Physiological validation of the concept of glycemic load in lean young adults.

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.

Increased saturated triacylglycerol levels in plasma membranes of human neutrophils stimulated by lipopolysaccharide.

Neutrophils isolated from patients with bacterial infections or stimulated in vitro with lipopolysaccharide (LPS) produce a high resolution, lipid-dominated spectrum on 1H-NMR spectroscopy (May et al, 1993. J. Infect. Dis. 168: 386-392). We have investigated the origin of this lipid signal using NMR and chemical analyses of both whole neutrophils and purified plasma membranes. Plasma membranes from neutrophils that had been stimulated with 50 microg/ml LPS exhibited the high resolution 1H-NMR signal, and contained double the triacylglycerol (TAG) content of plasma membranes isolated from resting cells. Chemical analysis of the whole cells indicated that the TAG also increased at the cellular level (1.7-fold) after stimulation with LPS. Diradylglycerol increased 2- to 3-fold in both whole cells and plasma membranes after stimulation, but was only a minor component compared with TAG. The plasma membrane protein/phospholipid ratio increased 2.6-fold, whereas cholesterol (free and esterified) was unchanged. The membranes from LPS-stimulated neutrophils exhibited increased fluidity, as judged by increased merocyanine 540 binding, consistent with a 2-fold reduction in cholesterol/phospholipid ratio. LPS induced a shift in fatty acid content of whole cell polar lipids towards more oleic acid and less palmitic acid, whereas the neutral lipid fraction contained increased amounts of palmitic and stearic acids. The TAG fraction of plasma membrane lipids contained increased amounts of palmitic acid when prepared from cells stimulated with LPS. We conclude that the 1H-NMR signal in LPS-stimulated neutrophils arises from increased amounts of plasma membrane TAG with an elevated content of palmitic acid.