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. 2017 May 4;32(7):1382–1392. doi: 10.1093/humrep/dex087

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© The Author 2017. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Model for adiponectin signalling in rabbit blastocysts stimulated in vitro with adiponectin. After binding of adiponectin to its receptors, AMPK is activated via APPL1. AMPK regulates β-oxidation by ACC phosphorylation, leading to an increased protein amount of CPT1. Furthermore, adiponectin increases PPARα expression and thereby regulating fatty acid uptake. However, the amount of p38 MAPK, a downstream target of APPL1, was decreased in blastocysts cultured in vitro with adiponectin. Besides its ability to regulate embryonic lipid metabolism directly, adiponectin increases paracrine amount of IGFs and InsR and IGF1R transcription in rabbit blastocysts via AMPK, which may indirectly influence embryonic lipid metabolism ( Direct activation, Direct inhibition, Indirect regulation, = no change, increase).

Inline graphic — Model for adiponectin signalling in rabbit blastocysts stimulated in vitro with adiponectin. After binding of adiponectin to its receptors, AMPK is activated via APPL1. AMPK regulates β-oxidation by ACC phosphorylation, leading to an increased protein amount of CPT1. Furthermore, adiponectin increases PPARα expression and thereby regulating fatty acid uptake. However, the amount of p38 MAPK, a downstream target of APPL1, was decreased in blastocysts cultured in vitro with adiponectin. Besides its ability to regulate embryonic lipid metabolism directly, adiponectin increases paracrine amount of IGFs and InsR and IGF1R transcription in rabbit blastocysts via AMPK, which may indirectly influence embryonic lipid metabolism ( Direct activation, Direct inhibition, Indirect regulation, = no change, increase).