A low dietary intake of cod protein is sufficient to increase growth, improve serum and tissue fatty acid compositions, and lower serum postprandial glucose and fasting non-esterified fatty acid concentrations in obese Zucker fa/fa rats
Studies in rats suggest that fish proteins may improve lipid and glucose regulation and could thus be a potential tool in the treatment of obesity-related comorbidities. To date, all published rat studies on dietary fish protein have been designed with 50 or 100 % of dietary proteins from fish. As it is not common, nor advised, to consume fish as the only protein source in a healthy diet, mechanistic studies on the effects of diets with low dose fish proteins are needed. Here, we investigate whether a low dose of cod protein would affect glucose homeostasis and lipid metabolism in obese Zucker fa/fa rats.
Twelve male obese Zucker fa/fa rats consumed diets where cod proteins accounted for 25 % of the total protein intake with the remaining 75 % from casein (COD) or 100 % of protein as casein (CAS) for 4 weeks.
Rats fed COD achieved a higher body weight without affecting adiposity and thigh muscle mass after 4 weeks, but liver weight and hepatic cholesterol level were higher than in CAS-fed rats. Fasting serum level of non-esterified fatty acids and 2 h postprandial glucose level were lower in COD than in CAS. The fatty acid metabolism was beneficially affected by the COD diet, with e.g., higher ratio of n-3/n-6 PUFAs in serum, liver and adipose tissue when compared to CAS.
A low intake of cod protein (25 % of protein intake) was sufficient to beneficially affect lipid metabolism and postprandial glucose regulation in obese fa/fa rats.
KeywordsObesity Fish protein Insulin Tumor necrosis factor-alpha Inflammation
The present research has been supported by funding from the Bergen Medical Research Foundation.
Conflict of interest
I.H. is a minor shareholder in Seagarden AS. The other authors declare no conflicts of interest.
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