These results suggest that HFS diet intake results in higher bone mass in aged rats.
Such effects of HFS diet intake might have been induced by increased body weight.
However, the commercial diet had significantly higher basal diet intake compared to other experimental diets.
Rats were allowed to recover until liquid diet intake stabilized (at least 1 week) and were then returned to a standard chow diet.
Saitoh, S., Shimomura, Y. & Suzuki, M. Effect of a high-carbohydrate diet intake on muscle glycogen repletion after exercise in rats previously fed a high-fat diet.
Although moderate ethanol challenge failed to alter cardiomyocyte mechanical property under low fat diet intake, it accentuated high fat diet intake-induced changes in cardiomyocyte contractile function and intracellular Ca2+ handling.
Taken together, our results suggest that PTP1B knockout offers cardioprotection against high fat diet intake through activation of AMPK.
High fat diet intake triggered obesity, hyperinsulinemia, and hypertriglyceridemia, the effects of which were unaffected by catalase transgene.
However, the aim of this was not to evaluate the food intake per se, but to establish that the diet intake did not change significantly between the run-in and intervention periods.
High fat diet intake induced obesity, systemic glucose intolerance, cardiac hypertrophy, dampened metabolic ability, cardiac and intracellular Ca2 + derangements, the effects of which were accentuated by APN knockout.
Neither high fat diet intake nor moderate ethanol challenge affected protein or mRNA levels as well as phosphorylation of Akt and GSK3β in mouse hearts.
