Yu, Haidong ORCID: 0000-0001-6039-6076, Dilbaz, Sedat, Cossmann, Jonas, Hoang, Anh Cuong, Diedrich, Victoria, Herwig, Annika, Harauma, Akiko, Hoshi, Yukino, Moriguchi, Toru, Landgraf, Kathrin, Koerner, Antje, Lucas, Christina, Brodesser, Susanne, Balogh, Lajos, Thuroczy, Julianna, Karemore, Gopal ORCID: 0000-0002-7285-0624, Kuefner, Michael Scott, Park, Edwards A., Rapp, Christine, Travers, Jeffrey Bryant and Roeszer, Tames (2019). Breast milk alkylglycerols sustain beige adipocytes through adipose tissue macrophages. J. Clin. Invest., 129 (6). S. 2485 - 2500. ANN ARBOR: AMER SOC CLINICAL INVESTIGATION INC. ISSN 1558-8238

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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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Yu, HaidongUNSPECIFIEDorcid.org/0000-0001-6039-6076UNSPECIFIED
Dilbaz, SedatUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Cossmann, JonasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hoang, Anh CuongUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Diedrich, VictoriaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Herwig, AnnikaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Harauma, AkikoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hoshi, YukinoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Moriguchi, ToruUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Landgraf, KathrinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Koerner, AntjeUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Lucas, ChristinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Brodesser, SusanneUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Balogh, LajosUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Thuroczy, JuliannaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Karemore, GopalUNSPECIFIEDorcid.org/0000-0002-7285-0624UNSPECIFIED
Kuefner, Michael ScottUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Park, Edwards A.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Rapp, ChristineUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Travers, Jeffrey BryantUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Roeszer, TamesUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-138243
DOI: 10.1172/JCI125646
Journal or Publication Title: J. Clin. Invest.
Volume: 129
Number: 6
Page Range: S. 2485 - 2500
Date: 2019
Publisher: AMER SOC CLINICAL INVESTIGATION INC
Place of Publication: ANN ARBOR
ISSN: 1558-8238
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
ACTIVATED RECEPTOR-GAMMA; FACTOR ACETYLHYDROLASE; INSULIN-RESISTANCE; BOVINE COLOSTRUM; EARLY-CHILDHOOD; PROTEIN-KINASE; DEFICIENT MICE; FATTY-ACIDS; DIET; OBESITYMultiple languages
Medicine, Research & ExperimentalMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/13824

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