Circadian rhythms and appetite

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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)

Sleep deprivation, shift-work and appetite

In modern society, where shopping, eating, working and drinking are widely available 24hours a day,

PD Diagram
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).

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 . 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 . This is strongly correlated with the prevalence of obesity within the U.K which has shown to have trebled over the last 3 decades . 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 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).

Several epidemiologic studies have showing sleep deprivation to elevate the levels of the appetite stimulating hormone ghrelin and decrease circulating leptin levels [Fig. 1] . 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] .

Conclusion

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