Postprandial response diets

Anderson, J. W., O Neal, D. S., Riddell-Mason, S., Floore, T. L., Dillon, D. W., and Oeltgen, P. R. (1995). Postprandial serum glucose, insulin, and lipoprotein responses to high- and low-fiber diets. Metabolism 44, 848-854. 

Martini and Wood (2002) tested the bioavailability of 3 different sources of Ca in 12 healthy elderly subjects (9 women and 3 men of mean SEM age 70 3 and 76 6 years, respectively) in a 6-week crossover trial conducted in a Human Study Unit. Each Ca source supplied 1000 mg Ca/day and was ingested for 1 week with meals (as 500 mg Ca 2x/day), thus contributing to a high-Ca intake (1300 mg Ca/day). A low-Ca intake (300 mg Ca/day strictly from the basal diet) was adhered to for 1 week in-between each treatment. The Ca sources included skim milk, CCM-fortified OJ, and a dietary supplement of CaCOa. Assessment parameters were indirect measures predicted to reflect the relative bioavailability of Ca postprandially via an acute PTH suppression test (hourly for 4h). Longer-term responses to Ca supplementation were assessed via a number of urinary and serum hormone, mineral, and bone resorption biomarkers (i.e., vitamin D, Ca, phosphorus, and collagen t) e 1 N-telopeptide cross-links). 

Schneeman, B. O., Burton-Freeman, B., and Davis, P. (2003). Incorporating dairy foods into low and high fat diets increases the postprandial cholecystokinin response in men and women. J. Nutr. 133,4124-4128. 

The endothelial dysfunction during the postprandial phase after a meal rich in oxidized fat is almost certainly due to the cellular response to oxidized fat originating from this repeatedly heated fat. As in so many cases, the precise identity of this factor is not known. It is often assumed that it is a reactive molecule, derived from quantitatively the most important unsaturated fatty acid (linoleic acid) in the diet. Thus 9-, 11-, and 13-hydroperoxy-linoleic acids are possibilities, as are 8,9- or 11,12-epoxy-linoleic acids. However, the relative amount of epoxy fatty acids in the diet is much less than that of hydroperoxy fats. Photooxidation products of oleic acid cannot be excluded either, and it is worth pointing out that this unsaturated fatty acid is quantitatively the most important fatty acid in Western and Mediterranean diets. What is also not clear is whether endothelial dysfunction during postprandial lipemia requires the induction of enzymes. 

Figure I. Postprandial glucose, insulin and BOHB responses in sheep, goats and llamas fed diets with high (HP) or low (LP) protein content.

It can be hypothesized that a reduction in the general and postprandial glycemic and insulinemic response may delay the development of insulin resistance and thus the development of diabetes (NIDDM) although there is very little direct evidence to support this hypothesis. However, diets high in both carbohydrate and dietary fiber have been reported to improve insulin sensitivity. Much of the research in this area has studied the effect of dietary fiber on the management rather than the prevention or etiology of diabetes. 

Postprandially, increased factor VUc concentrations have been demonstrated after consumption of diets rich in fat compared with fat-free meals (Figure 3). The response is stronger when more fat is consumed, but this occurs regardless of whether the fat is high in saturated or unsaturated fatty acids. Only meals with unrealistically high amounts of MCFA have been reported not to change factor VIIc levels in comparison with a meal providing a similar amount of olive oil. 

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