Researchers have uncovered how embryonic livers accumulate an important energy molecule even though they lacks the key enzyme responsible.
In adults, the liver stores glycogen, a sugar polymer that provides a steady supply of blood glucose when needed (e.g. during fasting). Glycogen production is controlled by an enzyme called glucokinase (GK), and mutations resulting in too much or too little GK will lead to hypo- and hyper-glycemia, respectively.
One interesting biological mystery has been that embryonic livers can store plenty of glycogen, yet they don't produce any GK; the liver only starts making this enzyme after newborns drink their first carbohydrate-rich milk.
Joan Guinovart and colleagues found that embryonic mouse livers circumvent the lack of GK by greatly overproducing (~200 fold higher than adult liver) another enzyme known as hexokinase (HK). Such as high amount is necessary because while HK can make glycogen, it's really inefficient.
However, unlike GK, HK makes glycogen independent of blood-glucose levels, and the researchers confirmed this by fasting pregnant mice and observing the embryonic livers did not alter their glycogen accumulation.
Thus, by using HK, embryos safeguard their glycogen production from any changes in maternal diet to ensure abundant storage. This is critical since glycogen is a newborn's principal source of energy in the critical time between birth and first milk meal.
This research was recently published in the Journal Of Biological Chemistry.
The above post is reprinted from materials provided by American Society for Biochemistry and Molecular Biology. Note: Materials may be edited for content and length.
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