All Title Author
Keywords Abstract

ISRN Obesity  2012 

Circadian Rhythms and Obesity in Mammals

DOI: 10.5402/2012/437198

Full-Text   Cite this paper   Add to My Lib

Abstract:

Obesity has become a serious public health problem and a major risk factor for the development of illnesses, such as insulin resistance and hypertension. Attempts to understand the causes of obesity and develop new therapeutic strategies have mostly focused on caloric intake and energy expenditure. Recent studies have shown that the circadian clock controls energy homeostasis by regulating the circadian expression and/or activity of enzymes, hormones, and transport systems involved in metabolism. Moreover, disruption of circadian rhythms leads to obesity and metabolic disorders. Therefore, it is plausible that resetting of the circadian clock can be used as a new approach to attenuate obesity. Feeding regimens, such as restricted feeding (RF), calorie restriction (CR), and intermittent fasting (IF), provide a time cue and reset the circadian clock and lead to better health. In contrast, high-fat (HF) diet leads to disrupted circadian expression of metabolic factors and obesity. This paper focuses on circadian rhythms and their link to obesity. 1. Introduction Obesity has become a serious and growing public health problem [1]. Attempts to develop new therapeutic strategies have mostly focused on energy expenditure and caloric intake. Recent studies link energy homeostasis to the circadian clock at the behavioral, physiological, and molecular levels [2–5], emphasizing that certain nutrients and the timing of food intake may play a significant role in weight gain [6]. Therefore, it is plausible that resetting of the circadian clock can be used as a new approach to attenuate obesity. 2. Circadian Rhythms Our planet revolves around its axis causing light and dark cycles of 24 hours. Organisms on our planet evolved to predict these cycles by developing an endogenous circadian (circa: about and dies: day) clock, which is synchronized to external time cues. This way, organisms ensure that physiological processes are carried out at the right time of the circadian cycle [7]. All aspects of physiology, including sleep-wake cycles, cardiovascular activity, endocrine system, body temperature, renal activity, gastrointestinal tract motility, and metabolism, are influenced by the circadian clock [7, 8]. Indeed, 10–20% of all cellular transcripts are cyclically expressed, most of which are tissue-specific [2, 9–13]. 3. The Circadian Clock The central circadian clock is located in the suprachiasmatic nuclei (SCN) of the brain anterior hypothalamus. The SCN clock is composed of multiple, single-cell oscillators synchronized to generate circadian rhythms [8, 14–16]. The

References

[1]  S. B. Wyatt, K. P. Winters, and P. M. Dubbert, “Overweight and obesity: prevalence, consequences, and causes of a growing public health problem,” American Journal of the Medical Sciences, vol. 331, no. 4, pp. 166–174, 2006.
[2]  O. Froy, “Metabolism and circadian rhythms—implications for obesity,” Endocrine Reviews, vol. 31, no. 1, pp. 1–24, 2010.
[3]  B. Marcheva, K. M. Ramsey, E. D. Buhr et al., “Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes,” Nature, vol. 466, no. 7306, pp. 627–631, 2010.
[4]  K. Oishi, H. Shirai, and N. Ishida, “CLOCK is involved in the circadian transactivation of peroxisome- proliferator-activated receptor α (PPARα) in mice,” Biochemical Journal, vol. 386, no. 3, pp. 575–581, 2005.
[5]  F. W. Turek, C. Joshu, A. Kohsaka et al., “Obesity and metabolic syndrome in circadian clock mutant nice,” Science, vol. 308, no. 5724, pp. 1043–1045, 2005.
[6]  D. M. Arble, J. Bass, A. D. Laposky, M. H. Vitaterna, and F. W. Turek, “Circadian timing of food intake contributes to weight gain,” Obesity, vol. 17, no. 11, pp. 2100–2102, 2009.
[7]  S. Panda, J. B. Hogenesch, and S. A. Kay, “Circadian rhythms from flies to human,” Nature, vol. 417, no. 6886, pp. 329–335, 2002.
[8]  S. M. Reppert and D. R. Weaver, “Coordination of circadian timing in mammals,” Nature, vol. 418, no. 6901, pp. 935–941, 2002.
[9]  R. A. Akhtar, A. B. Reddy, E. S. Maywood et al., “Circadian cycling of the mouse liver transcriptome, as revealed by cDNA microarray, is driven by the suprachiasmatic nucleus,” Current Biology, vol. 12, no. 7, pp. 540–550, 2002.
[10]  G. E. Duffield, J. D. Best, B. H. Meurers, A. Bittner, J. J. Loros, and J. C. Dunlap, “Circadian programs of transcriptional activation, signaling, and protein turnover revealed by microarray analysis of mammalian cells,” Current Biology, vol. 12, no. 7, pp. 551–557, 2002.
[11]  C. B. Green, J. S. Takahashi, and J. Bass, “The meter of metabolism,” Cell, vol. 134, no. 5, pp. 728–742, 2008.
[12]  B. Kornmann, N. Preitner, D. Rifat, F. Fleury-Olela, and U. Schibler, “Analysis of circadian liver gene expression by ADDER, a highly sensitive method for the display of differentially expressed mRNAs,” Nucleic Acids Research, vol. 29, no. 11, article E51, 2001.
[13]  K. F. Storch, O. Lipan, I. Leykin et al., “Extensive and divergent circadian gene expression in liver and heart,” Nature, vol. 417, pp. 78–83, 2002.
[14]  E. D. Herzog, J. S. Takahashi, and G. D. Block, “Clock controls circadian period in isolated suprachiasmatic nucleus neurons,” Nature Neuroscience, vol. 1, no. 8, pp. 708–713, 1998.
[15]  C. Liu, D. R. Weaver, S. H. Strogatz, and S. M. Reppert, “Cellular construction of a circadian clock: period determination in the suprachiasmatic nuclei,” Cell, vol. 91, no. 6, pp. 855–860, 1997.
[16]  D. K. Welsh, D. E. Logothetis, M. Meister, and S. M. Reppert, “Individual neurons dissociated from rat suprachiasmatic nucleus express independently phased circadian firing rhythms,” Neuron, vol. 14, no. 4, pp. 697–706, 1995.
