Hypoglycaemia is an important complication of insulin therapy in patients with diabetes. At the onset of the disease most patients recognize the symptoms (Fig. 42d) and are able to take remedial action, but ‘hypoglycaemia awareness’ decreases with the duration of insulin treatment so that after 20 years of diabetes up to a half of patients may have lost their awareness of the symptoms.
Severe hypoglycaemia, requiring the assistance of another person for treatment, is an important cause of morbidity and mortality in insulin treated diabetics. Family members, friends or school staff should be educated in recognition of the symptoms and how to treat it. Early symptoms can be treated with oral carbohydrate; if the patient is unable to swallow intramuscular glucagon is helpful as is buccal glucose gel. Patients and their relatives can be trained to administer intramuscular glucagon. If there is evidence of impaired consciousness medical advice should be sought and the patient treated with intravenous glucose.
Biosynthesis, storage and secretion
Glucagon is synthesized principally in the pancreatic a-cell, and is cleaved from a much larger precursor molecule, preproglucagon (179 amino acids in humans). The preproglucagon gene in humans is located on chromosome 2. Preproglucagon yields proglucagon (Fig. 42a). The N-terminal fragment of proglucagon is termed glicentin-related polypeptide fragment (GRPP), so-called because it contains glicentin (glucagon-like immunoreactivity-1), an intestinal glucagon sequence-containing polypeptide. GRPP and glucagon are stored together in the cell in granules, and released together in approximately equimolar quantities.
Both these peptides are also stored and released from cells in the gut, and glucagon and GRPP form part of a larger family of gut hormones (see Chapter 43). The glucagon content of a healthy human adult pancreas ranges from about 3–5 μg/g of net pancreas weight.
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