Dietary glycemic load, the mathematical product of the glycemic index (GI) of a food and its carbohydrate content, has been proposed as an indicator of the glucose response and insulin demand induced by a serving of food. To validate this concept in vivo, we tested the hypotheses that 1). portions of different foods with the same glycemic load produce similar glycemic responses; and 2). stepwise increases in glycemic load for a range of foods produce proportional increases in glycemia and insulinemia. In the first study, 10 healthy subjects consumed 10 different foods in random order in amounts calculated to have the same glycemic load as one slice of white bread. Capillary blood samples were taken at regular intervals over the next 2 h. The glycemic response as determined by area under the curve was not different from that of white bread for nine foods. However, lentils produced lower than predicted responses (P < 0.05). In the second study, another group of subjects was tested to determine the effects of increasing glycemic load using a balanced 5 x 5 Greco-Latin square design balanced for four variables: subject, dose, food and order. Two sets of five foods were consumed at five different glycemic loads (doses) equivalent to one, two, three, four and six slices of bread. Stepwise increases in glycemic load produced significant and predictable increases in both glycemia (P < 0.001) and insulinemia (P < 0.001). These findings support the concept of dietary glycemic load as a measure of overall glycemic response and insulin demand.

Leptin is reported to have effects in peripheral tissues that are independent of its central effects on food intake and body weight. In this study, the acute effects of a single dose of recombinant mouse leptin on lipid and glucose metabolism in lean and gold thioglucose-injected obese mice were examined. Changes were measured 2 h after leptin injection. In lean mice, liver and white adipose tissue (WAT) lipogenesis was inhibited. The activity of the pyruvate dehydrogenase complex (PDHCa), the rate-determining step for glucose oxidation, was reduced in heart, liver, quadriceps muscle, and both brown and white adipose tissues. Muscle and liver glycogen and liver triglyceride (TG) content was unchanged, but muscle TG was decreased. In obese mice, liver and WAT lipogenesis was inhibited and PDHCa reduced in heart and quadriceps muscle. Muscle and liver glycogen was decreased but not TG. Serum insulin was reduced in obese but not lean mice. These results are consistent with a role for leptin in the maintenance of steady-state energy stores by decreasing lipid synthesis and increasing fat mobilization, with decreased glucose oxidation occurring as a result of increased fatty acid oxidation.

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