[17]  J. J. Gooley, J. Lu, T. C. Chou, T. E. Scammell, and C. B. Saper, “Melanopsin in cells of origin of the retinohypothalamic tract,” Nature Neuroscience, vol. 4, no. 12, p. 1165, 2001.
[18]  R. J. Lucas, M. S. Freedman, D. Lupi, M. Munoz, Z. K. David-Gray, and R. G. Foster, “Identifying the photoreceptive inputs to the mammalian circadian system using transgenic and retinally degenerate mice,” Behavioural Brain Research, vol. 125, no. 1-2, pp. 97–102, 2001.
[19]  J. E. Quintero, S. J. Kuhlman, and D. G. McMahon, “The biological clock nucleus: a multiphasic oscillator network regulated by light,” Journal of Neuroscience, vol. 23, no. 22, pp. 8070–8076, 2003.
[20]  O. Froy, “Circadian rhythms, aging, and life span in mammals,” Physiology (Bethesda), vol. 26, pp. 225–235, 2011.
[21]  O. Froy and N. Chapnik, “Circadian oscillation of innate immunity components in mouse small intestine,” Molecular Immunology, vol. 44, no. 8, pp. 1954–1960, 2007.
[22]  C. Lee, J. P. Etchegaray, F. R. A. Cagampang, A. S. I. Loudon, and S. M. Reppert, “Posttranslational mechanisms regulate the mammalian circadian clock,” Cell, vol. 107, no. 7, pp. 855–867, 2001.
[23]  D. K. Welsh, S. H. Yoo, A. C. Liu, J. S. Takahashi, and S. A. Kay, “Bioluminescence imaging of individual fibroblasts reveals persistent, independently phased circadian rhythms of clock gene expression,” Current Biology, vol. 14, no. 24, pp. 2289–2295, 2004.
[24]  S. H. Yoo, S. Yamazaki, P. L. Lowrey et al., “PERIOD2::LUCIFERASE real-time reporting of circadian dynamics reveals persistent circadian oscillations in mouse peripheral tissues,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 15, pp. 5339–5346, 2004.
[25]  K. Saeb-Parsy, S. Lombardelli, F. Z. Khan, K. McDowall, I. T. H. Au-Yong, and R. E. J. Dyball, “Neural connections of hypothalamic neuroendocrine nuclei in the rat,” Journal of Neuroendocrinology, vol. 12, no. 7, pp. 635–648, 2000.
[26]  N. Burioka, Y. Fukuoka, M. Takata et al., “Circadian rhythms in the CNS and peripheral clock disorders: function of clock genes: influence of medication for bronchial asthma on circadian gene,” Journal of Pharmacological Sciences, vol. 103, no. 2, pp. 144–149, 2007.
[27]  B. J. Maron, J. Kogan, M. A. Proschan, G. M. Hecht, and W. C. Roberts, “Circadian variability in the occurrence of sudden cardiac death in patients with hypertrophic cardiomyopathy,” Journal of the American College of Cardiology, vol. 23, no. 6, pp. 1405–1409, 1994.
[28]  B. Staels, “When the Clock stops ticking, metabolic syndrome explodes,” Nature Medicine, vol. 12, no. 1, pp. 54–55, 2006.
[29]  S. Davis and D. K. Mirick, “Circadian disruption, shift work and the risk of cancer: a summary of the evidence and studies in Seattle,” Cancer Causes and Control, vol. 17, no. 4, pp. 539–545, 2006.
[30]  E. Filipski, V. M. King, X. M. Li et al., “Disruption of circadian coordination accelerates malignant growth in mice,” Pathologie Biologie, vol. 51, no. 4, pp. 216–219, 2003.
[31]  L. Fu, H. Pelicano, J. Liu, P. Huang, and C. C. Lee, “The circadian gene period2 plays an important role in tumor suppression and DNA-damage response in vivo,” Cell, vol. 111, pp. 41–50, 2002.
[32]  R. V. Kondratov, A. A. Kondratova, V. Y. Gorbacheva, O. V. Vykhovanets, and M. P. Antoch, “Early aging and age-related pathologies in mice deficient in BMAL1, the core component of the circadian clock,” Genes and Development, vol. 20, no. 14, pp. 1868–1873, 2006.
[33]  P. D. Penev, D. E. Kolker, P. C. Zee, and F. W. Turek, “Chronic circadian desynchronization decreases the survival of animals with cardiomyopathic heart disease,” American Journal of Physiology, vol. 275, no. 6, pp. H2334–H2337, 1998.
[34]  M. W. Hurd and M. R. Ralph, “The significance of circadian organization for longevity in the golden hamster,” Journal of Biological Rhythms, vol. 13, no. 5, pp. 430–436, 1998.
[35]  M. Karasek, “Melatonin, human aging, and age-related diseases,” Experimental Gerontology, vol. 39, no. 11-12, pp. 1723–1729, 2004.
[36]  A. Klarsfeld and F. Rouyer, “Effects of circadian mutations and LD periodicity on the life span of drosophila melanogaster,” Journal of Biological Rhythms, vol. 13, no. 6, pp. 471–478, 1998.
[37]  M. A. Hofman and D. F. Swaab, “Living by the clock: the circadian pacemaker in older people,” Ageing Research Reviews, vol. 5, no. 1, pp. 33–51, 2006.
[38]  K. Scarbrough, S. Losee-Olson, E. P. Wallen, and F. W. Turek, “Aging and photoperiod affect entrainment and quantitative aspects of locomotor behavior in Syrian hamsters,” American Journal of Physiology, vol. 272, no. 4, pp. R1219–R1225, 1997.
[39]  S. Yamazaki, M. Straume, H. Tei, Y. Sakaki, M. Menaker, and G. D. Block, “Effects of aging on central and peripheral mammalian clocks,” Proceedings of the National Academy of Sciences of the United States of America, vol. 99, no. 16, pp. 10801–10806, 2002.
[40]  U. Schibler, J. Ripperger, and S. A. Brown, “Peripheral circadian oscillators in mammals: time and food,” Journal of Biological Rhythms, vol. 18, no. 3, pp. 250–260, 2003.
