Maternal Fructose Intake Causes Developmental Reprogramming of Hepatic Mitochondrial Catalytic Activity and Lipid Metabolism in Weanling and Young Adult Offspring

Autor: Erin Vanessa LaRae Smith, Rebecca Maree Dyson, Christina M. G. Vanderboor, Ousseynou Sarr, Jane Anderson, Mary J. Berry, Timothy R. H. Regnault, Lifeng Peng, Clint Gray
Rok vydání: 2022
Předmět:
Male
Proteomics
mitochondrial metabolism
Excess fructose intake
QH301-705.5
Guinea Pigs
Hepatic metabolism
maternal fructose
excess fructose intake
developmental programming
hepatic metabolism
mitochondrial function
Mitochondria
Liver
Fructose
Weaning
Article
Oxidative Phosphorylation
Catalysis
Developmental programming
Fatty Acids
Monounsaturated
Inorganic Chemistry
Pregnancy
Tandem Mass Spectrometry
Animals
Humans
Physical and Theoretical Chemistry
Biology (General)
Molecular Biology
QD1-999
Triglycerides
Spectroscopy
Organic Chemistry
General Medicine
Lipid Metabolism
Computer Science Applications
Chemistry
Electron Transport Chain Complex Proteins
Maternal fructose
Mitochondrial metabolism
Prenatal Exposure Delayed Effects
Female
Mitochondrial function
Reactive Oxygen Species
Chromatography
Liquid
Zdroj: Paediatrics Publications
International Journal of Molecular Sciences, Vol 23, Iss 999, p 999 (2022)
International Journal of Molecular Sciences; Volume 23; Issue 2; Pages: 999
International Journal of Molecular Sciences
Popis: Excess dietary fructose is a major public health concern, yet little is known about its influence on offspring development and later-life disease when consumed in excess during pregnancy. To determine whether increased maternal fructose intake could have long-term consequences on offspring health, we investigated the effects of 10% w/v fructose water intake during preconception and pregnancy in guinea pigs. Female Dunkin Hartley guinea pigs were fed a control diet (CD) or fructose diet (FD; providing 16% of total daily caloric intake) ad libitum 60 days prior to mating and throughout gestation. Dietary interventions ceased at day of delivery. Offspring were culled at day 21 (D21) (weaning) and at 4 months (4 M) (young adult). Fetal exposure to excess maternal fructose intake significantly increased male and female triglycerides at D21 and 4 M and circulating palmitoleic acid and total omega-7 through day 0 (D0) to 4 M. Proteomic and functional analysis of significantly differentially expressed proteins revealed that FD offspring (D21 and 4 M) had significantly increased mitochondrial metabolic activities of β-oxidation, electron transport chain (ETC) and oxidative phosphorylation and reactive oxygen species production compared to the CD offspring. Western blotting analysis of both FD offspring validated the increased protein abundances of mitochondrial ETC complex II and IV, SREBP-1c and FAS, whereas VDAC1 expression was higher at D21 but lower at 4 M. We provide evidence demonstrating offspring programmed hepatic mitochondrial metabolism and de novo lipogenesis following excess maternal fructose exposure. These underlying asymptomatic programmed pathways may lead to a predisposition to metabolic dysfunction later in life.
Databáze: OpenAIRE
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