Insulin resistance and cigarette smoking

• Published in: The Lancet (British edition) Vol. 339; no. 8802; pp. 1128 - 1130
• Main Authors: Facchini, F.S., Hollenbeck, C.B., Jeppesen, J., Ida Chen, Y.-D., Reaven, G.M.
• Format: Journal Article
• Language: English
• Published: London Elsevier Ltd 09.05.1992; Lancet; Elsevier Limited
• Subjects: Academic Medical Centers; Adult; Alcohol Drinking - adverse effects; Biological and medical sciences; Blood; Blood Glucose - analysis; Body Mass Index; California - epidemiology; Cardiovascular diseases; Cholesterol; Cigarettes; Diabetes Complications; Energy Metabolism; Exercise; Female; Glucose; Glucose Tolerance Test; Humans; Hyperinsulinism - blood; Hyperinsulinism - epidemiology; Hyperinsulinism - etiology; Hyperlipidemias - blood; Hyperlipidemias - epidemiology; Hyperlipidemias - etiology; Insulin; Insulin - blood; Insulin Resistance; Lipoproteins, HDL - blood; Lipoproteins, LDL - blood; Lipoproteins, VLDL - blood; Male; Medical research; Medical sciences; Smoking; Smoking - adverse effects; Tobacco; Toxicology; Triglycerides - blood; California; Endocrinopathy; Human; Insulin; Negative therapeutic reaction; Diabetes mellitus; Tobacco smoking
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/0140-6736(92)90730-Q

Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0·66 [0·10] vs 0·39 [0·03] mmol/l, p<0·02) and cholesterol (0·45 [0·06] vs 0·23 [0·04] mmol/l, p<0·005) concentrations and lower high-density-lipoprotein cholesterol concentrations (1·16 [0·05] vs 1·51 [0·08] mmol/l, p<0·001). Although plasma glucose concentrations in response to the oral glucose load were similar in the two groups, plasma insulin response of the smokers was significantly higher (p<0·001). Finally, smokers had higher steady-state plasma glucose concentrations in response to a continuous infusion of glucose, insulin, and somatostatin (8·4 [0·2] vs 5·0 [0·3] mmol/l, p<0·001), despite similar steady-state plasma insulin concentrations. The findings show that chronic cigarette smokers are insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of coronary heart disease.