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1 Ceriello A: The possible role of postprandial hyperglycaemia in the pathogenesis of diabetic complications. Diabetologia 2003;46(suppl 1):M9-M16.

2 Liu S, Willet W, Stampfer M, et al: Prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr 2000;71:1455-1461.

3 Bonora E, Muggeo M: Postprandial blood glucose as a risk factor for cardiovascular disease in type II diabetes: the epidemiological evidence. Diabetologia 2001;44:2107-2114.

4 Crapo A, Insel J, Sperling M, Kolterman G: Comparison of serum glucose, insulin and glucagon responses to different types of complex carbohydrate in noninsulin-dependent diabetic patients. Am J Clin Nutr 1981;34:184-190.

5 Jenkins D, Wolever T, Taylor H, et al: Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981;34:362-366.

6 Bornet FRJ, Costagliola D, Rizkalla SW, et al: Insulinemic and glycemic indexes of six starch-rich foods taken alone and in a mixed meal by type 2 diabetes. Am J Clin Nutr 1987;45:588-595.

7 FAO/WHO: Carbohydrates in human nutrition. Report of a joint FAO/World Health Organization Expert Consultation. FAO Food and Nutrition, 1998, paper 66.

8 Wolever T, Mehling C: Long-term effect of varying the source or amount of dietary carbohydrate on postprandial plasma glucose, insulin, triacylglycerol, and free fatty acid concentrations in subjects with impaired glucose tolerance. Am J Clin Nutr 2003;77:612-621.

9 Barclay A, Brand-Miller J, Wolever T: Glycemic index, glycemic load, and glycemic response are not the same. Diabetes 2005;28:1839-1840.

10 Schulze M, Liu S, Rimm E, et al: Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women. Am J Clin Nutr 2004;80:348-356.

11 Brand-Miller J, Hayne S, Petocz P, Colagiuri S: Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care 2003;26:2261-2267.

12 Jarvi A, Karlstrom B, Granfeldt Y, et al: Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care 1999;22:10-18.

13 Rizkalla S, Taghrid L, Laromiguiere M, et al: Improved plasma glucose control, whole-body glucose utilization, and lipid profile on a low-glycemic index diet in type 2 diabetic men: a randomized controlled trial. Diabetes Care 2004;27:1866-1872.

14 Fontvieille A, Acosta M, Rizkalla S, et al: A moderate switch from high to low glycemic index foods for 3 weeks improves the metabolic control of type 1 (IDDM) diabetic subjects. Diabetes Nutr Metab 1988;1:139-143.

15 Fontvieille A, Rizkalla S, Penfornis A, et al: The use of low glycemic index foods improves metabolic control of diabetic patients over five weeks. Diabet Med 1992;9:1-7.

16 Bouché C, Rizkalla S, Luo J, et al: Five week, low-glycemic index diet decreases total fat mass and improves plasma lipid profile in moderately overweight nondiabetic subjects. Diabetes Care 2002;25:822-828.

17 Lerer-Metzger M, Rizkalla S, Luo J, et al: Effect of long-term low-glycemic index starchy food on plasma glucose and lipid concentrations and adipose tissue cellularity in normal and diabetic rats. Br J Nutr 1996;75:723-732.

18 Kabir M, Rizkalla S, Champ M, et al: Dietary amylose-amylopectin starch content affects glucose and lipid metabolism in adipocytes of normal and diabetic rats. J Nutr 1998;128: 35-43.

19 Kabir M, Rizkalla S, Quignard-Boulangé A, et al: A high glycemic index starch diet affects lipid storage-related enzymes in normal and to a lesser extent in diabetic rats. J Nutr 1998;128: 1878-1883.

20 Kabir M, Guerre-Millo M, Laromigiere M, et al: Negative regulation of leptin by chronic high glycemic index starch diet. Metabolism 2000;49:764-769.

Discussion

Dr. Katsilambros: Congratulations, I think that especially the study on adipocytes is very important. I would like to ask you if the low or high index diets in the rat were isoenergetic or were the rats fed ad libitum.

Dr. Slama: They were fed ad libitum.

Dr. Katsilambros: That is the difference then.

Dr. Slama: Yes, and the amount of carbohydrate was higher, 70% than the regular diet in the normal rats.

Dr. Katsilambros: It can be hypothesized that those rats on a low carbohydrate diet finally ate more calories than those on a high carbohydrate diet. In this sense this might explain the difference in your findings and the findings which I presented in the previous talk. This is 100% confirmed, it was in the past, it is in the present, and it will be in the future.

Dr. Schiffrin: Regarding the changes that you described in adipose tissue, was there more or less macrophage infiltration following the diet?

Dr. Slama: The macrophage story in adipose tissue is very recent, at least to my knowledge. When we did the study we didn't look at that. Perhaps in the future we will dissect, but for adipose tissue volume, adipose activity, tissue activity, it is certain, the adipocytes; but the macrophage I don't know.

Dr. Chiasson: I was just wondering are you interpreting the decrease in the size of the adipocyte due to a decrease in the insulin level?

