Interactive Effects of Macronutrients on Obesity and Metabolic Syndrome Development
Yudell, Barbara Elise
This item is only available for download by members of the University of Illinois community. Students, faculty, and staff at the U of I may log in with your NetID and password to view the item. If you are trying to access an Illinois-restricted dissertation or thesis, you can request a copy through your library's Inter-Library Loan office or purchase a copy directly from ProQuest.
Permalink
https://hdl.handle.net/2142/84964
Description
Title
Interactive Effects of Macronutrients on Obesity and Metabolic Syndrome Development
Author(s)
Yudell, Barbara Elise
Issue Date
2009
Doctoral Committee Chair(s)
Layman, Donald K.
Manabu Nakamura
Department of Study
Nutritional Sciences
Discipline
Nutritional Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Health Sciences, Nutrition
Language
eng
Abstract
In the second study, male Sprague-Dawley rats (N=24) were fed one of 6 diets for 30 days. Diets were based on a 2x3 factorial with 2 levels of protein (P10 and P20, percent energy), and 3 levels of fructose (F0, F20, and F40, percent energy, replacing glucose). Body composition was measured at the beginning and end points. P10 groups showed higher energy intake (P<0.0001) and percent fat (P<0.01) compared to P25 groups. Unexpectedly, replacing glucose with fructose attenuated this low protein effect without reducing lean mass. P10-40 had highest protein efficiency overall, which was 14% higher than P10-F0 (P<0.05). While fructose tended to increase blood pressure (P=0.06), this fructose effect was independent of adiposity. In liver, the integrated stress response (ISR) pathway was induced by low protein and fructose, suggesting inhibition of insulin signaling. However, glycogen was increased by low protein in both liver and muscle with concomitant decrease in protein tyrosine phosphatase 1B (PTP1B) expression, suggesting partial upregulation of insulin signaling. In muscle, the glucose transporter GLUT4 and PGC-1a were induced by both low protein and fructose. Low protein also induced pyruvate dehydrogenase 4 (PDK4) in skeletal muscle, suggesting decreased glucose oxidation but not glycolysis. Low protein increased plasma adiponectin (P<0.05), suggesting an enhanced role of adipose in energy metabolism. Increased protein efficiency by fructose may be mediated by induction of ISR in liver, and by GLUT4 and PGC-1a in muscle. Interactions of protein with carbohydrate metabolism support a significant contribution of protein to glycemic control when dietary protein is adequate. In total, these studies have confirmed the role of marginal protein deficiency in driving hyperphagia and increased adiposity, but have refuted other studies showing increased adiposity by dietary fat and fructose. When protein is marginally deficient, replacing glucose with fat or fructose unexpectedly spared amino acids and enhanced protein efficiency. No single macronutrient combination gave rise to metabolic syndrome, but instead, each diet was associated with unique metabolic regulation.
Use this login method if you
don't
have an
@illinois.edu
email address.
(Oops, I do have one)
IDEALS migrated to a new platform on June 23, 2022. If you created
your account prior to this date, you will have to reset your password
using the forgot-password link below.
