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Low birth weight male guinea pig offspring display increased visceral adiposity in early adulthood
Ousseynou Sarr1, Jennifer A Thompson2, Lin Zhao1
1Department of Obstetrics and Gynecology, Children's Health Research Institute, Lawson Health Research Institute, Western University, London, Ontario, Canada.
Insights
Low birth weight offspring from uteroplacental insufficiency pregnancies develop increased visceral fat. This is linked to altered gene and microRNA expression, impacting lipid synthesis and adipocyte development in adulthood.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Syndrome
Background:
- Uteroplacental insufficiency (UPI) during pregnancy is a known cause of intrauterine growth restriction (IUGR).
- IUGR is associated with an increased risk of developing visceral obesity in adulthood.
- The molecular mechanisms linking IUGR to adult obesity require further elucidation.
Purpose of the Study:
- To investigate the visceral adipose tissue molecular signature in low birth weight (LBW) offspring from UPI-induced IUGR pregnancies.
- To examine alterations in gene expression, protein phosphorylation, and microRNA profiles related to lipid synthesis in LBW guinea pigs.
Main Methods:
- Male guinea pig pups were categorized as normal birth weight (NBW) or LBW (induced by uterine artery ablation).
- Offspring were fed a control diet from weaning to 145 days (young adulthood) and then sacrificed.
- Epididymal white adipose tissue (EWAT) was analyzed for gene expression (lipid synthesis, lipolysis), protein phosphorylation (lipid synthesis regulators), and microRNA (miR) expression.
Main Results:
- LBW offspring exhibited similar body weights to NBW offspring at 145 days but had increased EWAT weight and lipid content, with adipocyte hypertrophy.
- Increased mRNA expression of lipid synthesis genes (ACC1, DGAT2, PPARγ1) and lipogenic genes (HSL, FABP4) was observed in LBW EWAT.
- Decreased phosphorylation of key lipid synthesis regulators (ACC, PPARγ) and increased expression of adipogenesis-related miRs (miR-24, miR-103-2) were found in LBW EWAT.
Conclusions:
- Adverse in utero conditions from UPI-induced IUGR lead to chronic alterations in lipid synthesis pathways in adult offspring.
- These molecular changes, including gene and miR expression and protein phosphorylation, are associated with increased visceral adiposity.
- LBW offspring from IUGR pregnancies display a distinct molecular signature in visceral adipose tissue, predisposing them to obesity.
Abstract:
Uteroplacental insufficiency (UPI)-induced intrauterine growth restriction (IUGR) predisposes individuals to adult visceral obesity. We postulated that low birth weight (LBW) offspring, from UPI-induced IUGR pregnancies, would display a visceral adipose lipogenic molecular signature involving altered gene expression, phosphorylation status of proteins of the lipid synthesis pathway and microRNA (miR) expression profile, occurring in association with increased visceral adiposity. Normal birth weight (NBW) and LBW (obtained by uterine artery ablation) male guinea pig pups were fed a control diet from weaning to 145 days and sacrificed. Despite being lighter at birth, LBW pups displayed body weights similar to NBW offspring at 145 days. At this age, which represents young adulthood, the relative weights of LBW epididymal white adipose tissue (EWAT) and lipid content were increased; which was consistent with adipocyte hypertrophy in the LBW offspring. Additionally, the mRNA expression of lipid synthesis-related genes including acetyl-CoA carboxylase 1 (ACC1), diglyceride acyltransferase 2 (DGAT2) and peroxisome proliferator-activated receptor gamma 1 (PPARγ1), was increased in LBW EWAT. Further, LBW EWAT displayed decreased phospho-ACC (Ser79) and phospho-PPARγ (Ser273) proteins. Moreover, the mRNA expression of hormone-sensitive lipase (HSL) and fatty acid binding protein 4 (FABP4), both involved in promoting adipose lipid storage, was increased in LBW EWAT. Finally, miR-24 and miR-103-2, miRs related to adipocyte development, were both increased in LBW EWAT. These findings indicate that, following an adverse in utero environment, lipid synthesis-related genes and miR expression, along with phosphorylation status of key regulators of lipid synthesis, appear to be chronically altered and occur in association with increased visceral adiposity in young adult IUGR male offspring.
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