In addition to total calorie intake there is also evidence that composition of the maternal diet can have long-term consequences on the metabolism of the offspring. Experimental animal models involving maternal protein restriction have suggested that adequate protein intake is critical in both development of the fetus and its long-term health. They have also provided insight into the possible underlying mechanisms.
Offspring of rat dams fed a low (8%) protein diet throughout the gestational period are consistently smaller at birth than offspring of a control diet containing 20% protein. Initially, the low-protein offspring have significantly improved glucose tolerance than the control offspring. In humans, small-for-gestational-age infants also display increased insulin sensitivity with respect to glucose disposal in early postnatal life. Offspring of dams fed a low-protein diet appear to undergo a greater age-dependent loss of glucose tolerance. By 15 months of age, the male low-protein offspring are considered to have developed glucose intolerance that is associated with insulin resistance and by 17 months of age this has progressed to type 2 diabetes.
Consistent with the thrifty phenotype hypothesis, the growth restriction of the tissues and organs of the low-protein offspring is not uniform. In the growth-restricted rats, brain growth is spared at the expense of the growth of other developing tissues. In addition to the altered structure and growth patterns, the insulin-sensitive tissues (skeletal muscle and adipose tissue) and organs (liver and pancreas) of the low-protein offspring have been metabolically programed to have altered functionality.
Recently, evidence has been provided suggesting that taurine supplementation to the maternal low-protein diet may benefit the health outcomes of the rat offspring. Maternal taurine supplementation was found to restore and normalize the vascularization of the offspring's endocrine pancreas. Despite these findings, there is little evidence to suggest that a maternal high-protein intake has overall beneficial effects on the metabolic health of the offspring. Some human epidemiological studies and human trials involving high-protein dietary supplementation have in fact demonstrated that the consumption of a high-animal-protein, low-carbohydrate diet throughout late pregnancy can lead to metabolic disturbances in the offspring when they reach adulthood. It has been suggested that these high-protein diets stimulate the hypothalamic-pituitary-adrenal axis and cause maternal cortisol levels to increase. As a result, the developing fetus is presented with the metabolic stress of being exposed to excess cortisol levels. This inappropriate exposure to cortisol during fetal life appears to program lifelong hypercorti-solemia and elevated blood pressure. It is likely that the type of protein is also important and this may in part explain some of these apparent discrepancies.
Adverse metabolic disturbances in offspring have therefore been demonstrated as consequential effects of both the in utero exposure to either maternal protein restriction or maternal high-protein consumption. The role of the carbohydrate level in these diets still needs to be ascertained. Nevertheless, it is essential that the optimal level of protein intake during pregnancy and lactation be clearly established so as to aid in the normal growth and development of the fetus.
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