Abnormal effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus

• Published in: Clinical endocrinology (Oxford) Vol. 46; no. 3; pp. 351 - 357
• Main Authors: Chiodera, P., Volpi, R., Capretti, L., Speroni, G., Necchi-Ghiri, S., Caffarri, G., Colla, R., Coiro, V.
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01.03.1997; Blackwell
• Subjects: Adult; Arginine Vasopressin - metabolism; Biological and medical sciences; Diabetes Mellitus, Type 1 - metabolism; Functional investigation of endocrine glands and genital system; Growth Hormone - metabolism; Humans; Hydrocortisone - metabolism; Insulin; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Pituitary Hormones - metabolism; Smoking - adverse effects; Smoking - metabolism; Endocrinopathy; Human; Immunopathology; Pathophysiology; Steroid hormone; Toxicity; 8-Arginine vasopressin; STH; Peptide hormone; Tobacco smoking; Autoimmune disease; Hydrocortisone; Glucocorticoid; Neuropeptide; Assay; Protein hormone; Adenohypophyseal hormone; Neurohypophyseal hormone; Adrenal hormone; Insulin dependent diabetes; Biological effect; Hormonal investigation
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1046/j.1365-2265.1997.1470945.x

OBJECTIVE We observed the effect of smoking two cigarettes on GH, AVP and cortisol secretion in patients with diabetes and normal subjects. DESIGN AND PATIENTS We tested 10 male smokers with insulin‐dependent diabetes mellitus (IDDM) and 10 normal smokers. On a different occasion, normal and diabetic smokers were tested with an insulin (0.15 U/kg body weight) tolerance test (ITT). MEASUREMENTS Hypoglycaemia‐induced hormonal responses in smokers were compared with those observed in 10 diabetic and 10 normal non smokers. RESULTS All subjects showed similar basal GH, cortisol and AVP levels. In the normal subjects, cigarette smoking induced a significant increase in circulating GH, AVP and cortisol levels, with mean peaks 3.3, 3 and 1.58 times higher than baseline, respectively. Smoking‐induced hormonal responses were significantly higher in diabetics (mean peak was 5.2 times higher than baseline for GH, 4.0 for AVP and 1.83 for cortisol). Insulin induced a similar hypoglycaemic nadir in all subjects at 30 minutes, even though the diabetic subjects had a delayed recovery in blood glucose levels. GH and AVP responses to hypoglycaemia were significantly higher in diabetic (mean peaks 11.5 and 3.2 times higher than baseline, respectively) than in normal (mean peaks 7.3 and 1.9) non‐smokers, whereas these groups showed similar cortisol responses (mean peak 2.3 times higher than baseline). Smoking did not change any hypoglycaemia‐induced hormonal rise in the normal controls, whereas it significantly enhanced GH, AVP and cortisol levels (mean peaks 14.5, 4 and 3.8 times higher than baseline, respectively) in diabetics. CONCLUSIONS In patients with IDDM, cigarette smoking not only elicits higher GH, AVP and cortisol responses than in normal subjects, but also enhances the counter‐regulatory hormone responses to insulin‐induced hypoglycaemia. These findings suggest interactions between nicotine inhaled with cigarette smoking and diabetes‐induced neuroendocrine alterations.