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Visualization and Quantification of Brown and Beige Adipose Tissues in Mice using [18F]FDG Micro-PET/MR Imaging
Published on: July 1, 2021
Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages
Haidong Yu1, Sedat Dilbaz1,2, Jonas Coßmann1
1Institute of Neurobiology, and.
Insights
Breast milk lipids called alkylglycerol-type (AKG-type) ether lipids protect infants from obesity by maintaining beige adipose tissue. This crucial mother-to-child lipid signaling is essential for healthy infant development and preventing adult obesity.
Area of Science:
- Lipid signaling
- Adipose tissue biology
- Infant nutrition
Background:
- Childhood obesity is a growing global health crisis, with early-onset obesity often leading to adult obesity and related diseases.
- Current infant nutrition, including formula, lacks specific protective lipid compounds found in breast milk.
- Understanding early-life metabolic programming is crucial for preventing long-term health issues.
Purpose of the Study:
- To identify specific lipid signaling pathways in breast milk that protect against infant obesity.
- To elucidate the mechanism by which these lipids influence adipose tissue development in infants.
- To explore the potential therapeutic implications of these findings for obesity prevention.
Main Methods:
- Analysis of lipid species in breast milk and their metabolism in infant adipose tissue.
- Investigation of the role of alkylglycerol-type (AKG-type) ether lipids in beige adipose tissue (BeAT) maintenance.
- Study of the interaction between adipose tissue macrophages (ATMs) and AKGs, including PAF production and IL-6/STAT3 signaling.
- Comparison of AKG signaling in infants versus adults, and in lean versus obese adipose tissue.
Main Results:
- Breast milk contains unique AKG-type ether lipids absent in infant formula and adult diets.
- AKGs promote infant beige adipose tissue (BeAT) development and prevent its conversion to white adipose tissue (WAT).
- Metabolism of AKGs by ATMs produces platelet-activating factor (PAF), activating IL-6/STAT3 signaling and BeAT development.
- Lack of AKG intake in infancy results in BeAT loss and increased fat accumulation.
- AKG signaling is infant-specific but reactivated in ATMs of obese adults, potentially reducing obesity.
Conclusions:
- AKG-type ether lipids in breast milk are essential for healthy adipose tissue development in infants.
- This mother-to-child lipid signaling pathway offers a protective mechanism against early-onset obesity.
- Targeting AKG metabolism could represent a novel strategy for obesity prevention and treatment.
Abstract:
Prevalence of obesity among infants and children below 5 years of age is rising dramatically, and early childhood obesity is a forerunner of obesity and obesity-associated diseases in adulthood. Childhood obesity is hence one of the most serious public health challenges today. Here, we have identified a mother-to-child lipid signaling that protects from obesity. We have found that breast milk-specific lipid species, so-called alkylglycerol-type (AKG-type) ether lipids, which are absent from infant formula and adult-type diets, maintain beige adipose tissue (BeAT) in the infant and impede the transformation of BeAT into lipid-storing white adipose tissue (WAT). Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of AKG intake in infancy leads to a premature loss of BeAT and increases fat accumulation. AKG signaling is specific for infants and is inactivated in adulthood. However, in obese adipose tissue, ATMs regain their ability to metabolize AKGs, which reduces obesity. In summary, AKGs are specific lipid signals of breast milk that are essential for healthy adipose tissue development.
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