Postprandial glucose, together with related hyperinsulinemia and lipidaemia, has been implicated in the development of chronic metabolic diseases like obesity, type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). In this review, available evidence is discussed on postprandial glucose in relation to body weight control, the development of oxidative stress, T2DM, and CVD and in maintaining optimal exercise and cognitive performance. There is mechanistic evidence linking postprandial glycaemia or glycaemic variability to the development of these conditions or in the impairment in cognitive and exercise performance. Nevertheless, postprandial glycaemia is interrelated with many other (risk) factors as well as to fasting glucose. In many studies, meal-related glycaemic response is not sufficiently characterized, or the methodology with respect to the description of food or meal composition, or the duration of the measurement of postprandial glycaemia is limited. It is evident that more randomized controlled dietary intervention trials using effective low vs. high glucose response diets are necessary in order to draw more definite conclusions on the role of postprandial glycaemia in relation to health and disease. Also of importance is the evaluation of the potential role of the time course of postprandial glycaemia.

This study examines the effect of the substitution of 6 g/day of fish oil in a saturated diet on glucose and fructose metabolism in healthy humans. Five subjects were submitted to two 3-wk controlled-diet periods (polyunsaturated/saturated = 0.21). During one period, 6 g/day of fat used for dressing were replaced by 6 g/day of fish oil [1.1 g/day of 20:5 (n-3) fatty acids and 0.7 g/day of 22:6 (n-3) fatty acids]. At the end of each period the subjects ingested a 1 g/kg fructose or glucose load 2 days apart. Plasma glucose fluxes were traced with the use of deuterated glucose and [U-13C]glucose. Substrate oxidation was measured by indirect calorimetry. Fish oil induced a 4% increase in basal and postload glycemia and a 40% decrease in insulinemia, whereas plasma C-peptide remained unaffected. Glucose fluxes were unaffected by fish oil, but carbohydrate (CHO) oxidation was reduced (fructose: 55.5 +/- 4.1 vs. 62.9 +/- 3.6 g/6 h; glucose: 36.7 +/- 4.7 vs. 50.5 +/- 4.7 g/6 h; all P < 0.05). Lipid oxidation was increased 35% by fish oil after both CHO loads. Nonoxidative glucose disposal was increased by fish oil (fructose: 9.4 +/- 2.5 vs. 2.9 +/- 1.1 g/6 h; glucose: 28.3 +/- 5.1 vs. 14.4 +/- 4.7 g/6 h; all P < 0.05). Fish oil could affect glucose transport and decrease CHO oxidation through the decrease in insulinemia and/or a specific effect on glycolytic pathway.

Twelve young healthy adults (five men, seven women) ingested four test meals on four occasions so we could examine the relationship between the rate of gastric emptying (GE) and the glucose response to different starchy foods. Each meal consisted of one food product containing 50 g starch: spaghetti, rice, French bread, or mashed potato. Basal and postprandial glucose and insulin responses were measured for 3 h. The foods were labeled with 3.7 MBq Tc99m-albumin and GE was studied by scintigraphy for 3 h. The rate of GE (expressed by the GE half-time) was fastest for mashed potatoes, then bread, rice, and slowest for spaghetti. Blood glucose and serum insulin responses were similar. A significant negative correlation was found between the GE half-time and the maximum variation in blood glucose level (r = -0.6, p less than 0.0001). The glucose response to all four foods is strongly related to the GE rate.

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Lactase-deficient subjects absorb lactose in yogurt more effectively than lactose in other dairy products. However, as all previous studies were performed without a double-blind design and only after a single ingestion of the test product, the mechanism of this enhanced absorption remains unclear. The aims of this double-blind study were 1) to evaluate lactose absorption after prolonged ingestion of yogurt and fermented-then-pasteurized milk (FPM) and 2) to assess the modification of the lactase activity of the duodenal mucosa. In 16 lactase-deficient subjects we confirmed that yogurt enhances lactose digestion, this beneficial effect being destroyed by pasteurization. Moreover, the long-term (8 d) ingestion of either yogurt or FPM does not modify the results of hydrogen breath tests in comparison with a 24-h ingestion. The mucosal lactase (Dahlquist method) and beta-galactosidase (ONPG method) activities were not significantly modified by yogurt or FPM ingestion. These results suggest that in lactase-deficient subjects no adaptation occurs after eating yogurt or FPM and that the increased lactose absorption in yogurt must be mainly related to an intraluminal process.