Insulin-induced hypoglycemia suppresses plasma parathyroid hormone levels in patients with adrenal insufficiency

• Published in: Metabolism, clinical and experimental clinical and experimental, 2004-10, Vol.53 (10), p.1251-1254
• Main Authors: Suliman, Abdulwahab M., Freaney, Rosemarie, McBrinn, Yvonne, Gibney, James, Murray, Barbara, Smith, Thomas P., McKenna, T.Joseph
• Format: Article
• Language: English
• Subjects: Adrenal Insufficiency - blood; Adrenal Insufficiency - drug therapy; Adrenals. Adrenal axis. Renin-angiotensin system (diseases); Biological and medical sciences; Blood Glucose - metabolism; Calcium - blood; Collagen Type I - metabolism; Endocrinopathies; Female; Glucocorticoids - therapeutic use; Humans; Hypoglycemia - chemically induced; Hypoglycemia - metabolism; Hypoglycemic Agents; Insulin; Magnesium - blood; Male; Medical sciences; Middle Aged; Non tumoral diseases. Target tissue resistance. Benign neoplasms; Parathyroid Hormone - blood; Phosphates - blood
• ISSN: 0026-0495; 1532-8600
• DOI: 10.1016/j.metabol.2004.01.005

Hypoglycemia has been reported to cause suppression of parathyroid hormone (PTH) levels in serum in normal subjects. It is possible that increasing cortisol levels in response to hypoglycemia was responsible. To examine this possibility the acute PTH response to insulin administration and resulting hypoglycemia was examined in patients with adrenal insufficiency. The possible acute impact of insulin-induced hypoglycemia on bone formation and bone resorption in the absence of an endogenous cortisol response was also examined. A prospective open study was undertaken to examine the acute effects of insulin and resulting hypoglycemia on PTH levels, on bone formation as indicated by serum levels of aminoterminal propeptide of type 1 procollagen (PINP), and on bone resorption as indicated by serum levels of β carboxy terminal telopeptide of type 1 collagen (β-CTx). Seven patients with adrenal insufficiency participated. These patients were studied on 3 occasions under different conditions: (1) when insulin was administered to induce hypoglycemia while the patients received their routine glucocorticoid replacement; (2) when the patients received their routine glucocorticoid replacement, but were not rendered hypoglycemic; and (3) when they did not receive glucocorticoid replacement and were not rendered hypoglycemic, ie, untreated. This facilitated isolation of the PTH response to insulin and hypoglycemia from the effects of the normal increase in endogenous cortisol levels in response to hypoglycemia. Blood samples were taken at baseline and after 3 hours while the subjects continued fasting for measurement of plasma glucose, serum ionized calcium (Cai), magnesium, phosphate, PINP, PTH, and β-CTx. Insulin 0.075 IU/kg body weight was given intravenously after the first blood sample. The usual morning glucocorticoid replacement dose was given 20 minutes after the baseline blood sample was obtained. After the administration of insulin, plasma glucose decreasedl from 4.8 ± 0.5 to 2.7 ± 0.5 mmol/L, mean ± SD ( P < .0001). PTH was not influenced by time or glucocorticoid treatment, but decreased in response to insulin-induced hypoglycemia ( P < .05). Serum levels of PINP and β-CTx decreased when untreated between 9 am and 12 pm ( P < .05), but were not independently influenced by insulin-induced hypoglycemia or glucocorticoid treatment. Serum levels of Cai increased and serum phosphate levels decreased in response to insulin-induced hypoglycemia, while serum phosphate