Dr. Slama: No, because it has also been observed in insulinopenic rats at least, but I don't know why it is so. Perhaps the disposition of the free fatty acids plays a major role. The free fatty levels are really much less after the low glycemic index diet. I think that you know better than I the role which is supposed to be played by free fatty acids. We, as doctors and also as physiologists, have been used to studying life at a steady state, at a basal level, but probably the most important aspect of nutrition is postprandial. It seems obvious that nutrition does things also postprandially, and the hypothesis of Ceriello [1] and others on oxidative stress and many other aspects should also play a role. I don't know exactly what the major determinant of the phenomenon is, but in one study on animals it has been observed every time, and this is probably the most striking effect of a low glycemic index, the effect on adipocytes.

Dr. Chiasson: In the postprandial profile between carbohydrate alone or within a mixed meal, you showed that the mixed meal had a lower rise in postprandial plasma glucose. Do you think that this is due only to the difference in the insulin profile?

Dr. Slama: It could be due to dilution of the calories; it could be due more certainly to increased fat intake, and perhaps also to protein intake and insulin secretion. So it is probably a mixed phenomenon which I can't fully explain, but the fact is here and it is well documented in the literature.

Dr. Chiasson: What is well documented? Are you saying that it modifies the absorption?

Dr. Slama: It is well demonstrated that when you eat a mixed meal, you obtain a lower glucose increase for the same amount of carbohydrate.

Dr. Chiasson: Yes, but usually that is mainly due to the disposition of glucose rather than to the absorption.

Dr. Slama: No idea; I have not seen that. If you say so I will look at the results, but I have not measured that. It is said that fat decreases stomach emptying and it plays a role, but perhaps it is also absorbed in the gut.

Dr. Chiasson: We have looked at absorption, labeling the carbohydrate, and whether it was given alone or within a mixed meal. We had exactly the same absorption profile, suggesting that the differences would be more in the disposition of the glucose absorbed and the insulin response. If you have fat in your meal then you would expect that you are creating insulin resistance and it will go higher up and so that could explain the lower profile within the mixed meal.

Dr. Halimi: I have a comment regarding the possible limits of the glycemic index which is based on the measure of peripheral glycemia and insulinemia, i.e. post-hepatic glycemia and post-hepatic insulinemia. However, we know that the liver plays a major role in normal people, which is quite different in the metabolic syndrome, in steatosis and in type-2 diabetes. Yet the glycemic index cannot take into account the respective roles of the different tissues (gut, liver, peripheral) involved in this complex process.

Dr. Slama: There are two things. First, in the first part of this morning's session the question was raised on peak value, raising time and negative part, etc. I think that the postprandial blood glucose excursion should be seen as a disturbance in a very finely tuned system, and the postprandial excursion is perhaps an overflow of the capability of the body to really maintain blood glucose around 1 g. It is an overflow. So the less brutal the disturbance is, the easier it will be for the body to maintain. To sustain what I am saying I refer to work we have done and published in a confidential review of nutrition in small laboratory pigs with Lang et al. [2, 3]. I don't remember all the details but these pigs had a catheter in the carotid artery and another in the portal vein. These pigs were put on glucose clamp and they had a tube in the stomach to really know what we were addressing. With the low glycemic index, the blood glucose excursion was lower and all the glucose was absorbed, as seen by the glucose clamp but not by blood glucose excursion. It is also the same on the insulin level in the portal vein but not in the peripheral vein.

Dr. Jianquin Sun: I have a question regarding some of the inconsistent results from different clinical trials in terms of glycemic control or lipid profile. Could you explain what is the reason for that result?

Dr. Slama: I think that we can also discuss paper by paper but I have not read all the papers so I cannot really answer your question. As I already said there are low glycemic index foods and low glycemic index foods. For example, as we already said, pizza and chocolate bars have very low glycemic index but in my opinion they are not to be recommended as daily foods. So if in one study they use such foods and in others they do not, of course the results will be totally different. So we have to look very carefully at every methodological aspect: the way the glycemic index of foods was calculated, the way the food was administered, and so on. So I cannot give a general answer to your important question. Because of course these critics are addressed to the glycemic index, not reproducibility, variability. For me this is not really convincing. Why should the glycemic food, starchy food, give exactly the same value? But day after day it makes a difference, and in all the studies I have seen and done myself, I have never seen a discrepancy.

References

1 Ceriello A: Postprandial hyperglycemia and diabetes complications: is it time to treat? Diabetes 2005;54:1-7.

2 Lang V, Vaugelade P, Bernard F, et al: Euglycemic hyperinsulinemic clamp to assess posthep-atic glucose appearance after carbohydrate loading. 1. Validation in pigs. Am J Clin Nutr 1999;69:1174-1182.

3 Lang V, Bornet FR, Vaugelade P, et al: Euglycemic hyperinsulinemic clamp to assess posthep-atic glucose appearance after carbohydrate loading. 2. Evaluation of corn and mung bean starches in healthy men. Am J Clin Nutr 1999;69:1183-1188.

Bantle JP, Slama G (eds): Nutritional Management of Diabetes Mellitus and Dysmetabolic Syndrome. Nestlé Nutr Workshop Ser Clin Perform Program, vol 11, pp 83-95, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2006.

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