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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Neonatal hyperoxia leads to white adipose tissue remodeling and susceptibility to hypercaloric diet
Alyson Deprez1,2, Marie-Amélie Lukaszewski1, Coraline De Sousa Do Outeiro1
1Sainte Justine University Hospital (CHU Sainte-Justine) and Research Centre, Department of Pediatrics, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.
Insights
Preterm birth conditions alter white adipose tissue, increasing adult metabolic disease risk. Neonatal hyperoxia causes lasting tissue changes, making it more vulnerable to high-fat diets.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Physiology
Background:
- Preterm birth increases adult cardiovascular and metabolic disease risk.
- White adipose tissue (WAT) is crucial for metabolic homeostasis.
- The impact of preterm birth on WAT is not well understood.
Purpose of the Study:
- To investigate the long-term effects of preterm birth conditions on white adipose tissue (WAT).
- To assess the combined impact of neonatal hyperoxia and a hypercaloric diet on metabolic health.
Main Methods:
- A rodent model simulating preterm birth conditions (neonatal hyperoxia).
- Evaluation of adult perirenal WAT and liver after a high-fat, high-fructose diet (HFFD).
- Analysis of WAT fibrosis, macrophage infiltration, adipocyte size, liver lipids, and triglycerides.
Main Results:
- Neonatal hyperoxia induced WAT fibrosis and macrophage infiltration.
- HFFD exacerbated metabolic dysfunction in hyperoxia-exposed rats, causing adipocyte hypertrophy, liver lipid accumulation, and increased triglycerides.
- Preterm birth conditions led to lasting WAT changes and increased susceptibility to diet-induced metabolic harm.
Conclusions:
- Preterm birth-related conditions have persistent, detrimental effects on WAT.
- These changes suggest a developmental programming of WAT that contributes to long-term metabolic risk in adults born preterm.
- WAT programming may underlie the increased metabolic disease risk observed in preterm-born individuals.
Abstract:
Individuals born preterm are at higher risk of cardiovascular and metabolic diseases in adulthood, through mechanisms not completely understood. White adipose tissue in humans and rodents is a dynamic endocrine organ and a critical player in the regulation of metabolic homeostasis. However, the impact of preterm birth on white adipose tissue remains unknown. Using a well-established rodent model of preterm birth-related conditions in which newborn rats are exposed during postnatal days 3-10 to 80% of oxygen, we evaluated the impact of transient neonatal hyperoxia on adult perirenal white adipose tissue (pWAT) and liver. We further assessed the effect of a second hit with a high-fat high-fructose hypercaloric diet (HFFD). We evaluated 4-month-old adult male rats after 2 months of HFFD. Neonatal hyperoxia led to pWAT fibrosis and macrophage infiltration without modification in body weight, pWAT weight, or adipocyte size. In animals exposed to neonatal hyperoxia vs. room air control, HFFD resulted in adipocyte hypertrophy, lipid accumulation in the liver, and increased circulating triglycerides. Overall, preterm birth-related conditions had long-lasting effects on the composition and morphology of pWAT, along with a higher susceptibility to the deleterious impact of a hypercaloric diet. These changes suggest a developmental pathway to long-term metabolic risk factors observed clinically in adults born preterm through programming of white adipose tissue.
