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Rhythmic control of energy balance - to understand how our internal clocks regulate energy metabolism


Project Description

24-hour rhythms are present in virtually all aspects of our behaviour and physiology. These rhythms are underpinned by circadian clocks that run throughout the body, and act within each tissue to orchestrate many organ functions and rhythmic activities (e.g. glucose homeostasis in the liver). In mammals, circadian timing is headed by a ’master clock’ located in a small area of the brain called the suprachiasmatic nucleus (SCN). The SCN synchronises clocks in the rest of the body, so that functioning of different organ systems are coordinated with each other. It has recently become clear that our circadian clocks are intimately linked to energy metabolism, and diminished circadian rhythmicity is now considered a hallmark feature of metabolic diseases such as obesity and diabetes. It is therefore critical that we understand how our internal clocks regulate energy metabolism, and how a disruption of circadian timing may contribute to metabolic disease.

In many tissues, circadian clock genes (the machinery that drives the clock) are closely connected to metabolic pathways. Importantly this connection is reciprocal, meaning that the clock not only drives the rhythmic activity of key metabolic genes, but is itself strongly influenced by metabolism and cellular energy status. For example, when nocturnal laboratory mice are forced to feed only during the day, many aspects of their physiology become disconnected from the SCN, which remains locked to environmental light cycles. Thus, the strong influence of diet and eating behaviour on circadian clocks suggests that abnormal energy supply (over consumption of high-calorie foods, or disordered eating habits) will be effective at dampening circadian control of metabolism. This raises three important questions: 1) are some of our body clocks particularly susceptible to diet-induced disruption; 2) how does the loss of clock function within these ’susceptible’ clocks impact on overall metabolic or behavioural rhythms; 3) what critical components form the clock-metabolic interface in such tissues. We welcome applications from students wishing to examine these questions.

Funding Notes

Applications are invited from self-funded students. This project has a Band 3 fee. Details of our different fee bands can be found on our website (View Website). For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (View Website).

As an equal opportunities institution we welcome applicants from all sections of the community regardless of gender, ethnicity, disability, sexual orientation and transgender status. All appointments are made on merit.

Informal enquiries may be made directly to the primary supervisor.

References

Bechtold DA, Loudon AS (2013) Hypothalamic clocks and rhythms in feeding behaviour. Trends Neurosci. 36(2):74-82.

Li J, Hand LE, Meng QJ, Loudon AS, Bechtold DA (2011) GPR50 Interacts with TIP60 to Modulate Glucocorticoid Receptor Signalling. PLoS One 6(8):e23725.

Bechtold DA, Gibbs JE, Loudon AS. (2010) Circadian dysfunction in disease. Trends Pharmacol Sci 31(5):191-8.

Meng QJ*, Maywood ES*, Bechtold DA*, Lu WQ, Li J, Gibbs JE, Chesham J, Rajamohan F, Knafels F, Ohren JF, Walton KM, Wager TT, Hastings MH, Loudon AS. (2010) Entrainment of disrupted circadian behavior through inhibition of CK1 enzymes. PNAS 107(34):15240-5

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