Experimental Data

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Our first experimental work in this field consisted of designing a method to test the concept in animals (i.e. in rats: to validate the GI concept in acute conditions). We, thus, conditioned the rats to consume any presented meal within the next 5 min if they wanted to eat after an overnight fast. Different foods were then tested, i.e. glucose powder, different foods rich in amylose or resistant starch (like mung beans), and different types of corn starch rich in amylopectin (like waxy corn starch). We demonstrated that the classification of starchy foods utilized in human nutrition was also done experimentally [17].

Consequently, we aimed to evaluate the chronic consequences of consuming low and high GI foods in rats. We used diabetic (STZ-n2: low streptozotocin dose injected on the 2nd day after birth) and nondiabetic male Sprague-Dawley rats. They were fed either a low or a high GI diet for 3 and 12 weeks. At the end of the nutritional periods, the activity and gene expression of different proteins, in different tissues, implicated in glucose and lipid metabolism were evaluated. Four of our studies all produced the same type of results: each study gave a more mechanistic explanation than the preceding one.

• Glucose metabolism was improved in diabetic and nondiabetic rats; the postprandial insulin profiles were lower with low GI foods.

• Circulating lipid levels: The most reproducible result observed with low GI was a significant reduction of plasma cholesterol and triglyceride levels.

• Size of adipocytes, metabolism and gene expression: Again, the most reproducible result observed in all types of experimental animals was a reduction in the diameter of the adipocytes in rats fed a low GI diet compared to those fed a high GI diet. These adipocytes during the low GI period were more metabolically active with an ex vivo increase in insulin-stimulated 14C-glucose transport and oxidation but a decrease in lipogenesis [18]. A decrease in the activity and gene expression of lipogenic enzymes was also found [19]. Leptin levels as well as its gene expression in epididy-mal adipose tissue were found to be decreased just before the increase in adiposity in the high GI fed rats [20].

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