Effect of large bowel fermentation on insulin, glucose, free fatty acids, and glucagon-like peptide 1 (7-36) amide in patients with coronary heart disease

Insulin resistance syndrome has recently been described as a unifying hypot hesis to explain the relationship between the many risk factors of coronary heart disease. Carbohydrate that is malabsorbed and fermented in the colon has been demonstrated to decrease insulin response to a glucose load and i mprove other risk factors associated with coronary heart disease, although the mechanism remains unclear. The object of the present study was to inves tigate whether this observation could be explained by the production of fer mentation products induced by malabsorbed carbohydrate in the colon, or by stimulating the incretin glucagon-like peptide 1 (7-36) amide that is relea sed from the large bowel. We used lactulose as a model for resistant starch carbohydrate. Ten insulin-resistant male volunteers, who had undergone pre vious coronary artery bypass grafting, volunteered to take part in the stud y and underwent 6 d of lactulose loading (15 g/d for 2 d and 30 g/d for 4 d ). There was no significant change in insulin, glucose, free fatty acids, o r glucagon-like peptide 1 (7-36) amide response to an oral glucose toleranc e test following the lactulose despite a significant rise in breath hydroge n. Large bowel fermentation stimulated by lactulose appears to have no sign ificant effect on insulin, glucose, free fatty acids, and glucagon-like pep tide 1 (7-36) response in patients with coronary heart disease. Nutrition 1 999;15:183-188. (C)Elsevier Science Inc. 1999.