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Adiponectin Deficiency Alters Placenta Function but Does Not Affect Fetal Growth in Mice
Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Unit for Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.
Vise andre og tillknytning
2022 (engelsk)Inngår i: International Journal of Molecular Sciences, ISSN 1661-6596, E-ISSN 1422-0067, Vol. 23, nr 9, artikkel-id 4939Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Adiponectin administration to pregnant mice decreases nutrient transport and fetal growth. An adiponectin deficiency, on the other hand, as seen in obese women during pregnancy, alters fetal growth; however, the mechanism is unclear. To determine the role of adiponectin on placenta function and fetal growth, we used adiponectin knockout, adiponectin heterozygote that displays reduced adiponectin levels, and wild-type mice on a control diet or high fat/high sucrose (HF/HS) diet. Triglycerides (TGs) in the serum, liver, and placenta were measured using colorimetric assays. Gene expression was measured using quantitative RT-PCR. Adiponectin levels did not affect fetal weight, but it reduced adiponectin levels, increased fetal serum and placenta TG content. Wildtype dams on a HF/HS diet protected the fetuses from fatty acid overload as judged by increased liver TGs in dams and normal serum and liver TG levels in fetuses, while low adiponectin was associated with increased fetal liver TGs. Low maternal adiponectin increased the expression of genes involved in fatty acid transport; Lpl and Cd36 in the placenta. Adiponectin deficiency does not affect fetal growth but induces placental dysfunction and increases fetal TG load, which is enhanced with obesity. This could lead to imprinting effects on the fetus and the development of metabolic dysfunction in the offspring. 

sted, utgiver, år, opplag, sider
MDPI, 2022. Vol. 23, nr 9, artikkel-id 4939
Emneord [en]
adiponectin, fetal growth, placenta, triglycerides
HSV kategori
Forskningsprogram
Translationell medicin TRIM
Identifikatorer
URN: urn:nbn:se:his:diva-21132DOI: 10.3390/ijms23094939ISI: 000795395700001PubMedID: 35563332Scopus ID: 2-s2.0-85129085040OAI: oai:DiVA.org:his-21132DiVA, id: diva2:1657716
Forskningsfinansiär
Swedish Research Council, 2013-07107Swedish Research Council, 2020-02485Swedish Research Council, 2020-01463Diabetesfonden, DIA2019-419Magnus Bergvall Foundation, 2018-02891Åke Wiberg Foundation, M17-0113Adlerbertska Research Foundation, E 2017/26Hjalmar Svensson's Research Foundation, HJSV2017070
Merknad

CC BY 4.0

Attribution 4.0 International (CC BY 4.0)

© 2022 by the authors. Licensee MDPI, Basel, Switzerland.

Correspondence: anna.benrick@gu.se or anna.benrick@his.se

This research was funded by the Swedish Research Council (2013-07107, 2020-02485, 2020-01463), the NovoNordisk Foundation (NNF19OC0056601), the Swedish Diabetes Foundation (DIA2019-419), the Diabetes Research and Wellness Foundation, Magnus Bergvall Foundation (2018-02891), Åke Wiberg Foundation (M17-0113), Adlerbertska Foundation (E 2017/26), Hjalmar Svensson Foundation (HJSV2017070), and The Royal Society of Arts and Sciences in Gothenburg (2019-330).

Tilgjengelig fra: 2022-05-12 Laget: 2022-05-12 Sist oppdatert: 2022-07-13bibliografisk kontrollert

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