Abstract
Palatable foods lead to overeating, and it is almost a forgone conclusion that it is also an important contributor to the current obesity epidemic - there is even talk about food addiction. However, the cause-effect relationship between taste and obesity is far from clear. As discussed here, there is substantial evidence for altered taste sensitivity, taste-guided liking and wanting, and neural reward processing in the obese, but it is not clear whether such traits cause obesity or whether obesity secondarily alters these functions. Studies with calorie restriction-induced weight loss and bariatric surgery in humans and animal models suggest that at least some of the obesity-induced alterations are reversible and consequently represent secondary effects of the obese state. Thus, both genetic and non-genetic predisposition and acquired alterations in taste and reward functions appear to work in concert to aggravate palatability-induced hyperphagia. In addition, palatability is typically associated with high energy content, further challenging energy balance regulation. The mechanisms responsible for these alterations induced by the obese state, weight loss, and bariatric surgery, remain largely unexplored. Better understanding would be helpful in designing strategies to promote healthier eating and prevention of obesity and the accompanying chronic disease risks.