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Cigarette smoking is associated with elevated adrenal androgen response to adrenocorticotropin
A Hautanen1, M Mänttäri, M Kupari
1Department of Clinical Chemistry, University of Helsinki, Finland.
Insights
Smoking significantly impacts male steroid levels, increasing adrenal androgens like androstenedione and dehydroepiandrosterone sulfate (DHEAS). This suggests smoking impairs adrenal cortex hydroxylase activity, affecting hormone production.
Area of Science:
- Endocrinology
- Metabolic Health
- Toxicology
Background:
- Cigarette smoking is a known factor influencing various physiological processes.
- Endogenous steroid profiles are critical for male health and metabolic function.
- Previous research indicates smoking's complex relationship with hormone levels.
Purpose of the Study:
- To investigate the effects of cigarette smoking on endogenous steroid levels in men.
- To compare steroid profiles between smokers and non-smokers in dyslipidemic and general male populations.
- To explore potential mechanisms linking smoking to altered adrenal steroidogenesis.
Main Methods:
- Analysis of basal and ACTH-stimulated steroid concentrations in two male cohorts (n=189 and n=100).
- Measurement of androstenedione, dehydroepiandrosterone sulfate (DHEAS), cortisol, and other steroid hormones.
- Assessment of lipid profiles and apolipoprotein AI in one cohort.
Main Results:
- Smokers exhibited higher basal androstenedione and DHEAS levels and androstenedione/cortisol ratios.
- ACTH stimulation revealed increased androstenedione and dehydroepiandrosterone (DHEA) concentrations in smokers.
- Smokers showed altered lipid profiles (lower HDL-cholesterol, higher triglycerides) but similar testosterone and SHBG levels.
Conclusions:
- Smoking appears to decrease adrenal cortex 21- or 11 beta-hydroxylase activity.
- This leads to an increased secretion of adrenal androgens in male smokers.
- Smoking-induced alterations in steroidogenesis may contribute to metabolic disturbances.
Abstract:
Cigarette smoking alters the pattern of endogenous steroid levels. We examined this phenomenon in two separate male groups. Group A consisted of 189 dyslipidemic men participating in the Helsinki Heart Study and group B of 100 men including patients with heart disease and healthy controls. The subjects in the latter group underwent ACTH-testing. In group A, smokers had significantly higher basal androstenedione and dehydroepiandrosterone sulfate (DHEAS) levels and androstenedione/cortisol ratios than nonsmokers. Mean concentrations of cortisol, dehydroepiandrosterone (DHEA), androstanediol glucuronide, testosterone, and sex-hormone binding globulin (SHBG) did not differ between smokers and nonsmokers. In group B, smokers had lower high density lipoprotein (HDL)-cholesterol and apolipoprotein AI and higher triglyceride levels than nonsmokers. Basal androstenedione and ACTH stimulated androstenedione and DHEA concentrations were higher in smokers. No significant differences were found in basal insulin, SHBG, estrone, estradiol, testosterone, free testosterone, and dihydrotestosterone concentrations between smokers and nonsmokers. These results suggest that smoking decreases the activity of either 21- or 11 beta-hydroxylase in the adrenal cortex, which results in increased secretion of adrenal androgens.