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Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages
Haidong Yu, … , Jeffrey Bryant Travers, Tamás Röszer
Haidong Yu, … , Jeffrey Bryant Travers, Tamás Röszer
Published May 13, 2019
Citation Information: J Clin Invest. 2019;129(6):2485-2499. https://doi.org/10.1172/JCI125646.
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Research Article Immunology Metabolism

Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages

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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.

Authors

Haidong Yu, Sedat Dilbaz, Jonas Coßmann, Anh Cuong Hoang, Victoria Diedrich, Annika Herwig, Akiko Harauma, Yukino Hoshi, Toru Moriguchi, Kathrin Landgraf, Antje Körner, Christina Lucas, Susanne Brodesser, Lajos Balogh, Julianna Thuróczy, Gopal Karemore, Michael Scott Kuefner, Edwards A. Park, Christine Rapp, Jeffrey Bryant Travers, Tamás Röszer

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Figure 2

Lack of breastfeeding and lack of neonatal AKG intake reduce beige adipocyte content in the iAT.

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Lack of breastfeeding and lack of neonatal AKG intake reduce beige adipo...
(A–C) Color-coded CIM showing the relative transcript level of UCP1 in human infant iAT. Also see Supplemental Figure 6A. (A) Breastfed infants, (B) formula-fed infants; age in years and the individual identifier number are indicated for each sample. (C) CIM showing relative UCP1 level in 0.3- to 1.0-yearold infants. UCP1 level was normalized to 3 reference genes (ACTB, TBP, HPRT1), and individual values were compared with the mean value of the 2 study groups. (D) Histology and BeAT content of the iAT in breastfed and formula-fed human infants. Scale bars: 100 μm (H&E); 25 μm (UCP1). (E) Scheme of artificial rearing (AR) experiment. (F) Histology of the iAT at P10 and P34 in breastfed and AR mice. ac, white adipocyte. Scale bars: 80 μm. (G) BeAT content of the iAT at P34. (H) CIM showing relative UCP1 level in iAT on P10 and P34. **P < 0.01; ***P < 0.001, Student’s 2-tailed unpaired t test (D); 1-way ANOVA with Dunnett’s post hoc test (G).
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