Circadian rhythms and appetite: Difference between revisions

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Several epidemiologic studies have showing sleep deprivation to elevate the levels of the appetite stimulating hormone ghrelin and decrease circulating leptin levels [Fig. 1] <ref> Taheri ''et. al'' (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. ''PLoS Medicine'' '''1'''(3):e62.</ref><ref name=Spiegel04/>.  These changes in appetite regulatory hormones could be the causes of increased food intake in these sleep deprived adults where a rise in body weight is also observed [Fig. 2] <ref name=Taheri04/>.
Several epidemiologic studies have showing sleep deprivation to elevate the levels of the appetite stimulating hormone ghrelin and decrease circulating leptin levels [Fig. 1] <ref name=Taheri04> Taheri ''et. al'' (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. ''PLoS Medicine'' '''1'''(3):e62.</ref><ref name=Spiegel04/>.  These changes in appetite regulatory hormones could be the causes of increased food intake in these sleep deprived adults where a rise in body weight is also observed [Fig. 2] <ref name=Taheri04/>.


   
   

Revision as of 09:01, 12 October 2010

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This article is currently being developed as part of an Eduzendium student project in the framework of a course entitled Appetite and Obesity at University of Edinburgh. The course homepage can be found at CZ:(U00984) Appetite and Obesity, University of Edinburgh 2010.
For the course duration, the article is closed to outside editing. Of course you can always leave comments on the discussion page. The anticipated date of course completion is 01 February 2011. One month after that date at the latest, this notice shall be removed.
Besides, many other Citizendium articles welcome your collaboration!


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Begin your article with a brief overview of the scope of the article on interest group. Include the article name in bold in the first sentence.[1]

Remember you are writing an encyclopedia article; it is meant to be readable by a wide audience, and so you will need to explain some things clearly, without using unneccessary jargon. But you don't need to explain everything - you can link specialist terms to other articles about them - for example adipocyte or leptin simply by enclosing the word in double square brackets.

You can write your article directly onto the wiki- but at first you'll find it easier to write it in Word and copy and paste it onto the wiki.

Construct your article in sections and subsections, with headings and subheadings like this:

Introduction

The control of food intake is a flexible system whereby internal and external environmental cues can alter the timing of feeding and appetite. The suprachiasmatic nucleus in the hypothalamus is the vital coordinator of these stimuli that ultimately generates known as circadian rhythms.

Circadian rhythms are driven by the light and dark cycles of the earth which through alteration of gene expression elicit a host of physiological responses including fluctuations in the hormones involved in appetite and food intake.

It has been well documented that food intake itself can regulate these rhythms and yet the neural mechanisms by which this occurs remains elusive. It has recently been proposed that there exists a ‘food entrainable oscillator’ that exists independently from the SCN which controls food anticipation activity.

Various factors such as have been known to influence circadian rhythms indeed our modern day lifestyle has highlighted new factors that influence these delicate balances including jet-lag and shift work.

SCN, the biological clock

Suprachiasmatic Nucleus

Suprachiasmatic nucleus of the anterior hypothalamus is the main regulator of circadian rhythms. SCN is made of neuronal and glial cells, with most of the neurons being GABAergic. Main input into SCN is light. Light is transmitted from retina via the retinohypothalamic tract to SCN. (Froy, 2010) Vasoactive intrinsic polypeptide in SCN activates and synchronises SCN neurons and coordinates behavioural rhythms. SCN signals to peripheral oscillators using the following actors: TGFα, prokinecticin 2 and cardiotrophin like cytokine and neuronal connections to prevent dampening of circadian rhythms in the tissues. (Froy, 2010) SCN efferent fibres terminate around the arcuate nucleus of ventromedial hypothalamus (VMH) and paraventricular nucleus PVN, areas involved in regulation of food intake and corticosteroid release. (Froy, 2010) SCN innervates sub-paraventricular zone (SPZ) and dorsomedial hypothalamus (DMH) which in-turn innervate PVN and lateral hypothalamus, areas which regulate corticosteroid release and wakefulness / feeding cycle. (Froy, 2010) DMH regulates sleep-wakefulness and feeding cycles among others and degeneration of DMH results in severe impairment of those cycles. (Froy, 2010) SCN selectively innervates preautonomic nervous system neurons found in dorsal and ventral borders of PVN.As pre-autonomic neurons in the hypothalamus are connected to sympathetic and parasympathetic system, this allows SCN to control energy homeostasis. (Froy, 2010) SCN receives information on hormones and metabolites, which are present in the bloodstream and cannot cross blood-brain barrier, via its dense reciprocal interactions with ventromedial arcuate nucleus (vmARC). vmARC receives the above information through its connection with circumventricular median eminence. Circumventricular median eminence is a structure within the brain which is free of blood-brain barrier and hormones can easily reach their receptors on neurons. Gastrin-releasing peptide interacts with SCN and results in light-like resetting of SCN. (Froy, 2010)