[41]  O. Froy, D. C. Chang, and S. M. Reppert, “Redox potential: differential roles in dCRY and mCRY1 functions,” Current Biology, vol. 12, no. 2, pp. 147–152, 2002.
[42]  S. M. Reppert and D. R. Weaver, “Molecular analysis of mammalian circadian rhythms,” Annual Review of Physiology, vol. 63, pp. 647–676, 2001.
[43]  M. J. Zylka, L. P. Shearman, D. R. Weaver, and S. M. Reppert, “Three period homologs in mammals: differential light responses in the suprachiasmatic circadian clock and oscillating transcripts outside of brain,” Neuron, vol. 20, no. 6, pp. 1103–1110, 1998.
[44]  E. J. Eide and D. M. Virshup, “Casein kinase I: another cog in the circadian clockworks,” Chronobiology International, vol. 18, no. 3, pp. 389–398, 2001.
[45]  E. J. Eide, M. F. Woolf, H. Kang et al., “Control of mammalian circadian rhythm by CKIε-regulated proteasome-mediated PER2 degradation,” Molecular and Cellular Biology, vol. 25, no. 7, pp. 2795–2807, 2005.
[46]  D. Whitmore, N. Cermakian, C. Crosio et al., “A clockwork organ,” Biological Chemistry, vol. 381, no. 9-10, pp. 793–800, 2000.
[47]  E. J. Eide, H. Kang, S. Crapo, M. Gallego, and D. M. Virshup, “Casein kinase I in the mammalian circadian clock,” Methods in Enzymology, vol. 393, article no. 19, pp. 408–418, 2005.
[48]  M. Garaulet and J. A. Madrid, “Chronobiological aspects of nutrition, metabolic syndrome and obesity,” Advanced Drug Delivery Reviews, vol. 62, no. 9-10, pp. 967–978, 2010.
[49]  T. Hirota and Y. Fukada, “Resetting mechanism of central and peripheral circadian clocks in mammals,” Zoological Science, vol. 21, no. 4, pp. 359–368, 2004.
[50]  A. Kohsaka and J. Bass, “A sense of time: how molecular clocks organize metabolism,” Trends in Endocrinology and Metabolism, vol. 18, no. 1, pp. 4–11, 2007.
[51]  A. J. Davidson, O. Casta?ón-Cervantes, and F. K. Stephan, “Daily oscillations in liver function: diurnal vs circadian rhythmicity,” Liver International, vol. 24, no. 3, pp. 179–186, 2004.
[52]  S. E. la Fleur, “Daily rhythms in glucose metabolism: suprachiasmatic nucleus output to peripheral tissue,” Journal of Neuroendocrinology, vol. 15, no. 3, pp. 315–322, 2003.
[53]  S. E. La Fleur, A. Kalsbeek, J. Wortel, and R. M. Buijs, “A suprachiasmatic nucleus generated rhythm in basal glucose concentrations,” Journal of Neuroendocrinology, vol. 11, no. 8, pp. 643–652, 1999.
[54]  K. M. Ramsey, B. Marcheva, A. Kohsaka, and J. Bass, “The clockwork of metabolism,” Annual Review of Nutrition, vol. 27, pp. 219–240, 2007.
[55]  A. Kalsbeek, M. Ruiter, S. E. La Fleur, C. Cailotto, F. Kreier, and R. M. Buijs, “Chapter 17: the hypothalamic clock and its control of glucose homeostasis,” Progress in Brain Research, vol. 153, pp. 283–307, 2006.
[56]  S. Yamazaki, Y. Ishida, and S. I. Inouye, “Circadian rhythms of adenosine triphosphate contents in the suprachiasmatic nucleus, anterior hypothalamic area and caudate putamen of the rat—negative correlation with electrical activity,” Brain Research, vol. 664, no. 1-2, pp. 237–240, 1994.
[57]  C. Cailotto, S. E. La Fleur, C. Van Heijningen et al., “The suprachiasmatic nucleus controls the daily variation of plasma glucose via the autonomic output to the liver: are the clock genes involved?” European Journal of Neuroscience, vol. 22, no. 10, pp. 2531–2540, 2005.
[58]  S. Zvonic, Z. E. Floyd, R. L. Mynatt, and J. M. Gimble, “Circadian rhythms and the regulation of metabolic tissue function and energy homeostasis,” Obesity, vol. 15, no. 3, pp. 539–543, 2007.
[59]  S. Zvonic, A. A. Ptitsyn, S. A. Conrad et al., “Characterization of peripheral circadian clocks in adipose tissues,” Diabetes, vol. 55, no. 4, pp. 962–970, 2006.
[60]  H. Ando, H. Yanagihara, Y. Hayashi et al., “Rhythmic messenger ribonucleic acid expression of clock genes and adipocytokines in mouse visceral adipose tissue,” Endocrinology, vol. 146, no. 12, pp. 5631–5636, 2005.
[61]  M. S. Bray and M. E. Young, “Circadian rhythms in the development of obesity: potential role for the circadian clock within the adipocyte,” Obesity Reviews, vol. 8, no. 2, pp. 169–181, 2007.
[62]  M. Ruiter, S. E. La Fleur, C. Van Heijningen, J. Van der Vliet, A. Kalsbeek, and R. M. Buijs, “The daily rhythm in plasma glucagon concentrations in the rat is modulated by the biological clock and by feeding behavior,” Diabetes, vol. 52, no. 7, pp. 1709–1715, 2003.
[63]  S. F. De Boer and J. Van Der Gugten, “Daily variations in plasma noradrenaline, adrenaline and corticosterone concentrations in rats,” Physiology and Behavior, vol. 40, no. 3, pp. 323–328, 1987.
[64]  R. S. Ahima, D. Prabakaran, and J. S. Flier, “Postnatal leptin surge and regulation of circadian rhythm of leptin by feeding: implications for energy homeostasis and neuroendocrine function,” Journal of Clinical Investigation, vol. 101, no. 5, pp. 1020–1027, 1998.
