shp, small heterodimer partner, sirt1, sirtuin 1, tef, thyrotroph embryonic factor, tgr5, g protein-coupled bile acid receptor, ttfl, transcriptional translational feedback loop

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