One of the roles of the liver is the detoxification of the unconjugated bilirubin (UCB) produced during haemoglobin metabolism. In newborns the whole functions of the liver are not completelly activated, thus, in the first days of life, the amount of blood UCB can increase to potentially toxic levels. When entering the tissues, UCB is responsible for the yellow skin and sclera color, but most importantly UCB can induce a neurological damages, such as auditory, motor, and cognitive deficits (transitory or permanent), or even death, if not treated.
The Gilbert syndrome: When bilirubin turns to protection
Differently from the neonatal jaundice, mutations in the promoter of the UGT1A1, the haptic enzyme responsible for the transformation and clearance of unconjugated bilirubin, lead to a minimal increase of the blood bilirubin levels (higher than the normal value of 1mg/dL, condition known as Gilbert syndrome). This small increase of blood UCB seems to play a protective function preventing the onset of metabolic syndrome (obesity), diabetes, cardiovascular diseases, and certain cancers, possibly due to the anti-inflammatory and anti-oxidant properties of the bilirubin itself.
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