Isken, F., Klaus, S., Petzke, K. J., Loddenkemper, C., Pfeiffer, A. F. H. and Weickert, M. O.. (2010) Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype. American Journal of Physiology: Endocrinology and Metabolism, Vol.298 (No.2). E287-E295. ISSN 0193-1849

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Abstract

Isken F, Klaus S, Petzke KJ, Loddenkemper C, Pfeiffer AF, Weickert MO. Impairment of fat oxidation under high-vs. low-glycemic index diet occurs before the development of an obese phenotype. Am J Physiol Endocrinol Metab 298: E287-E295, 2010. First published November 24, 2009; doi:10.1152/ajpendo.00515.2009.-Exposure to high vs. low glycemic index (GI) diets increases fat mass and insulin resistance in obesity-prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice (n = 10 per group) to long-term (20 wk) or short-term (6 wk) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week 5) marked increase in body fat mass and liver fat, a gene expression profile in liver consistent with elevated lipogenesis, and, after long-term exposure, significantly reduced glucose clearance following a glucose load. The long-term high-GI diet also led to a delayed switch to both carbohydrate and fat oxidation in the postprandial state, indicating reduced metabolic flexibility. In contrast, no difference in carbohydrate oxidation was observed after short-term high-vs. low-GI exposure. However, fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention, at a time where most measured phenotypic markers including body fat mass were comparable between groups. Thus long-term high-GI feeding resulted in an obese, insulin-resistant, and metabolically inflexible phenotype in obesity-prone C57BL/6J mice. Early onset and significantly impaired fatty acid oxidation preceded these changes, thereby indicating a potentially causal involvement.

Item Type:	Journal Article
Subjects:	R Medicine > RC Internal medicine Q Science > QP Physiology
Divisions:	Faculty of Medicine > Warwick Medical School
Library of Congress Subject Headings (LCSH):	Obesity, Glycemic index, Adipose tissues, Insulin resistance, Phenotype
Journal or Publication Title:	American Journal of Physiology: Endocrinology and Metabolism
Publisher:	American Physiological Society
ISSN:	0193-1849
Official Date:	February 2010
Volume:	Vol.298
Number:	No.2
Number of Pages:	9
Page Range:	E287-E295
Identification Number:	10.1152/ajpendo.00515.2009
Status:	Peer Reviewed
Publication Status:	Published
Funder:	Deutsche Forschungs Gesellschaft (DFG), German Ministry of Education and Science (BMBF)
Grant number:	PF 164/14-1 (DFG), 0313826A (BMBF)
URI:	http://wrap.warwick.ac.uk/id/eprint/16611

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