High-fat diet decreases energy expenditure and expression of genes controlling lipid metabolism, mitochondrial function and skeletal system development in the adipose tissue, along with increased expression of extracellular matrix remodelling- and inflammation-related genes.
The aim of the present study was to identify the genes differentially expressed in the visceral adipose tissue in a well-characterised mouse model of high-fat diet (HFD)-induced obesity. Male C57BL/6J mice (n 20) were fed either HFD (189 % of energy from fat) or low-fat diet (LFD, 42 % of energy from fat) for 16 weeks. HFD-fed mice exhibited obesity, insulin resistance, dyslipidaemia and adipose collagen accumulation, along with higher levels of plasma leptin, resistin and plasminogen activator inhibitor type 1, although there were no significant differences in plasma cytokine levels. Energy intake was similar in the two diet groups owing to lower food intake in the HFD group; however, energy expenditure was also lower in the HFD group than in the LFD group. Microarray analysis revealed that genes related to lipolysis, fatty acid metabolism, mitochondrial energy transduction, oxidation-reduction, insulin sensitivity and skeletal system development were down-regulated in HFD-fed mice, and genes associated with extracellular matrix (ECM) components, ECM remodelling and inflammation were up-regulated. The top ten up- or down-regulated genes include Acsm3, mt-Nd6, Fam13a, Cyp2e1, Rgs1 and Gpnmb, whose roles in the deterioration of obesity-associated adipose tissue are poorly understood. In conclusion, the genes identified here provide new therapeutic opportunities for prevention and treatment of diet-induced obesity.
Department of Food Science and Nutrition,Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Myung-Sook
MS
Choi
Department of Food Science and Nutrition,Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Young-Je
YJ
Kim
Center for Food and Nutritional Genomics Research, Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Eun-Young
EY
Kwon
School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Jae Young
JY
Ryoo
School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Sang Ryong
SR
Kim
Center for Food and Nutritional Genomics Research, Kyungpook National University,1370 San-Kyuk Dong Puk-Ku,Daegu702-701,Republic of Korea.
Un Ju
UJ
Jung
D052436:Adipose Tissue, White / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D050154:Adiposity; D000818:Animals; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D003066:Coenzyme A Ligases / Q000235:genetics / Q000378:metabolism*; D019392:Cytochrome P-450 CYP2E1 / Q000235:genetics / Q000378:metabolism*; D059305:Diet, High-Fat / Q000009:adverse effects; D004734:Energy Metabolism; D005109:Extracellular Matrix / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D020690:GTPase-Activating Proteins / Q000235:genetics / Q000378:metabolism; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D015971:Gene Expression Regulation, Enzymologic; D007333:Insulin Resistance; D008297:Male; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000201:enzymology / Q000276:immunology / Q000378:metabolism; D018482:Muscle, Skeletal / Q000201:enzymology / Q000276:immunology / Q000378:metabolism; D009245:NADH Dehydrogenase / Q000235:genetics / Q000378:metabolism*; D009765:Obesity / Q000209:etiology / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
D015415:Biomarkers; D020690:GTPase-Activating Proteins; D019392:Cytochrome P-450 CYP2E1; D009245:NADH Dehydrogenase; D003066:Coenzyme A Ligases
Inflammation