An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is injected into a patient's vein, after which blood glucose is measured at regular intervals. This procedure is performed to assess pituitary function, adrenal function, insulin sensitivity,[1][2] and sometimes for other purposes. An ITT is usually ordered and interpreted by an endocrinologist.
When used to assess insulin sensitivity, a standard dose of insulin is administered, and blood glucose is monitored with frequent sampling. The plasma glucose disappearance rate (KITT) indicates the degree of whole-body insulin sensitivity, and correlates well with the gold-standard glucose clamp technique.[1]
When used for assessing the integrity of the hypothalamic–pituitary–adrenal axis (HPA), insulin injections are continued to the point of inducing extreme hypoglycemia below 2.2 mmol/L (40 mg/dL). Patient must have symptomatic neuroglycopenia to trigger counter-regulatory cascade. Glucose levels below 2.2 mmol/L are insufficient absent symptoms. The brain must register low glucose levels. In response, adrenocorticotropic hormone (ACTH) and growth hormone (GH) are released as a part of the stress mechanism. ACTH elevation causes the adrenal cortex to release cortisol. Normally, both cortisol and GH serve as counterregulatory hormones, opposing the action of insulin, i.e. acting against the hypoglycemia.[3]
ITT to the point of extreme hypoglycemia is considered to be the gold standard for assessing the integrity of the HPA. Sometimes ITT is performed to assess the adrenal function, e.g. before surgery. It is assumed that the ability to respond to insulin-induced hypoglycemia translates into appropriate cortisol rise in the stressful event of acute illness or major surgery.[4] The extreme hypoglycemic version of the ITT is potentially very dangerous and must be undertaken with great care, because it can iatrogenically induce the equivalent of a diabetic coma. A health professional must attend it at all times. Other provocation tests which cause much less release of growth hormone include the use of glucagon, arginine and clonidine.
^ abOkita K, Iwahashi H, Kozawa J, Okauchi Y, Funahashi T, Imagawa A, Shimomura I (May 4, 2014). "Usefulness of the insulin tolerance test in patients with type 2 diabetes receiving insulin therapy". J Diabetes Investig. 5 (3): 305–312. doi:10.1111/jdi.12143. PMC 4020335. PMID 24843779.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^"Insulin Tolerance Test (ITT)". Melior Discovery. Retrieved 1 October 2019.
^Greenwood FC, Landon J, Stamp TC (1965). "The plasma sugar, free fatty acid, cortisol, and growth hormone response to insulin. I. In control subjects". J Clin Invest. 45 (4): 429–. doi:10.1172/JCI105357. PMC 292717. PMID 5937021.
^Plumpton FS, Besser GM (1969). "The adrenocortical response to surgery and insulin-induced hypoglycaemia in corticosteroid-treated and normal subjects". Br J Surg. 56 (3): 216–219. doi:10.1002/bjs.1800560315. PMID 5776687. S2CID 29500731.
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