Circadian rhythms and appetite/Bibliography

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A list of key readings about Circadian rhythms and appetite.
Please sort and annotate in a user-friendly manner. For formatting, consider using automated reference wikification.

Ishida et.al, 1999 “Biological clocks” Proc. Natl. Acad. Sci. USA. 96(16):8819–8820 (The above review focuses on genes between species that are responsible for determining the circadian behaviour, particularly on switch genes which regulate function of many circadian rhythm genes. This summary establishes molecular mechanism of biological clock in humans.)


Turek et.al, 2005 “Obesity and Metabolic Syndrome in Circadian Clock mutant mice” Science 308: 1043-45 (The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus. The knockout studies have determined the precise effect of Clock gene products on feeding behaviour and rhythmicity in behaviour.)

Froy, O 2010 “Metabolism and Circadian Rhythms - Implications for Obesity” Endocrine Reviews 31:1-24. (The review consistently explains the effect of circadian rhythm and feeding behaviour. The circadian clock has been reported to regulate metabolism and energy homeostasis in the liver and other peripheral tissues. This is achieved by mediating the expression and/or activity of certain metabolic enzymes and transport systems and their interaction with suprachiasmatic nucleus (SCN), the core clock mechanism.)

Schibler, U. et al. (2002) A Web of Circadian Pacemakers. Cell 111: 919-922 (It’s a nice minireview discussing the role of circadian pacemakers and their interactions, useful of background information.)

Feillet, C. A. (2010) Food for Thoughts: Feeding Time and Hormonal Secretion. Journal of Neuroendocrinology 22:620-628 (Discuses the influence of hormones on feeding behaviour in mice)

Yannielli, P. C. et al. (2007) Ghrelin Effects on the Circadian System of Mice. The Journal of Neuroscience 27(11):2890-2895. (Useful for discussing how hormones can feedback and influence the SCN regulation and ultimately feeding times).

Shea, S. et al. (2005) Independent Circadian Sleep/Wake Regulation of Adippokines and Glucose in Humans. The Journal of Clinical Endocrinology & Metabolism. 90:2537-2544 (A useful study looking at hormone fluctuations in humans that are involved in food intake regulation: "Our data imply that alterations in the sleep/wake schedule would lead to an increased daily range in the circulating leptin.. which by influencing food intake and energy balance could be implicated in the increased prevalence of obesity in the shift work population.")

Mendoza J. & Challet E. (2009) Brain Clocks: From the Suprachiasmatic Nuclei to a Cerebral Network. The Neuroscientist 15: 5 (“The daily variations of physiology and behavior are controlled by a highly complex system comprising of a master circadian clock in the suprachiasmatic nuclei (SCN) of the hypothalamus, extra-SCN cerebral clocks, and peripheral oscillators…. pathophysiological alterations of internal timing that are deleterious for health may result from internal desynchronization within the network of cerebral clocks.”)


Escobar C. et. al (2009) Peripheral oscillators: the driving force for food-anticipatory Activity. European Journal of Neuroscience, 30: 1665–1675 (“In this review, which is aimed especially at discussing the contribution of the peripheral oscillators, we have put together the accumulating evidence that the clock gene machinery as we know it today is not sufficient to explain food entrainment… food entrainment is initiated by a repeated metabolic state of scarcity that drives an oscillating network of brain nuclei in interaction with peripheral oscillators.”)


Mistleberger E. & Marchant E. (1999) Enhanced Food-Anticipatory Circadian Rhythms in the Genetically obese Zucker Rat. Physiology & Behaviour 66(2): 329-335 (“…the central actions of leptin may mediate the inhibitory effects of obesity on the expression of food-anticipatory rhythms in rats, but do not mediate the inhibitory effects of ad lib food access, and do not serve as necessary internal entrainment cues or clock components for the food entrainable circadian system.”)


Mendoza J. (2006) Circadian Clocks: Setting Time by Food. Journal of Neuroendocrinology 19: 127-137 (“…the reward and motivational value of food can also be a potent synchroniser for the SCN clock. This suggests that energy metabolism and motivational properties of food can influence the clock mechanism of the SCN.")

Gimble J.M. et. al (2009) Circadian biology and sleep: missing links in obesity and metabolism? Obesity Reviews, 10(suppl 2):1-5 (This is a good review, highlighting “…circadian biology at the basic and clinical levels in the context of nutrition, obesity and sleep medicine… questions presented by the changing interface between technology, lifestyle and biological rhythms.”)


Kalsbeek et al.(2007) Minireview: Circadian Control of Metabolism by the Suprachiasmatic Nuclei. Endocrinology 2007 148:5635-5639


Rennie K.L. & Jebb S.A. (2005) Prevalence of obesity in Great Britain. Obesity Reviews, 6:11-12 (“Since 1980 the prevalence of obesity in Great Britain in adults has almost trebled.”)

Spiegel K. et. al (2004) Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141:846-50. (“Sleep restriction was associated with average reductions in the anorexigenic hormone leptin (decrease, 18%; P = 0.04), elevations in the orexigenic factor ghrelin (increase, 28%; P < 0.04), and increased hunger (increase, 24%; P < 0.01) and appetite (increase, 23%; P = 0.01)… Short sleep duration in young, healthy men is associated with decreased leptin levels, increased ghrelin levels, and increased hunger and appetite.”)

Taheri S. et. al (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Medicine, 1(3):e62. (“…Participants underwent nocturnal polysomnography and reported on their sleep habits through questionnaires and sleep diaries. Following polysomnography, morning, fasted blood samples were evaluated for serum leptin and ghrelin, two key opposing hormones in appetite regulation… Relationships among these measures, BMI, and sleep duration (habitual and immediately prior to blood sampling) were examined… A U-shaped curvilinear association between sleep duration and BMI was observed… Participants with short sleep had reduced leptin and elevated ghrelin. These differences in leptin and ghrelin are likely to increase appetite, possibly explaining the increased BMI observed with short sleep duration…”)