Clock Genes

Princess Fiona

Sleep deprivation, shift-work and appetite

In modern society, where shopping, eating, working and drinking are widely available 24hours a day, major health implications have been linked as a result. This availability of around the clock activities has defied our bodies internal clock of the vital hours of sleep it requires [2]. Over the last few decades where technology and social activities has dramatically advanced, the number of hours of sleep young adults get has decreased within the range of 1-2hours [3]. This is strongly correlated with the prevalence of obesity within the U.K which has shown to have trebled over the last 3 decades [4]. Although the rise in this obesity epidemic has been shown to be multi-factorial, sleep deprivation is just another factor to add to the list needing to be addressed in this ever rising health problem.


Figure 1. The relationship between sleep duration and changes in serum leptin and ghrelin levels. (a) Mean leptin levels against average nightly sleep duration. As the number of hours sleep increases the levels of serum leptin also increases. Standard errors for half-hour increments of average nightly sleep. (b) Mean ghrelin levels against total number of hours sleep. As the total number of hours sleep decreases, the mean levels of ghrelin increases. Standard errors for half-hour increments of total sleep time. This figure has been adapted from Taheri et. al (2004).


Several epidemiologic studies have showing sleep deprivation to elevate the levels of the appetite stimulating hormone ghrelin and decrease circulating leptin levels [Fig. 1] [5][3]. These changes in appetite regulatory hormones could be the causes of increased food intake in these sleep deprived adults where a rise in body weight is also observed [Fig. 2] [5].


Figure 2. The relationship between average nightly sleep and changes in body mass index (BMI). As the average nightly hours of sleep decreases below 7 hours, the mean BMI increases. Furthermore, more than an average of 8 hours sleep also causes a rise in mean BMI. Standard errors for 45-min intervals of average nightly sleep. This figure has been adapted from Taheri et. al (2004).

Conclusion

etc.

About References

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<ref>Person A ''et al.''(2010) The perfect reference for subpart 1 ''J Neuroendocrinol'' 36:36-52</ref> <ref>Author A, Author B (2009) Another perfect reference ''J Neuroendocrinol'' 25:262-9</ref>.

Look at the reference list below to see how this will look.[6] [7]

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Select your references carefully - make sure they are cited accurately, and pay attention to the precise formatting style of the references. Your references should be available on PubMed and so will have a PubMed number. (for example PMID: 17011504) Writing this without the colon, (i.e. just writing PMID 17011504) will automatically insert a link to the abstract on PubMed (see the reference to Johnsone et al. in the list.) [8]

Use references sparingly; there's no need to reference every single point, and often a good review will cover several points. However sometimes you will need to use the same reference more than once.


How to write the same reference twice:

Reference: Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431 PMID 17072591

First time: <ref name=Berridge07>Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. ''Psychopharmacology'' 191:391–431 PMID 17072591 </ref>

Second time:<ref name=Berridge07/>

This will appear like this the first time [9] and like this the second time [9]

Figures and Diagrams

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References

  1. See the "Writing an Encyclopedia Article" handout for more details.
  2. Gimble J.M. et. al (2009) Circadian biology and sleep: missing links in obesity and metabolism? Obesity Reviews 10(suppl 2):1-5.
  3. 3.0 3.1 Spiegel 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.
  4. Rennie K.L. & Jebb S.A. (2005) Prevalence of obesity in Great Britain. Obesity Reviews 6:11-12.
  5. 5.0 5.1 Taheri et. al (2004) Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Medicine 1(3):e62.
  6. Person A et al. (2010) The perfect reference for subpart 1 J Neuroendocrinol 36:36-52
  7. Author A, Author B (2009) Another perfect reference J Neuroendocrinol 25:262-9
  8. Johnstone LE et al. (2006)Neuronal activation in the hypothalamus and brainstem during feeding in rats Cell Metab 2006 4:313-21. PMID 17011504
  9. 9.0 9.1 Berridge KC (2007) The debate over dopamine’s role in reward: the case for incentive salience. Psychopharmacology 191:391–431 PMID 17072591