title: Intrauterine growth retardation increases the susceptibility of pigs to high-fat diet-induced mitochondrial dysfunction in skeletal muscle.
abstract: It has been recognized that there is a relationship between prenatal growth restriction and the development of metabolic-related diseases in later life, a process involved in mitochondrial dysfunction. In addition, intrauterine growth retardation (IUGR) increases the susceptibility of offspring to high-fat (HF) diet-induced metabolic syndrome. Recent findings suggested that HF feeding decreased mitochondrial oxidative capacity and impaired mitochondrial function in skeletal muscle. Therefore, we hypothesized that the long-term consequences of IUGR on mitochondrial biogenesis and function make the offspring more susceptible to HF diet-induced mitochondrial dysfunction. Normal birth weight (NBW), and IUGR pigs were allotted to control or HF diet in a completely randomized design, individually. After 4 weeks of feeding, growth performance and molecular pathways related to mitochondrial function were determined. The results showed that IUGR decreased growth performance and plasma insulin concentrations. In offspring fed a HF diet, IUGR was associated with enhanced plasma leptin levels, increased concentrations of triglyceride and malondialdehyde (MDA), and reduced glycogen and ATP contents in skeletal muscle. High fat diet-fed IUGR offspring exhibited decreased activities of lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G6PD). These alterations in metabolic traits of IUGR pigs were accompanied by impaired mitochondrial respiration function, reduced mitochondrial DNA (mtDNA) contents, and down-regulated mRNA expression levels of genes responsible for mitochondrial biogenesis and function. In conclusion, our results suggest that IUGR make the offspring more susceptible to HF diet-induced mitochondrial dysfunction.
authors.affiliation: Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan, People's Republic of China.
authors.forename: Jingbo
authors.initials: J
authors.lastname: Liu
authors.forename: Daiwen
authors.initials: D
authors.lastname: Chen
authors.forename: Ying
authors.initials: Y
authors.lastname: Yao
authors.forename: Bing
authors.initials: B
authors.lastname: Yu
authors.forename: Xiangbing
authors.initials: X
authors.lastname: Mao
authors.forename: Jun
authors.initials: J
authors.lastname: He
authors.forename: Zhiqing
authors.initials: Z
authors.lastname: Huang
authors.forename: Ping
authors.initials: P
authors.lastname: Zheng
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004272:DNA, Mitochondrial / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects*; D004435:Eating; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000378:metabolism; D020738:Leptin / Q000097:blood; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D024821:Metabolic Syndrome; D008928:Mitochondria / Q000378:metabolism*; D028361:Mitochondrial Diseases / Q000209:etiology*; D018482:Muscle, Skeletal / Q000503:physiopathology*; D011247:Pregnancy; D006180:Proton-Translocating ATPases / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D013552:Swine / Q000254:growth & development; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D004272:DNA, Mitochondrial; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D014280:Triglycerides; D019344:Lactic Acid; D006003:Glycogen; D005954:Glucosephosphate Dehydrogenase; D006180:Proton-Translocating ATPases