What are the harmful effects of hypoglycaemia? Briefly describe the physiological role of hormones in the prevention of hypoglycaemia?

 

Outline:

·        Effects of low blood sugar on brain

·        Key hormones involved:

- glucagon

- epinephrine

- cortisol

- growth hormone

 

Essay:

            Hypoglycaemia is defined by a blood glucose concentration of 45 mg/dL or less. It is usually caused by an exaggerated insulin release following a meal, or low blood glucose ocurring during fasting though this is rare. Alcohol consumption in individuals who are starved or have engaged in prolonged, strenuous exercise can also produce hypoglycaemia. The brain is most affected by a low blood glucose level. The central nervous system has an absolute requirement for a continuous supply of blood-borne glucose to serve as a fuel for energy metabolism. Transient hypoglycaemia can cause cerebral dysfunction, whereas severe, prolonged hypoglycaemia causes brain death. Neuroglycopenia – the impaired delivery of glucose to the brain results in impairment of brain function causing headache, confusion, slurred speech, seizures, coma, and death.

 

            There are two overlapping glucose-regulating systems that are activated by hypoglycaemia: the islets of Langerhans, which release glucagon, and receptors in the hypothalamus, which respond to abnormally low concentration of blood glucose. The hypothalamic glucoreceptors can trigger both the secretoin of epinephrine (mediated by the autonomic nervous system) and release of ACTH and growth hormone by the anterior pituitary.

 

            Hypoglycaemia is combated by decreased release of insulin and increased secretion of glucagon, epinephrine, cortisol, and growth hormone. Glucagon and epinephrine are most important in the acute, short-term regulation of blood glucose levels. Glucagon stimulates hepatic glycogenolysis and gluconeogenesis, increasing blood glucose levels. Epinephrine promotes glycogenolysis and lipolysis, inhibits insulin secretion, and inhibits the insulin-mediated uptake of glucose by peripheral tissues.

 

            Cortisol and growth hormone are less important in the short-term maintenance of blood glucose concentrations. They play a more important role in the long-term management of glucose metabolism. Cortisol increases the hepatic output of glucose from glycogen stores and inhibit insulin-mediated glucose uptake in muscle and adipose tissue. It mobilizes muscle protein for gluconeogenesis by increasing protein degradation and inhibiting protein synthesis and increasing the rate of entry of amino acids into blood. Growth hormone causes decreased glucose uptake by insulin-sensitive tissues and increase plasma free fatty acids and ketoacids.

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