CASE FILES: BIOCHEMISTRY
A N S W E R TO C A SE 26: SO M O G Y I E F F E C T
A 56-year-old man with a long history of insulin diabetes with
evening hypoglycemia and fasting morning hyperglycemia.
Biochemical mechanism of hypoglycemia: The low nighttime serum
blood sugar stimulates the counter-regulatory hormones to try to raise
the glucose level. These include epinephrine, glucagon, cortisol, and
growth hormone, which affect the glucose level and raise it by the time
morning comes around.
C L IN IC A L C O R R E L A T IO N
This individual has a classic manifestation of the Somogyi effect, which is
fasting morning hyperglycemia in response to hypoglycemia in the early
morning and late night hours. The danger is that if nighttime blood glucose
levels are not measured, the physician may interpret the patient as having
hyperglycemia and require even higher doses of insulin. This would be exactly
the wrong treatment, since the hypoglycemia is leading to counter-regulatory
hormone reaction, and a very low sugar level bound to the high level in the
morning. The diagnosis is established by measuring a 2
glucose level, and
when confirmed, then the bedtime NPH insulin (intermediate to long acting)
needs to be decreased.
A PPR O A C H TO G L U C O SE A N D C O U N T E R -
R E G U L A T O R Y H O R M O N E S
Understand regulation of glycogen and glucose production.
Understand how insulin and epinephrine affect glucose levels.
Be familiar with the regulation of glucagons.
Know about diabetic ketoacidosis and biochemical mechanism.
Epinephrine: Adrenaline; a catecholamine hormone derived from the
amino acids phenylalanine or tyrosine that is synthesized and secreted
by the adrenal medulla in response to stress.
GLUT 2: Glucose transporter isoform 2; a transport protein located on the
plasma membrane of liver, pancreas, intestine, and kidney that will allow
glucose to cross the membrane depending on the concentration gradient.
GLUT 2 is the transporter that enables export of glucose from the liver.
Ketoacidosis: An elevation of the ketone body concentration that decreases
the pH of the arterial blood to a pathologic condition.