The increased prevalence of obesity in our society is a cause for serious concern. Although
lifestyle and diet changes are successful ways to lose weight, a high percentage of people
weight cycle, also known as “yoyo” dieting. Evidence suggests weight cycling is no more
detrimental to a person’s health than remaining obese, but there still remains speculation over
the mechanisms involved in weight regain. One such model proposes the “food addiction”
model, whereby a deficit in reward function can lead to a blunted reward response to eating,
leading to over consumption.
In this thesis, I aim to clarify the role of mesolimbic dopamine signalling. Firstly, a short, medium
and chronic high fat (HF) feeding study was used to assess the development of changes in
dopamine signalling. Secondly, to assess the effects of a single weight cycle on dopamine
signalling, mice were fed control or HF diets, and swapped diet every 6 weeks. Finally, to assess
the effect of rapid weight change, lean and DIO mice swapped to a HF diet or control diet for a
week, respectively.
Chronic HF diet increased dopamine-related gene expression and showed a similar expression
profile as short term HF feeding. Medium term HF feeding on the other hand showed a decrease
in dopamine related gene expression. Weight cycling appeared to have no clear uniform effect
on dopamine-related gene expression.
Rapid weight gain showed little change in dopamine-related gene expression in the reward
areas. Conversely, rapid weight loss induced a decrease in tyrosine hydroxylase (TH) and
dopamine receptor 2 (D2R) mRNA in the VTA, but with little change elsewhere.
In conclusion, my data does not support the “food addiction” model of changes in dopamine
signalling contributing to obesity. Similarly, there appears to be little effect on dopamine gene
expression with rapid changes in body weight.