[65]  B. Bodosi, J. Gardi, I. Hajdu, E. Szentirmai, F. Obal Jr., and J. M. Krueger, “Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal diurnal cycle, restricted feeding, and sleep deprivation,” American Journal of Physiology, vol. 287, no. 5, pp. R1071–R1079, 2004.
[66]  J. L. Downs and H. F. Urbanski, “Aging-related sex-dependent loss of the circulating leptin 24-h rhythm in the rhesus monkey,” Journal of Endocrinology, vol. 190, no. 1, pp. 117–127, 2006.
[67]  S. P. Kalra, M. Bagnasco, E. E. Otukonyong, M. G. Dube, and P. S. Kalra, “Rhythmic, reciprocal ghrelin and leptin signaling: new insight in the development of obesity,” Regulatory Peptides, vol. 111, no. 1–3, pp. 1–11, 2003.
[68]  A. Kalsbeek, E. Fliers, J. A. Romijn et al., “The suprachiasmatic nucleus generates the diurnal changes in plasma leptin levels,” Endocrinology, vol. 142, no. 6, pp. 2677–2685, 2001.
[69]  S. Sukumaran, R. R. Almon, D. C. DuBois, and W. J. Jusko, “Circadian rhythms in gene expression: relationship to physiology, disease, drug disposition and drug action,” Advanced Drug Delivery Reviews, vol. 62, no. 9-10, pp. 904–917, 2010.
[70]  X. M. Guan, J. F. Hess, H. Yu, P. J. Hey, and L. H. T. Van Der Ploeg, “Differential expression of mRNA for leptin receptor isoforms in the rat brain,” Molecular and Cellular Endocrinology, vol. 133, no. 1, pp. 1–7, 1997.
[71]  C. X. Yi, J. Van Der Vliet, J. Dai, G. Yin, L. Ru, and R. M. Buijs, “Ventromedial arcuate nucleus communicates peripheral metabolic information to the suprachiasmatic nucleus,” Endocrinology, vol. 147, no. 1, pp. 283–294, 2006.
[72]  J. M. Zigman, J. E. Jones, C. E. Lee, C. B. Saper, and J. K. Elmquist, “Expression of ghrelin receptor mRNA in the rat and the mouse brain,” Journal of Comparative Neurology, vol. 494, no. 3, pp. 528–548, 2006.
[73]  G. Boden, X. Chen, and M. Polansky, “Disruption of circadian insulin secretion is associated with reduced glucose uptake in first-degree relatives of patients with type 2 diabetes,” Diabetes, vol. 48, no. 11, pp. 2182–2188, 1999.
[74]  E. Van Cauter, K. S. Polonsky, and A. J. Scheen, “Roles of circadian rhythmicity and sleep in human glucose regulation,” Endocrine Reviews, vol. 18, no. 5, pp. 716–738, 1997.
[75]  M. H. Oster, T. W. Castonguay, C. L. Keen, and J. S. Stern, “Circadian rhythm of corticosterone in diabetic rats,” Life Sciences, vol. 43, no. 20, pp. 1643–1645, 1988.
[76]  A. Velasco, I. Huerta, and B. Marin, “Plasma corticosterone, motor activity and metabolic circadian patterns in streptozotocin-induced diabetic rats,” Chronobiology International, vol. 5, no. 2, pp. 127–135, 1988.
[77]  Y. Shimomura, M. Takahashi, H. Shimizu et al., “Abnormal feeding behavior and insulin replacement in STZ-induced diabetic rats,” Physiology and Behavior, vol. 47, no. 4, pp. 731–734, 1990.
[78]  V. Spallone, L. Bernardi, L. Ricordi et al., “Relationship between the circadian rhythms of blood pressure and sympathovagal balance in diabetic autonomic neuropathy,” Diabetes, vol. 42, no. 12, pp. 1745–1752, 1993.
[79]  R. Heptulla, A. Smitten, B. Teague, W. V. Tamborlane, Y. Z. Ma, and S. Caprio, “Temporal patterns of circulating leptin levels in lean and obese adolescents: relationships to insulin, growth hormone, and free fatty acids rhythmicity,” Journal of Clinical Endocrinology and Metabolism, vol. 86, no. 1, pp. 90–96, 2001.
[80]  J. Licinio, “Longitudinally sampled human plasma leptin and cortisol concentrations are inversely correlated,” Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 3, p. 1042, 1998.
[81]  F. Perfetto, R. Tarquini, G. Cornélissen et al., “Circadian phase difference of leptin in android versus gynoid obesity,” Peptides, vol. 25, no. 8, pp. 1297–1306, 2004.
[82]  M. F. Saad, M. G. Riad-Gabriel, A. Khan, et al., “Diurnal and ultradian rhythmicity of plasma leptin: effects of gender and adiposity,” The Journal of Clinical Endocrinology & Metabolism, vol. 83, no. 2, pp. 453–459, 1998.
[83]  A. Gavrila, C. K. Peng, J. L. Chan, J. E. Mietus, A. L. Goldberger, and C. S. Mantzoros, “Diurnal and ultradian dynamics of serum adiponectin in healthy men: comparison with leptin, circulating soluble leptin receptor, and cortisol patterns,” The Journal of Clinical Endocrinology & Metabolism, vol. 88, no. 6, pp. 2838–2843, 2003.
[84]  B. O. Yildiz, M. A. Suchard, M. L. Wong, S. M. McCann, and J. Licinio, “Alterations in the dynamics of circulating ghrelin, adiponectin, and leptin in human obesity,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 28, pp. 10434–10439, 2004.
[85]  B. Guo, S. Chatterjee, L. Li et al., “The clock gene, brain and muscle Arnt-like 1, regulates adipogenesis via Wnt signaling pathway,” FASEB Journal, vol. 26, pp. 3453–3463, 2012.
[86]  S. Shimba, N. Ishii, Y. Ohta et al., “Brain and muscle Arnt-like protein-1 (BMAL1), a component of the molecular clock, regulates adipogenesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 102, no. 34, pp. 12071–12076, 2005.
[87]  S. Shimba, T. Ogawa, S. Hitosugi, et al., “Deficient of a clock gene, brain and muscle Arnt-like protein-1 (BMAL1), induces dyslipidemia and ectopic fat formation,” PLoS One, vol. 6, article e25231, 2011.
