Ashok Yadav/LinkedIn
Feb 26, 2026, 15:39
Ashok Yadav: Placental Glycogen as a Vital Energy Reserve for Fetal and Placental Health
Ashok Yadav, Biology Educator of Biology Faculty at Apex Academy, shared a post on LinkedIn:
”Placental glycogen storage serves as a vital energy reserve, primarily thought to support fetal growth and maintain glucose levels when maternal supply fluctuates. While its exact function in humans is still debated, animal models provide significant evidence for its role in both fetal development and placental health.
Functions of Placental Glycogen
- Fetal Energy Support: It is widely hypothesized that placental glycogen acts as a ‘buffer,’releasing glucose during periods of high fetal demand, particularly in late gestation.
- Local Placental Fuel: The placenta is a highly metabolic organ; glycogen stores may provide direct energy for its own functions, such as hormone production and maintaining vasomotor activity in placental blood vessels.
- Pathological Protection: In cases of maternal diabetes, the placenta may store excess glucose as glycogen to protect the fetus from hyperglycemia.
Dynamics and Storage Locations
- Temporal Peaks: In humans, glycogen accumulation peaks in the first trimester and declines toward term. In mice, it peaks around embryonic day 15.5.
- Cellular Storage:
- Mice: Specialized glycogen trophoblast cells in the junctional zone are the primary storage site.
- Humans: Storage occurs in extravillous trophoblasts (EVTs) located in the basal plate.
Clinical Significance
- Growth Complications: Both abnormally high and low placental glycogen levels are linked to Intrauterine Growth Restriction (IUGR) and pre-eclampsia.
- Diabetes: Maternal diabetes often leads to aberrant glycogen storage, which can disrupt normal metabolic communication between mother and fetus.
- Genetic Disorders: Rare conditions like Glycogen Storage Disease Type IV can show specific placental involvement, potentially allowing for prenatal diagnosis via biopsy.”
Stay updated with Hemostasis Today.
-
May 29, 2026, 09:53Yassin Taher: Recognizing Clonal Eosinophilic Disorders in Pediatric Hypereosinophilic Syndrome
-
May 29, 2026, 09:52Sergio Emanuel Kaiser: Ruvonoflast and a New Anti-Inflammatory Strategy for Residual Cardiovascular Risk
-
May 29, 2026, 09:50Maria Symiakaki: Advancing Cardiovascular Prevention at the 2026 Congress of the European Atherosclerosis Society
-
May 29, 2026, 09:37Katie Baca-Motes: What Can Menstrual Cycle Physiology Tell Us About Health Beyond Reproduction?
-
May 29, 2026, 09:35Torben Boelk: Bringing Plasma Donation to the Heart of Leipzig
-
May 29, 2026, 04:37Josefin Ahnström: How Andexanet Alfa Impacts TFPIα Function
-
May 29, 2026, 03:19Building Safer Systems for Anticoagulation Management – ISTH
-
May 29, 2026, 03:07Early Diagnosis Can Change the Lives of Women With Haemophilia – EHC
-
May 29, 2026, 02:41Ifeanyichukwu Ifechidere: The Biggest DOAC Myth in Coagulation – ‘No Monitoring Required’