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      Is Open Access

      Circadian rhythms in liver metabolism and disease

      , *

      Acta Pharmaceutica Sinica. B

      Elsevier

      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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          Most cited references 119

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          Obesity and metabolic syndrome in circadian Clock mutant mice.

          The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. We found that homozygous Clock mutant mice have a greatly attenuated diurnal feeding rhythm, are hyperphagic and obese, and develop a metabolic syndrome of hyperleptinemia, hyperlipidemia, hepatic steatosis, hyperglycemia, and hypoinsulinemia. Expression of transcripts encoding selected hypothalamic peptides associated with energy balance was attenuated in the Clock mutant mice. These results suggest that the circadian clock gene network plays an important role in mammalian energy balance.
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            Restricted feeding uncouples circadian oscillators in peripheral tissues from the central pacemaker in the suprachiasmatic nucleus.

             F Fleury,  Tu Le,  F Damiola (2000)
            In mammals, circadian oscillators exist not only in the suprachiasmatic nucleus, which harbors the central pacemaker, but also in most peripheral tissues. It is believed that the SCN clock entrains the phase of peripheral clocks via chemical cues, such as rhythmically secreted hormones. Here we show that temporal feeding restriction under light-dark or dark-dark conditions can change the phase of circadian gene expression in peripheral cell types by up to 12 h while leaving the phase of cyclic gene expression in the SCN unaffected. Hence, changes in metabolism can lead to an uncoupling of peripheral oscillators from the central pacemaker. Sudden large changes in feeding time, similar to abrupt changes in the photoperiod, reset the phase of rhythmic gene expression gradually and are thus likely to act through a clock-dependent mechanism. Food-induced phase resetting proceeds faster in liver than in kidney, heart, or pancreas, but after 1 wk of daytime feeding, the phases of circadian gene expression are similar in all examined peripheral tissues.
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              Adverse metabolic and cardiovascular consequences of circadian misalignment.

              There is considerable epidemiological evidence that shift work is associated with increased risk for obesity, diabetes, and cardiovascular disease, perhaps the result of physiologic maladaptation to chronically sleeping and eating at abnormal circadian times. To begin to understand underlying mechanisms, we determined the effects of such misalignment between behavioral cycles (fasting/feeding and sleep/wake cycles) and endogenous circadian cycles on metabolic, autonomic, and endocrine predictors of obesity, diabetes, and cardiovascular risk. Ten adults (5 female) underwent a 10-day laboratory protocol, wherein subjects ate and slept at all phases of the circadian cycle-achieved by scheduling a recurring 28-h "day." Subjects ate 4 isocaloric meals each 28-h "day." For 8 days, plasma leptin, insulin, glucose, and cortisol were measured hourly, urinary catecholamines 2 hourly (totaling approximately 1,000 assays/subject), and blood pressure, heart rate, cardiac vagal modulation, oxygen consumption, respiratory exchange ratio, and polysomnographic sleep daily. Core body temperature was recorded continuously for 10 days to assess circadian phase. Circadian misalignment, when subjects ate and slept approximately 12 h out of phase from their habitual times, systematically decreased leptin (-17%, P < 0.001), increased glucose (+6%, P < 0.001) despite increased insulin (+22%, P = 0.006), completely reversed the daily cortisol rhythm (P < 0.001), increased mean arterial pressure (+3%, P = 0.001), and reduced sleep efficiency (-20%, P < 0.002). Notably, circadian misalignment caused 3 of 8 subjects (with sufficient available data) to exhibit postprandial glucose responses in the range typical of a prediabetic state. These findings demonstrate the adverse cardiometabolic implications of circadian misalignment, as occurs acutely with jet lag and chronically with shift work.
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                Author and article information

                Contributors
                Journal
                Acta Pharm Sin B
                Acta Pharm Sin B
                Acta Pharmaceutica Sinica. B
                Elsevier
                2211-3835
                2211-3843
                02 February 2015
                March 2015
                02 February 2015
                : 5
                : 2
                : 113-122
                Affiliations
                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
                S2211-3835(15)00005-2
                10.1016/j.apsb.2015.01.003
                4629216
                © 2015 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.

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

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