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Premature impairment of methylation pathway and cardiac metabolic dysfunction in fa/fa obese Zucker rats

De Castro, N. M., Yaqoob, P., De la Fuente, M., Baeza, I. and Claus, S. P. (2013) Premature impairment of methylation pathway and cardiac metabolic dysfunction in fa/fa obese Zucker rats. Journal of Proteome Research, 12 (4). pp. 1935-1945. ISSN 1535-3907

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To link to this item DOI: 10.1021/pr400025y


Increasing evidence suggests that obesity is a chronic inflammatory disease, in which adipose tissue is involved in a network of endocrine signals to modulate energy homeostasis. These oxidative-inflammatory pathways, which are associated with cardiovascular complications, are also observed during the aging process. In this study, we investigated the interaction between aging and the development of obesity in a hyperphagic rat model. Metabolic profiles of the liver, white adipose tissue (WAT) and heart from young and adult Zucker lean (fa/+) and obese (fa/fa) rats were characterized using a (1)H NMR-based metabonomics approach. We observed premature metabolic modifications in all studied organs in obese animals, some of which were comparable to those observed in adult lean animals. In the cardiac tissue, young obese rats displayed lower lactate and scyllo-inositol levels associated with higher creatine, choline and phosphocholine levels, indicating an early modulation of energy and membrane metabolism. An early alteration of the hepatic methylation and transsulfuration pathways in both groups of obese rats indicated that these pathways were affected before diabetic onset. These findings therefore support the hypothesis that obesity parallels some metabolic perturbations observed in the aging process and provides new insights into the metabolic modifications occurring in pre-diabetic state.

Item Type:Article
Divisions:Interdisciplinary centres and themes > Chemical Analysis Facility (CAF) > NMR (CAF)
Life Sciences > School of Chemistry, Food and Pharmacy > Department of Food and Nutritional Sciences > Food Microbial Sciences Research Group
ID Code:31301
Publisher:American Chemical Society

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