Adiponectin regulates glycogen metabolism at the human fetal–maternal interface

Area of Science:

• Reproductive biology
• Endocrinology
• Cellular metabolism

Background:

• Early pregnancy relies on histiotrophic nutrition from endometrial secretions.
• Glycogen is crucial for fetal development, but its metabolism at the fetal-maternal interface is unclear.
• Adiponectin, a cytokine regulating homeostasis, is a potential key factor.

Purpose of the Study:

• To elucidate the role of adiponectin in glycogen metabolism at the fetal-maternal interface.
• To investigate adiponectin's effects on endometrial stromal cells (EnSCs) and trophoblasts.
• To understand adiponectin's contribution to early pregnancy nutrition.

Main Methods:

• Investigated adiponectin's impact on glucose transporter 1 expression and glucose catabolism in EnSCs.
• Assessed adiponectin's influence on glycogen synthesis, accumulation, and secretion in EnSCs.
• Examined adiponectin's effect on glycogen endocytosis by human villous trophoblasts.
• Analyzed glycogen degradation in placental cells.

Main Results:

• Adiponectin increases glucose uptake and glycogen synthesis in EnSCs.
• Adiponectin promotes glycogen accumulation and secretion from EnSCs via phosphoinositide-3 kinase activation.
• Adiponectin significantly reduces glycogen endocytosis by trophoblasts.
• Endocytosed glycogen is degraded into glucose in placental lysosomes.

Conclusions:

• Adiponectin plays a dual role: promoting endometrial glycogen synthesis and reducing placental glycogen uptake.
• Adiponectin is potentially vital for conceptus nutrition during the first trimester by controlling uterine and placental glycogen metabolism.