Hanne Sørup Tastesen:
Dietary protein in the prevention of diet‐induced obesity and co‐morbidities

Date: 15-05-2014    Supervisor: Karsten Kristiansen & Lise Madsen

Background: Obesity and related co‐morbidities are increasing problems worldwide and nutritional approaches to prevent and alleviate these diseases are thus of great interest. High‐protein diets have been shown to prevent and alleviate obesity and co‐morbidities in rodents and humans through increased energy expenditure and satiety. Similarly, protein from different sources and in different forms has been shown to modulate obesity and co‐morbidities. However, the impact of protein from different sources consumed at normal dietary levels remains to be further elucidated. Obesity‐prone C57BL/6J mice were fed obesity‐promoting diets with protein from different sources, in different forms and at different levels to evaluate the affect on development of obesity, glucose intolerance and dyslipidemia.

Results: In the present study the dietary level of protein, 16 versus 32 percent energy from protein, was found to be negligible in development of obesity and co‐morbidities in mice. Seafood protein with high endogenous taurine and glycine contents was found to prevent diet‐induced adiposity and dyslipidemia, both in ad libitum and pair‐fed settings. The ability of seafood proteins to prevent these metabolic disturbances was found to associate with the high endogenous taurine and glycine concentrations and to concur with increased energy expenditure and a tendency towards increased voluntary locomotor activity. Consumption of a seafood protein‐mixture prevented diet‐induced development of obesity as compared to intake of chicken filet and preserved glucose tolerance compared to casein intake. Hydrolyzed casein was shown to prevent obesity compared to intact casein, which was associated with increased spontaneous locomotor activity in hydrolyzed casein‐fed mice. No increase in energy expenditure, as assessed by indirect calorimetry, was observed after four weeks, but after eight weeks adaptations towards increased energy expenditure‐capacity was present concurrent with altered energy substrate utilization in hydrolyzed caseinfed mice compared to mice fed the intact protein.

Conclusions: We found that the source and form of protein has great impact on development and prevention of diet‐induced adiposity, dyslipidemia, hyperinsulinemia and impairment of glucose tolerance through modulations of voluntary locomotor activity, energy expenditure and energy substrate metabolism in mice.