Exploring the causes of obesity development and obesity resistance
- Research Opportunity
- Honours students
- Number of Honour Places Available
- Department / Centre
- Medicine and Radiology
- Austin Health
|Dr Barbara Famfirstname.lastname@example.org||Personal web page|
|A/Professor Sof Andrikopoulosemail@example.com||Personal web page|
|Dr Evelyn Marinfirstname.lastname@example.org|
Summary The global obesity epidemic is worsening both here in Australia and in other Westernised countries and it is clear that current therapies, particularly those involving public health measures are ineffective in curbing this surge
The global obesity epidemic is worsening both here in Australia and in other Westernised countries and it is clear that current therapies, particularly those involving public health measures are ineffective in curbing this surge. There is much evidence in the literature to suggest that this epidemic is not solely due to individuals over-eating and not exercising adequately, but powerful biological factors existing that increase the chances of developing obesity when in an environment of plentiful and calorie rich foods. We have developed a mouse model of diet-induced obesity in which there is a clear divergence of the population into those that are prone to weight gain whilst on a high-energy dense (HED) diet and those that are resistant to this diet. We have evidence that changes in nutrient specific gut receptor expression (involved in gut microbiota action) rather than central changes may be more closely linked to the differences in body weight gain responses. Our unique mouse model allows us to further unravel other metabolic consequences obesity proneness and in particular obesity resistance. By characterizing these features that create this metabolic profiling, we will gain critical insights and generate important new knowledge about obesity development that are likely to lead to new approaches for future obesity management.
School Research Themes
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Department / Centre
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Research NodeAustin Health
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