[88]  A. Chawla and M. A. Lazar, “Induction of Rev-ErbAα, an orphan receptor encoded on the opposite strand of the α-thyroid hormone receptor gene, during adipocyte differentiation,” Journal of Biological Chemistry, vol. 268, no. 22, pp. 16265–16269, 1993.
[89]  I. P. Torra, V. Tsibulsky, F. Delaunay et al., “Circadian and glucocorticoid regulation of Rev-erbα expression in liver,” Endocrinology, vol. 141, no. 10, pp. 3799–3806, 2000.
[90]  H. Cho, X. Zhao, M. Hatori et al., “Regulation of circadian behaviour and metabolism by REV-ERB-alpha and REV-ERB-beta,” Nature, vol. 485, pp. 123–127, 2012.
[91]  N. Preitner, F. Damiola, Luis-Lopez-Molina et al., “The orphan nuclear receptor REV-ERBα controls circadian transcription within the positive limb of the mammalian circadian oscillator,” Cell, vol. 110, no. 2, pp. 251–260, 2002.
[92]  T. K. Sato, S. Panda, L. J. Miraglia, et al., “A functional genomics strategy reveals Rora as a component of the mammalian circadian clock,” Neuron, vol. 43, no. 4, pp. 527–537, 2004.
[93]  P. Lau, S. J. Nixon, R. G. Parton, and G. E. Muscat, “RORalpha regulates the expression of genes involved in lipid homeostasis in skeletal muscle cells: caveolin-3 and CPT-1 are direct targets of ROR,” The Journal of Biological Chemistry, vol. 279, no. 35, pp. 36828–36840, 2004.
[94]  H. R. Ueda, W. Chen, A. Adachi, et al., “A transcription factor response element for gene expression during circadian night,” Nature, vol. 418, no. 6897, pp. 534–539, 2002.
[95]  L. A. Solt, Y. Wang, S. Banerjee, et al., “Regulation of circadian behaviour and metabolism by synthetic REV-ERB agonists,” Nature, vol. 485, pp. 62–68, 2012.
[96]  S. Kersten, B. Desvergne, and W. Wahli, “Roles of PPARS in health and disease,” Nature, vol. 405, no. 6785, pp. 421–424, 2000.
[97]  P. Lefebvre, G. Chinetti, J. C. Fruchart, and B. Staels, “Sorting out the roles of PPARα in energy metabolism and vascular homeostasis,” Journal of Clinical Investigation, vol. 116, no. 3, pp. 571–580, 2006.
[98]  L. Canaple, J. Rambaud, O. Dkhissi-Benyahya et al., “Reciprocal regulation of brain and muscle Arnt-like protein 1 and peroxisome proliferator-activated receptor α defines a novel positive feedback loop in the rodent liver circadian clock,” Molecular Endocrinology, vol. 20, no. 8, pp. 1715–1727, 2006.
[99]  I. Inoue, Y. Shinoda, M. Ikeda et al., “CLOCK/BMAL1 is involved in lipid metabolism via transactivation of the peroxisome proliferator-activated receptor (PPAR) response element,” Journal of Atherosclerosis and Thrombosis, vol. 12, no. 3, pp. 169–174, 2005.
[100]  R. Gutman, M. Barnea, L. Haviv, N. Chapnik, and O. Froy, “Peroxisome proliferator-activated receptor alpha (PPARalpha) activation advances locomotor activity and feeding daily rhythms in mice,” International Journal of Obesity, vol. 36, pp. 1131–1134, 2012.
[101]  B. Grimaldi and P. Sassone-Corsi, “Circadian rhythms: metabolic clockwork,” Nature, vol. 447, no. 7143, pp. 386–387, 2007.
[102]  C. Liu, S. Li, T. Liu, J. Borjigin, and J. D. Lin, “Transcriptional coactivator PGC-1α integrates the mammalian clock and energy metabolism,” Nature, vol. 447, no. 7143, pp. 477–481, 2007.
[103]  D. Carling, “AMP-activated protein kinase: balancing the scales,” Biochimie, vol. 87, no. 1, pp. 87–91, 2005.
[104]  D. G. Hardie, S. A. Hawley, and J. W. Scott, “AMP-activated protein kinase—development of the energy sensor concept,” Journal of Physiology, vol. 574, no. 1, pp. 7–15, 2006.
[105]  H. U. Jee, S. Yang, S. Yamazaki et al., “Activation of 5′-AMP-activated kinase with diabetes drug metformin induces casein kinase Iε (CKIε)-dependent degradation of clock protein mPer2,” Journal of Biological Chemistry, vol. 282, no. 29, pp. 20794–20798, 2007.
[106]  K. A. Lamia, U. M. Sachdeva, L. Di Tacchio et al., “AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation,” Science, vol. 326, no. 5951, pp. 437–440, 2009.
[107]  O. Froy and R. Miskin, “Effect of feeding regimens on circadian rhythms: implications for aging and longevity,” Aging, vol. 2, no. 1, pp. 7–27, 2010.
[108]  M. Barnea, L. Haviv, R. Gutman, N. Chapnik, Z. Madar, and O. Froy, “Metformin affects the circadian clock and metabolic rhythms in a tissue-specific manner,” Biochim Biophys Acta, vol. 1822, pp. 1796–1180, 2012.
[109]  C. Canto and J. Auwerx, “Caloric restriction, SIRT1 and longevity,” Trends in Endocrinology and Metabolism, vol. 20, no. 7, pp. 325–331, 2009.
[110]  M. C. Haigis and L. P. Guarente, “Mammalian sirtuins—emerging roles in physiology, aging, and calorie restriction,” Genes and Development, vol. 20, no. 21, pp. 2913–2921, 2006.
[111]  C. Cantó, Z. Gerhart-Hines, J. N. Feige et al., “AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity,” Nature, vol. 458, no. 7241, pp. 1056–1060, 2009.
[112]  G. Asher, D. Gatfield, M. Stratmann et al., “SIRT1 regulates circadian clock gene expression through PER2 deacetylation,” Cell, vol. 134, no. 2, pp. 317–328, 2008.
