Mellora Sharman AREV 2017

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Approach to Hypoglycaemia and Canine Insulinomas Glycaemic Control Glucose is obtained from a variety of sources including digestion and absorption of carbohydrates; breakdown of glycogen (liver and muscles); and synthesis from lactate, pyruvate, amino acids, glycerol via gluconeogenesis. Several hormones are responsible for maintaining circulating blood glucose concentrations within a narrow range (Table 1). Hormones involved in Regulation of Glucose Hormone

Released From:

Action

Effect

Insulin

Pancreatic islets

Glucagon

Pancreatic islets

Adrenaline

Adrenal medulla

Thyroxine

Thyroid

Cortisol

Adrenal Cortex

Growth Hormone

Anterior Pituitary

Increases glucose entry to cells Stimulates glycogen production from glucose Enhances fatty acid synthesis from glucose Suppresses lipolysis Increases protein synthesis Suppresses proteolysis and gluconeogenesis Stimulates release of glucose from glycogen (glycogenolysis) Increases glucose synthesis from fatty acids and amino acids (gluconeogenesis) Increases lipolysis Stimulates growth hormone release Rapidly increases glucose release from glycogen Stimulates glucagon release Stimulates release of fatty acids from adipose tissue Increases glycogenolysis Enhances absorption of glucose and other simple carbohydrates from intestines Increase gluconeogenesis Chronically antagonises all aspects of insulin activity Antagonises insulin (chronically) and reduces peripheral glucose utilization Stimulates lipolysis Decreases glucagon, growth hormone and insulin secretion Decreases secretion and absorption in the gastrointestinal tract

Somatostatin Pancreatic islets

↑ ↑

The primary ‘fuel sensor’ of the body is the pancreatic β-cells, and these respond to changes in plasma levels of various energy substrates and hormones. Signals from energy substrates such as glucose, amino acids, various hormones (insulin, glucagon-like peptide, somatostatin, and adrenalin), and neurotransmitters (nor-adrenaline, acetylcholine) result in glycaemic control. In this scenario glucose is the principle stimulus for insulin release. Very simply stated, glucose metabolism within βcells results in generation of metabolic intermediates, increased cytosolic ATP/ADP and an increase in intracellular calcium ions. Ultimately this combination of events triggers exocytosis of stored insulin into the circulation. The release of insulin in response to elevated blood glucose tends to be biphasic, with an initial rapid ‘first-phase’ release of pre-formed insulin, resulting in a quick peak over several minutes, with a subsequent decline to low level secretion. This is followed by a gradual


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Mellora Sharman AREV 2017 by Innovation in Health Center - Issuu