Cortisol and growth hormone are released after 1 to 2 hours of hypoglycemia being detected but have a more protracted effect in raising blood glucose, through gluconeogenesis, reducing peripheral glucose utilization and promoting lipolysis so adipose tissue can be used an alternative energy source ( 1). Gluconeogenesis is primarily achieved by the conversion of specific amino acids and glycerol to glucose and urea ( 2, 6). The actions of glucagon and epinephrine are physiologically counteractive to those of insulin and therefore these hormones promote glycogenolysis, gluconeogenesis, inhibit insulin secretion, and limit peripheral glucose uptake by tissues ( 1). Glucagon, from pancreatic alpha cells, and epinephrine from the adrenal medulla, are the initial hormones that are released within minutes in response to hypoglycemia but have a short duration of action. Decreasing blood glucose concentration simultaneously stimulates the release of the counter-regulatory hormones. After the initial post-prandial insulin peak, insulin concentrations begin to decline due to inhibitory feedback from decreasing plasma glucose concentration (< 3.3 mmol/L or 60 mg/dL) and the excretion of insulin by the kidney ( 1, 5). Insulin also promotes production of triglyceride in adipose tissue and of protein and glycogen in skeletal muscle ( 1). Insulin serves to temporarily halt gluconeogenesis and glycogenolysis, stimulate glucose uptake and utilization by insulin-sensitive cells, promote production and storage of glycogen, and inhibit glucagon secretion ( 1, 2) the net effect being prevention of sustained hyperglycemia. The release of insulin from pancreatic beta cells is signaled when glucose is > 6 mmol/L (110 mg/dL) ( 4). After a meal, glucose, amino acids, and gastrointestinal hormones (gastrin, secretin, cholecystokinin, and gastric inhibitory peptide) rise in the plasma. However, hepatic autoregulation, independent of counter regulatory hormones is also vitally important in modulating blood glucose levels ( 3). In the clinically normal animal, the body maintains euglycemia primarily via equilibrium between the glucose-lowering hormone insulin and the glucose-elevating hormones glucagon, cortisol, epinephrine, norepinephrine, and growth hormone (diabetogenic hormones or counter-regulatory hormones) ( 2). Glucose in the body is derived from 3 sources: i) intestinal absorption from the digestion of carbohydrates, ii) dissolution of glycogen (the storage form of glucose) via glycogenolysis predominantly in the liver but also in the muscle, and iii) synthesis of glucose (gluconeogenesis), mostly by the liver, from non-carbohydrate sources e.g., lactate, pyruvate, amino acids, and glycerol, but also a significant amount by the kidneys ( 1).
Laboratory error from improper sample handling or submission, use of a human glucometer, leukemia/polycythemia vera Infection (e.g., sepsis, severe canine babesiosis)ĭecreased hepatic glycogenesis and increased glucose utilizationĭeficiency of enzymes required for glycogen conversion Increased glucose utilization by the tumor but also due to secretion of insulin analogues Severe hepatic disease such as hepatitis, cirrhosis, neoplasia, amyloidosis, hepatotoxinsĭecreased glucose production from lack of a counter-regulatory hormone (i.e., cortisol)ĭecreased glucose production from lack of a counter-regulatory hormone (i.e., growth hormone or adrenocorticotropic hormone)Įxcess glucose utilization due to hypersecretion of insulinĮxtra-pancreatic tumors (e.g., hepatocellular carcinoma, hepatoma, leiomyosarcoma, leiomyoma) Beta blockers via suspected interference of counter- regulatory mechanisms Inadequate intake and depletion of glycogen storesĭrug and toxin associated causes such as iatrogenic insulin overdose, xylitol toxicity, oral hypoglycemic agents (usually sulfonylureas), beta blockersĮxcess glucose utilization due to hypersecretion of insulin and increased tissue sensitivity to insulin. Inadequate glycogen stores, limited fat and muscle mass Neonatal/juvenile or toy breed juvenile hypoglycemia Extreme exercise (e.g., hunting dog hypoglycemia)Įxcess glucose utilization and inadequate glycogen stores
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