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Effects of stress hormones on energy balance and metabolic diseaseSupervisor

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

Project Description

The prevalence of obesity continues to increase at an alarming rate, associated with marked increases in diabetes and cardiovascular disease (CVD). This has been largely attributed to changes in lifestyle, including the consumption of highly palatable and energy-dense foods and reduced physical activity. More recently, stress has been recognised as an important contributor to these rising disease rates (1).

Increased levels of stress hormones (glucocorticoids) associate with obesity (particularly abdominal obesity) and metabolic diseases such as diabetes and CVD. Glucocorticoids promote redistribution of body fat, stimulate liver glucose production and oppose the actions of insulin, leading to insulin resistance. In addition to these peripheral effects, glucocorticoids can act within the brain to stimulate food intake and have the potential to regulate glucose homeostasis via neuropeptide circuitry in the hypothalamus (2).

The aim of this project is to examine mechanisms by which stress and over-exposure to glucocorticoids lead to obesity and metabolic disease (3). We have a long-standing interest in the hypothalamic regulation of appetite (4, 5), which will form a key part of these studies. We will use animal models of stress or glucocorticoid exposure and/or dietary manipulations (e.g. high fat feeding) to investigate effects on genes within the brain that regulate feeding, satiety and glucose homeostasis. Cell models will also be used to investigate neuronal responses to glucocorticoids at the cellular level. Molecular tools will include qRT-PCR, Western blotting, immunohistochemistry, in-situ analysis, chromatin immunoprecipitation and AAV knockdown of genes.

Overall, this project will investigate novel mechanisms by which stress impacts on regulation of food intake and energy balance, leading to development of metabolic disease.

Funding Notes

This project has a Band 3 fee. Details of our different fee bands can be found on our website. For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website. Informal enquiries may be made directly to the primary supervisor.

References

1. Bose M, Olivan B, Laferrere B (2009) Stress and obesity: the role of the hyopthalamo-pituitary-adrenal axis in metabolic disease. Current Opinion in Endocrinology, Diabetes and Obesity 16(5):340-6

2. Yi CX, Foppen E, Abplanalp W, Gao Y, Alkemade A, la Fleur SE, Serlie MJ, Fliers E, Buijs RM, Tschop MH, Kalsbeek A (2012). Glucocorticoid signaling in the arcuate nucleus modulates hepatic insulin sensitivity. Diabetes 61(2):339-45

3. Harno E, Cottrell EC, Keevil BG, DeSchoolmeester J, Bohlooly-Y M, Anderssen H, Turnbull AV, Leighton B, White A (2013). 11-Dehydrocorticosterone Causes Metabolic Syndrome, Which Is Prevented when 11-HSD1 is Knocked Out in livers of male mice. Endocrinology 154(10):3599-609

4. Pritchard LE, Oliver RL, McLoughlin JD, Birtles S, Lawrence CB, Turnbull AV & White A (2003) Pro-opiomelanocortin (POMC) derived peptides in rat cerebrospinal fluid (CSF) and hypothalamic extracts: evidence that secretion is regulated with respect to energy balance. Endocrinology 144 (3):760-6

5. Pritchard L E and White A (2007) Minireview: Neuropeptide Processing and Its Impact on Melanocortin Pathways. Endocrinology 148 (9): 4201-7

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