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Obesity, type 2 diabetes and the thrifty genotype hypothesis


Bristol Medical School

About the Project

Rationale
The thrifty genotype hypothesis suggests that certain populations may have an inherent genetic predisposition to promote fat storage. This is a distinct survival advantage during times of scarcity or famine, but in a modern environment of plenty and prosperity, this same genotype can engender the public health disaster that is the obesity epidemic.

The fat sand rat (Psammomys obesus) is an excellent experimental model for the thrifty gene phenomenon. Psammomys obesus is a terrestrial rodent of the gerbil subfamily that usually lives in sandy deserts. Fat sand rats live in burrows, which are often located under the bushes on which they forage, which have little nutritional value. Under these conditions of scarcity, the fat sand rats remain lean. However, when fed a diet of normal laboratory rodent chow they become obese .

Feeding and fat metabolism are governed by a dialogue between the brain and adipose tissues. This dialogue goes wrong in obesity; food is consumed in excess of bodily energy requirements, with the excess energy stored as adipose tissue. A number of brain regions have been strongly implicated in this dialogue. In this study, we will focus on two key regions in the hypothalamus – the arcuate nucleus (ARC) and the paraventricular nucleus (PVN).

Aims & Objectives
Hypothesis - that the thrifty genotype of the fat sand rat engenders distinct patterns of gene expression in adipose tissues and in brain regions responsible for appetite and adiposity. Using RNA sequencing, the student will ask how the white fat, brown fat, ARC and PVN transcriptomes of male Psammomys obesus respond to plenty compared to scarcity.

Methods
*Husbandry and physiological analysis of adult fat sand rats
* Illumina deep sequencing (RNAseq)
*Bioinformatic analysis of RNAseq datasets and systems analysis
*Expression validation using qPCR, in situ hybridisation, Western blotting and immunocytochemistry.

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