[113]  Y. Nakahata, M. Kaluzova, B. Grimaldi et al., “The NAD+-dependent deacetylase SIRT1 modulates CLOCK-mediated chromatin remodeling and circadian control,” Cell, vol. 134, no. 2, pp. 329–340, 2008.
[114]  Y. Nakahata, S. Sahar, G. Astarita, M. Kaluzova, and P. Sassone-Corsi, “Circadian control of the NAD+ salvage pathway by CLOCK-SIRT1,” Science, vol. 324, no. 5927, pp. 654–657, 2009.
[115]  J. Rutter, M. Reick, L. C. Wu, and S. L. McKnight, “Regulation of clock and NPAS2 DNA binding by the redox state of NAD cofactors,” Science, vol. 293, no. 5529, pp. 510–514, 2001.
[116]  J. Rutter, M. Reick, and S. L. McKnight, “Metabolism and the control of circadian rhythms,” Annual Review of Biochemistry, vol. 71, pp. 307–331, 2002.
[117]  K. Oishi, G. I. Atsumi, S. Sugiyama et al., “Disrupted fat absorption attenuates obesity induced by a high-fat diet in Clock mutant mice,” FEBS Letters, vol. 580, no. 1, pp. 127–130, 2006.
[118]  K. Oishi, N. Ohkura, M. Wakabayashi et al., “CLOCK is involved in obesity-induced disordered fibrinolysis in ob/ob mice by regulating PAI-1 gene expression,” Journal of Thrombosis and Haemostasis, vol. 4, no. 8, pp. 1774–1780, 2006.
[119]  R. D. Rudic, P. McNamara, A. M. Curtis et al., “BMAL1 and CLOCK, two essential components of the circadian clock, are involved in glucose homeostasis,” PLoS Biology, vol. 2, no. 11, article e377, 2004.
[120]  S. Yang, A. Liu, A. Weidenhammer et al., “The role of mPer2 clock gene in glucocorticoid and feeding rhythms,” Endocrinology, vol. 150, no. 5, pp. 2153–2160, 2009.
[121]  V. M. Cassone and F. K. Stephan, “Central and peripheral regulation of feeding and nutrition by the mammalian circadian clock: implications for nutrition during manned space flight,” Nutrition, vol. 18, no. 10, pp. 814–819, 2002.
[122]  F. K. Stephan, “The “other” circadian system: food as a Zeitgeber,” Journal of Biological Rhythms, vol. 17, no. 4, pp. 284–292, 2002.
[123]  O. Froy, N. Chapnik, and R. Miskin, “Long-lived αMUPA transgenic mice exhibit pronounced circadian rhythms,” American Journal of Physiology, vol. 291, no. 5, pp. E1017–E1024, 2006.
[124]  B. Grasl-Kraupp, W. Bursch, B. Ruttkay-Nedecky, A. Wagner, B. Lauer, and R. Schulte-Hermann, “Food restriction eliminates preneoplastic cells through apoptosis and antagonizes carcinogenesis in rat liver,” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, no. 21, pp. 9995–9999, 1994.
[125]  K. I. Honma, S. Honma, and T. Hiroshige, “Critical role of food amount for prefeeding corticosterone peak in rats,” The American Journal of Physiology, vol. 245, no. 3, pp. R339–R344, 1983.
[126]  A. Boulamery-Velly, N. Simon, J. Vidal, J. Mouchet, and B. Bruguerolle, “Effects of three-hour restricted food access during the light period on circadian rhythms of temperature, locomotor activity, and heart rate in rats,” Chronobiology International, vol. 22, no. 3, pp. 489–498, 2005.
[127]  R. Hara, K. Wan, H. Wakamatsu et al., “Restricted feeding entrains liver clock without participation of the suprachiasmatic nucleus,” Genes to Cells, vol. 6, no. 3, pp. 269–278, 2001.
[128]  J. Hirao, S. Arakawa, K. Watanabe, K. Ito, and T. Furukawa, “Effects of restricted feeding on daily fluctuations of hepatic functions including P450 monooxygenase activities in rats,” Journal of Biological Chemistry, vol. 281, no. 6, pp. 3165–3171, 2006.
[129]  R. E. Mistlberger, “Circadian food-anticipatory activity: formal models and physiological mechanisms,” Neuroscience and Biobehavioral Reviews, vol. 18, no. 2, pp. 171–195, 1994.
[130]  C. A. Comperatore and F. K. Stephan, “Entrainment of duodenal activity to periodic feeding,” Journal of Biological Rhythms, vol. 2, no. 3, pp. 227–242, 1987.
[131]  M. Saito, E. Murakami, and M. Suda, “Circadian rhythms in disaccharidases of rat small intestine and its relation to food intake,” Biochimica et Biophysica Acta, vol. 421, no. 1, pp. 177–179, 1976.
[132]  K. Horikawa, Y. Minami, M. Iijima, M. Akiyama, and S. Shibata, “Rapid damping of food-entrained circadian rhythm of clock gene expression in clock-defective peripheral tissues under fasting conditions,” Neuroscience, vol. 134, no. 1, pp. 335–343, 2005.
[133]  K. Oishi, K. Miyazaki, and N. Ishida, “Functional CLOCK is not involved in the entrainment of peripheral clocks to the restricted feeding: entrainable expression of mPer2 and BMAL1 mRNAs in the heart of Clock mutant mice on Jcl:ICR background,” Biochemical and Biophysical Research Communications, vol. 298, no. 2, pp. 198–202, 2002.
[134]  F. K. Stephan, J. M. Swann, and C. L. Sisk, “Anticipation of 24-hr feeding schedules in rats with lesions of the suprachiasmatic nucleus,” Behavioral and Neural Biology, vol. 25, no. 3, pp. 346–363, 1979.
[135]  F. Damiola, N. Le Minli, N. Preitner, B. Kornmann, F. Fleury-Olela, and U. Schibler, “Restricted feeding uncouples circadian oscillators in peripheral tissues from the central pacemaker in the suprachiasmatic nucleus,” Genes and Development, vol. 14, no. 23, pp. 2950–2961, 2000.
