Recent clinical research has established that high dairy product intake can significantly reduce body weight and fat mass. Dietary calcium may reduce body weight and fat mass, however, recent studies demonstrate that this effect is enhanced by dairy product intake. Our own studies suggest that dietary calcium intervention increases lipid oxidation in human volunteers and improved vitamin D status is associated with increased energy expenditure. These as well as several other mechanisms have been proposed to mediate the impact of dairy product consumption on body fat mass, including 1) reducing food intake; 2) formation of calcium and fatty acid complexes leading to reduced fat absorption; 3) increasing adipocyte lipolysis; and 4) reducing lipogenesis. These metabolic alterations are potentially mediated by calcium regulated hormones. The objective of these studies is to determine the mechanism(s) by which inclusion of dairy products in the diet induces changes in body composition. Our central hypothesis is that in muscle, increased lipid oxidation is induced by dietary calcium intake and increased energy expenditure is induced by vitamin D intake. We further hypothesize that increased lipolysis from the adipocyte is mediated by dairy product intake. We will address these hypotheses by determining the independent and cooperative effects of the following on overall body mechanisms regulating energy balance: 1) dietary calcium and vitamin D; and 2) dairy product intake with dietary calcium and vitamin D. Identifying the mechanisms by which dairy product intake regulates energy balance will contribute to determining when and how dairy product intake results in changes in body composition. This information would be important in helping to establish dietary recommendations for dairy products or its' components to aid in reducing the growing numbers of obese and overweight individuals and their attendant health problems.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
1R01DK069965-01A1
Application #
6983329
Study Section
Integrative Physiology of Obesity and Diabetes Study Section (IPOD)
Program Officer
Yanovski, Susan Z
Project Start
2005-08-15
Project End
2008-07-31
Budget Start
2005-08-15
Budget End
2006-07-31
Support Year
1
Fiscal Year
2005
Total Cost
$260,481
Indirect Cost
Name
Purdue University
Department
Nutrition
Type
Other Domestic Higher Education
DUNS #
072051394
City
West Lafayette
State
IN
Country
United States
Zip Code
47907
Camarillo, Ignacio G; Clah, Leon; Zheng, Wei et al. (2014) Maternal exercise during pregnancy reduces risk of mammary tumorigenesis in rat offspring. Eur J Cancer Prev 23:502-5
Carrillo, Andres E; Flynn, Michael G; Pinkston, Catherine et al. (2013) Impact of vitamin D supplementation during a resistance training intervention on body composition, muscle function, and glucose tolerance in overweight and obese adults. Clin Nutr 32:375-81
Chang, Eugene; Donkin, Shawn S; Teegarden, Dorothy (2009) Parathyroid hormone suppresses insulin signaling in adipocytes. Mol Cell Endocrinol 307:77-82
Li, Jia; Fleet, James C; Teegarden, Dorothy (2009) Activation of rapid signaling pathways does not contribute to 1 alpha,25-dihydroxyvitamin D3-induced growth inhibition of mouse prostate epithelial progenitor cells. J Cell Biochem 107:1031-6
Taber, Laura M; Adams, Lynn S; Teegarden, Dorothy (2009) Mechanisms of nuclear vitamin D receptor resistance in Harvey-ras-transfected cells. J Nutr Biochem 20:629-37
Siddiqui, Shamim M K; Chang, Eugene; Li, Jia et al. (2008) Dietary intervention with vitamin D, calcium, and whey protein reduced fat mass and increased lean mass in rats. Nutr Res 28:783-90
Teegarden, Dorothy; Gunther, Carolyn W (2008) Can the controversial relationship between dietary calcium and body weight be mechanistically explained by alterations in appetite and food intake? Nutr Rev 66:601-5
Li, Jia; Byrne, Mary E; Chang, Eugene et al. (2008) 1alpha,25-Dihydroxyvitamin D hydroxylase in adipocytes. J Steroid Biochem Mol Biol 112:122-6