Eating -- particularly eating fat-rich foods -- causes cells in the small intestine to produce a hormone called cholecystokinin, or CCK. CCK stimulates digestion and gut peristalsis (the motion that propels food along the digestive tract), and also triggers satiation -- the full feeling that prompts you to stop eating.

The study by Luyer and colleagues shows that fat-induced CCK can also dampen inflammation in the gut, as rats fed a high-fat diet were protected against lethal bacteria-induced shock whereas those fed a low-fat diet were not. CCK sent signals to the brain through the vagus nerve, the nerve that provides the electrical regulation for many internal organs, including the gut and the heart. In response to CCK, vagus nerve endings in the gut released a neurotransmitter called acetylcholine. Acetylcholine then bound to proteins on immune cells and turned the cells off.

The authors think this pathway might explain why the immune system doesn't react to food proteins and normal gut bacteria as if they were foreign invaders. They also suggest that triggering this fat-driven chain of events in patients might provide a way to reduce inflammatory complications after surgery.

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While all the exercise groups saw improvements in peak VO2 and TTE after completing their exercise regimens, the researchers noticed some interesting trends.

"We found that when we compared the low amount/moderate intensity group to the low amount/vigorous intensity group, we did not see a significant improvement in peak oxygen consumption," Duscha said. "However, when we increased the amount of exercise from 12 to 20 miles “ at the same intensity “ we did see an improvement in peak oxygen consumption."

Also, although no statistically significant difference was detected between the low amount/moderate intensity group and the low amount/high intensity group, the researchers did see a trend toward both a separate and combined effect of exercise intensity and amount on increased peak VO2 levels.

The Duke team was led by cardiologist William Kraus, M.D., who received a $4.3 million grant from the National Heart, Lung and Blood Institute in 1998 to investigate the effects of exercise on sedentary overweight adults at risk for developing heart disease and/or diabetes. The results of that five-year trial, known as STRRIDE (Studies of Targeted Risk Reduction Interventions through Defined Exercise), and other analyses of the data collected, began to be published in 2002.

The Duke team is currently enrolling patients in STRRIDE II, in which researchers are seeking to determine the effects of weight training, alone and in combination with aerobic training, on cardiovascular health.

Joining Duscha were Duke colleagues Cris Slentz, Ph.D., Johanna Johnson, Daniel Bensimhon, M.D., and Kenneth Knetzger. Joseph Houmard, Ph.D., East Carolina University, was also a member of the team.

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