[136]  K. A. Stokkan, S. Yamazaki, H. Tei, Y. Sakaki, and M. Menaker, “Entrainment of the circadian clock in the liver by feeding,” Science, vol. 291, no. 5503, pp. 490–493, 2001.
[137]  J. D. Lin, C. Liu, and S. Li, “Integration of energy metabolism and the mammalian clock,” Cell Cycle, vol. 7, no. 4, pp. 453–457, 2008.
[138]  H. Sherman, I. Frumin, R. Gutman et al., “Long-term restricted feeding alters circadian expression and reduces the level of inflammatory and disease markers,” Journal of Cellular and Molecular Medicine, vol. 15, pp. 2745–2759, 2011.
[139]  H. Sherman, Y. Genzer, R. Cohen, N. Chapnik, Z. Madar, and O. Froy, “Timed high-fat diet resets circadian metabolism and prevents obesity,” FASEB Journal, vol. 26, pp. 3493–3502, 2012.
[140]  J. J. Gooley, A. Schomer, and C. B. Saper, “The dorsomedial hypothalamic nucleus is critical for the expression of food-entrainable circadian rhythms,” Nature Neuroscience, vol. 9, no. 3, pp. 398–407, 2006.
[141]  G. J. Landry, M. M. Simon, I. C. Webb, and R. E. Mistlberger, “Persistence of a behavioral food-anticipatory circadian rhythm following dorsomedial hypothalamic ablation in rats,” American Journal of Physiology, vol. 290, no. 6, pp. R1527–R1534, 2006.
[142]  G. J. Landry, G. R. Yamakawa, I. C. Webb, R. J. Mear, and R. E. Mistlberger, “The dorsomedial hypothalamic nucleus is not necessary for the expression of circadian food-anticipatory activity in rats,” Journal of Biological Rhythms, vol. 22, no. 6, pp. 467–478, 2007.
[143]  M. Mieda, S. C. Williams, J. A. Richardson, K. Tanaka, and M. Yanagisawa, “The dorsomedial hypothalamic nucleus as a putative food-entrainable circadian pacemaker,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 32, pp. 12150–12155, 2006.
[144]  A. J. Davidson, S. L. T. Cappendijk, and F. K. Stephan, “Feeding-entrained circadian rhythms are attenuated by lesions of the parabrachial region in rats,” American Journal of Physiology, vol. 278, no. 5, pp. R1296–R1304, 2000.
[145]  J. Mendoza, M. Angeles-Castellanos, and C. Escobar, “Differential role of the accumbens Shell and Core subterritories in food-entrained rhythms of rats,” Behavioural Brain Research, vol. 158, no. 1, pp. 133–142, 2005.
[146]  R. E. Mistlberger and D. G. Mumby, “The limbic system and food-anticipatory circadian rhythms in the rat: ablation and dopamine blocking studies,” Behavioural Brain Research, vol. 47, no. 2, pp. 159–168, 1992.
[147]  A. J. Davidson, “Search for the feeding-entrainable circadian oscillator: a complex proposition,” American Journal of Physiology, vol. 290, no. 6, pp. R1524–R1526, 2006.
[148]  R. E. Mistlberger and E. G. Marchant, “Enhanced food-anticipatory circadian rhythms in the genetically obese Zucker rat,” Physiology and Behavior, vol. 66, no. 2, pp. 329–335, 1999.
[149]  S. Pitts, E. Perone, and R. Silver, “Food-entrained circadian rhythms are sustained in arrhythmic Clk/Clk mutant mice,” American Journal of Physiology, vol. 285, no. 1, pp. R57–R67, 2003.
[150]  J. S. Pendergast, W. Nakamura, R. C. Friday, F. Hatanaka, T. Takumi, and S. Yamazaki, “Robust food anticipatory activity in BMAL1-deficient mice,” PLoS ONE, vol. 4, no. 3, Article ID e4860, 2009.
[151]  K. F. Storch and C. J. Weitz, “Daily rhythms of food-anticipatory behavioral activity do not require the known circadian clock,” Proceedings of the National Academy of Sciences of the United States of America, vol. 106, no. 16, pp. 6808–6813, 2009.
[152]  C. A. Feillet, J. A. Ripperger, M. C. Magnone, A. Dulloo, U. Albrecht, and E. Challet, “Lack of food anticipation in Per2 mutant mice,” Current Biology, vol. 16, no. 20, pp. 2016–2022, 2006.
[153]  R. E. Mistlberger, “Circadian rhythms: perturbing a food-entrained clock,” Current Biology, vol. 16, no. 22, pp. R968–R969, 2006.
[154]  E. J. Masoro, I. Shimokawa, Y. Higami, C. A. McMahan, and B. P. Yu, “Temporal pattern of food intake not a factor in the retardation of aging processes by dietary restriction,” Journals of Gerontology A, vol. 50, no. 1, pp. B48–B53, 1995.
[155]  J. Koubova and L. Guarente, “How does calorie restriction work?” Genes and Development, vol. 17, no. 3, pp. 313–321, 2003.
[156]  E. J. Masoro, “Overview of caloric restriction and ageing,” Mechanisms of Ageing and Development, vol. 126, no. 9, pp. 913–922, 2005.
[157]  G. S. Roth, M. A. Lane, D. K. Ingram et al., “Biomarkers of caloric restriction may predict longevity in humans,” Science, vol. 297, no. 5582, p. 811, 2002.
[158]  G. S. Roth, J. A. Mattison, M. A. Ottinger, M. E. Chachich, M. A. Lane, and D. K. Ingram, “Aging in rhesus monkeys: relevance to human health interventions,” Science, vol. 305, no. 5689, pp. 1423–1426, 2004.
[159]  R. Weindruch and R. S. Sohal, “Caloric intake and aging,” The New England Journal of Medicine, vol. 337, no. 14, pp. 986–994, 1997.
[160]  E. Challet, I. Caldelas, C. Graff, and P. Pévet, “Synchronization of the molecular clockwork by light- and food-related cues in mammals,” Biological Chemistry, vol. 384, no. 5, pp. 711–719, 2003.
