Please use this identifier to cite or link to this item: https://doi.org/10.1186/s12986-016-0135-5
Title: Metabolic gene expression profile in circulating mononuclear cells reflects obesity-associated metabolic inflexibility
Authors: Baig, S 
Parvaresh Rizi, E
Shabeer, M 
Chhay, V 
Mok, S.F 
Loh, T.P 
Magkos, F 
Vidal-Puig, A
Tai, E.S 
Khoo, C.M 
Toh, S.-A 
Keywords: 6 phosphofructokinase
peroxisome proliferator activated receptor alpha
pyruvate dehydrogenase kinase 4
adult
aerobic metabolism
Article
chemical composition
clinical article
controlled study
disease association
fatty acid metabolism
gene expression profiling
gene induction
glucose oxidation
human
human cell
insulin resistance
lean body weight
male
mononuclear cell
obesity
phenotype
respiratory quotient
transcription regulation
Issue Date: 2016
Citation: Baig, S, Parvaresh Rizi, E, Shabeer, M, Chhay, V, Mok, S.F, Loh, T.P, Magkos, F, Vidal-Puig, A, Tai, E.S, Khoo, C.M, Toh, S.-A (2016). Metabolic gene expression profile in circulating mononuclear cells reflects obesity-associated metabolic inflexibility. Nutrition and Metabolism 13 (1) : 1-Aug. ScholarBank@NUS Repository. https://doi.org/10.1186/s12986-016-0135-5
Abstract: Background: Obesity is associated with an impaired ability to switch from fatty acid to glucose oxidation during the fasted to fed transition, particularly in skeletal muscle. However, whether such metabolic inflexibility is reflected at the gene transcription level in circulatory mononuclear cells (MNC) is not known. Methods: The whole-body respiratory quotient (RQ) and transcriptional regulation of genes involved in carbohydrate and lipid metabolism in MNC were measured during fasting and in response (up to 6 h) to high-carbohydrate and high-fat meals in nine lean insulin-sensitive and nine obese insulin-resistant men. Results: Compared to lean subjects, obese subjects had an impaired ability to increase RQ and switch from fatty acid to glucose oxidation following the high-carbohydrate meal (interaction term P < 0.05). This was accompanied by an impaired induction of genes involved in oxidative metabolism of glucose in MNC, such as phosphofructokinase (PFK), pyruvate dehydrogenase kinase 4 (PDK4), peroxisome proliferator-activated receptor alpha (PPAR?) and uncoupling protein 3 (UCP3) and increased expression of genes involved in fatty acid metabolism, such as fatty acid translocase (FAT/CD36) and fatty acid synthase (FASN) (P < 0.05). On the contrary, there were no differences in the gene expression profiles between lean and obese subjects following the high-fat meal. Conclusions: Postprandial expression profiles of genes involved in glucose and fatty acid metabolism in the MNC reflect the differing metabolic flexibility phenotypes of our cohort of lean and obese individuals. These differences in metabolic flexibility between the lean and obese are elicited by an acute meal challenge that is rich in carbohydrate but not fat. © 2016 The Author(s).
Source Title: Nutrition and Metabolism
URI: https://scholarbank.nus.edu.sg/handle/10635/173816
ISSN: 17437075
DOI: 10.1186/s12986-016-0135-5
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