This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Due to the increasing obesity risks, many lactating women are concerned about losing weight gained during pregnancy without adversely affecting their milk production. We have demonstrated previously that oral galactose which has low glycemic index compared to glucose, may provide a nutrient substrate that is converted to glucose, thus providing a substrate for lactose synthesis but not inhibit fat mobilization by increasing plasma glucose and insulin. The objective of this study is to determine the impact of a high (glucose) versus low (galactose) insulin stimulating oral carbohydrate meal on mobilization and oxidation of fat in post-partum and control women. We hypothesize that an isocaloric carbohydrate drink which does not stimulate insulin secretion, when compared to one which stimulates significant insulin secretion will promote fat mobilization and oxidation and will not affect on milk production in healthy lactating women. Should we demonstrate that the nature of the oral carbohydrate affects fatty acid mobilization and fat oxidation with no impact on lactose synthesis and milk production, we would have the scientific evidence to design a wider clinical trial of breast-feeding mothers who are desirous of losing weight while sustaining successful breast feeding. Hypothesis: Over a three day period, an isocaloric carbohydrate drink which does not stimulate insulin secretion (low glycemic index), when compared to one which stimulates significant insulin secretion (high glycemic index) will: i. Promote fat mobilization and oxidation. ii. Have no effect on milk production in healthy lactating women. This hypothesis will be tested in two different protocols. In protocol (1) the drink will be either just glucose or just galactose providing 55% of the subject''s daily basal metabolic needs. Protocol (2) will be the same as protocol (1) with the exception that the drink will be supplemented with extra 15% protein, essential fatty acids, minerals and vitamins. Thus, this drink will have exactly the same carbohydrate content as that used in protocol (1) but will provide 70% of the basal metabolic rate. The objective of this study is to determine whether low(galactose) versus high (glucose) glycemic index dietary carbohydrate content in a diet with reduced calories will facilitate fat mobilization and oxidation without adversely affecting milk production, or milk composition. Understanding the metabolic consequences of lactation on maternal metabolism and the regulation of lactose synthesis will give new insights into the regulation of human milk production, providing new strategies to improve the number of successfully breastfeeding women and to allow women to lose unwanted weight while maintaining adequate milk production. Many lactating women are concerned about losing weight gained during pregnancy. A large number of dietary approaches to achieve weight loss are available. Many high-carbohydrate foods common to Western diets produce a high glycemic response (high-glycemic index). These diets induce a rapid increase in blood glucose, resulting in insulin release which leads to inhibition of fat mobilization. Thus high-glycemic index diets may result in altering fuel partitioning in a way that may lead to body fat gain. On the other hand, diets that produce a low glycemic response (low-glycemic index diets) may enhance weight control because they promote satiety and minimize postprandial insulin secretion. Although regaining pre-pregnancy weight should be the goal, extreme dietary behaviors could impair milk production. It is postulated that the primary determinant of milk volume is lactose production. We have recently demonstrated that oral galactose, which has a low-glycemic index, provides a nutrient substrate that is converted to glucose and only minimally increases plasma glucose and insulin concentrations. Thus galactose is a potential substrate for lactose synthesis that might also promote fat mobilization.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000188-46
Application #
8166688
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2009-12-01
Project End
2010-11-30
Budget Start
2009-12-01
Budget End
2010-11-30
Support Year
46
Fiscal Year
2010
Total Cost
$9,156
Indirect Cost
Name
Baylor College of Medicine
Department
Pediatrics
Type
Schools of Medicine
DUNS #
051113330
City
Houston
State
TX
Country
United States
Zip Code
77030
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