[161]  E. Challet, L. C. Solberg, and F. W. Turek, “Entrainment in calorie-restricted mice: conflicting zeitgebers and free- running conditions,” American Journal of Physiology, vol. 274, no. 6, pp. R1751–R1761, 1998.
[162]  J. Mendoza, C. Graff, H. Dardente, P. Pevet, and E. Challet, “Feeding cues alter clock gene oscillations and photic responses in the suprachiasmatic nuclei of mice exposed to a light/dark cycle,” Journal of Neuroscience, vol. 25, no. 6, pp. 1514–1522, 2005.
[163]  D. Resuehr and J. Olcese, “Caloric restriction and melatonin substitution: effects on murine circadian parameters,” Brain Research, vol. 1048, no. 1-2, pp. 146–152, 2005.
[164]  J. Mendoza, K. Drevet, P. Pévet, and E. Challet, “Daily meal timing is not necessary for resetting the main circadian clock by calorie restriction,” Journal of Neuroendocrinology, vol. 20, no. 2, pp. 251–260, 2008.
[165]  O. Froy, N. Chapnik, and R. Miskin, “Relationship between calorie restriction and the biological clock: lessons from long-lived transgenic mice,” Rejuvenation Research, vol. 11, no. 2, pp. 467–471, 2008.
[166]  R. Michael Anson, Z. Guo, R. de Cabo et al., “Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 10, pp. 6216–6220, 2003.
[167]  O. Descamps, J. Riondel, V. Ducros, and A. M. Roussel, “Mitochondrial production of reactive oxygen species and incidence of age-associated lymphoma in OF1 mice: effect of alternate-day fasting,” Mechanisms of Ageing and Development, vol. 126, no. 11, pp. 1185–1191, 2005.
[168]  C. L. Goodrick, D. K. Ingram, M. A. Reynolds, J. R. Freeman, and N. Cider, “Effects of intermittent feeding upon weight and lifespan in inbred mice: interaction of genotype and age,” Mechanisms of Ageing and Development, vol. 55, no. 1, pp. 69–87, 1990.
[169]  I. Ahmet, R. Wan, M. P. Mattson, E. G. Lakatta, and M. Talan, “Cardioprotection by intermittent fasting in rats,” Circulation, vol. 112, no. 20, pp. 3115–3121, 2005.
[170]  A. Contestabile, E. Ciani, and A. Contestabile, “Dietary restriction differentially protects from neurodegeneration in animal models of excitotoxicity,” Brain Research, vol. 1002, no. 1-2, pp. 162–166, 2004.
[171]  D. E. Mager, R. Wan, M. Brown et al., “Caloric restriction and intermittent fasting alter spectral measures of heart rate and blood pressure variability in rats,” FASEB Journal, vol. 20, no. 6, pp. 631–637, 2006.
[172]  M. P. Mattson, “Energy intake, meal frequency, and health: a neurobiological perspective,” Annual Review of Nutrition, vol. 25, pp. 237–260, 2005.
[173]  S. Sharma and G. Kaur, “Neuroprotective potential of dietary restriction against kainate-induced excitotoxicity in adult male Wistar rats,” Brain Research Bulletin, vol. 67, no. 6, pp. 482–491, 2005.
[174]  M. P. Mattson, “Dietary factors, hormesis and health,” Ageing Research Reviews, vol. 7, no. 1, pp. 43–48, 2008.
[175]  M. P. Mattson, W. Duan, R. Wan, and Z. Guo, “Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations,” NeuroRx, vol. 1, no. 1, pp. 111–116, 2004.
[176]  O. Froy, N. Chapnik, and R. Miskin, “Effect of intermittent fasting on circadian rhythms in mice depends on feeding time,” Mechanisms of Ageing and Development, vol. 130, no. 3, pp. 154–160, 2009.
[177]  H. Yanagihara, H. Ando, Y. Hayashi, Y. Obi, and A. Fujimura, “High-fat feeding exerts minimal effects on rhythmic mRNA expression of clock genes in mouse peripheral tissues,” Chronobiology International, vol. 23, no. 5, pp. 905–914, 2006.
[178]  A. Kohsaka, A. D. Laposky, K. M. Ramsey et al., “High-fat diet disrupts behavioral and molecular circadian rhythms in mice,” Cell Metabolism, vol. 6, no. 5, pp. 414–421, 2007.
[179]  M. Barnea, Z. Madar, and O. Froy, “High-fat diet delays and fasting advances the circadian expression of adiponectin signaling components in mouse liver,” Endocrinology, vol. 150, no. 1, pp. 161–168, 2009.
[180]  M. Barnea, Z. Madar, and O. Froy, “High-fat diet followed by fasting disrupts circadian expression of adiponectin signaling pathway in muscle and adipose tissue,” Obesity, vol. 18, no. 2, pp. 230–238, 2010.
[181]  P. Cano, V. Jimenez-Ortega, A. Larrad, C. F. R. Toso, D. P. Cardinali, and A. I. Esquifino, “Effect of a high-fat diet on 24-h pattern of circulating levels of prolactin, luteinizing hormone, testosterone, corticosterone, thyroid-stimulating hormone and glucose, and pineal melatonin content, in rats,” Endocrine, vol. 33, no. 2, pp. 118–125, 2008.
[182]  M. C. Cha, C. J. Chou, and C. N. Boozer, “High-fat diet feeding reduces the diurnal variation of plasma leptin concentration in rats,” Metabolism: Clinical and Experimental, vol. 49, no. 4, pp. 503–507, 2000.
[183]  P. J. Havel, R. Townsend, L. Chaump, and K. Teff, “High-fat meals reduce 24-h circulating leptin concentrations in women,” Diabetes, vol. 48, no. 2, pp. 334–341, 1999.
[184]  J. Mendoza, P. Pévet, and E. Challet, “High-fat feeding alters the clock synchronization to light,” Journal of Physiology, vol. 586, no. 24, pp. 5901–5910, 2008.
[185]  M. Hatori, C. Vollmers, A. Zarrinpar, et al., “Time-restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high-fat diet,” Cell Metabolism, vol. 15, pp. 848–860, 2012.

Full-Text

comments powered by Disqus