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Layman, Donald K. Manabu Nakamura Yudell, Barbara Elise 2015-09-25T22:31:09Z 2015-09-25T22:31:09Z 10000-01-01 2009 2009 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. Made available in DSpace on 2015-09-25T22:31:09Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3363122.pdf: 1318760 bytes, checksum: b699ccc427fb8f8b56e12c134b0f4abb (MD5) Previous issue date: 2009 Embargo set by: Seth Robbins for item 86245 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs U of I Only 89 p. Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2009. http://hdl.handle.net/2142/84964 (MiAaPQ)AAI3363122 eng Health Sciences, Nutrition Interactive Effects of Macronutrients on Obesity and Metabolic Syndrome Development text Nutritional Sciences Nutritional Sciences University of Illinois at Urbana-Champaign Dissertation Ph.D.