Introduction Improvement in glycemic control is likely to reduce the risk of diabetic complication, while its effect on erectile dysfunction (ED) remains unclear. Aim The aim of this study was to evaluate the association of glycemic control with risk of ED in type 2 diabetics. Methods A self-administered questionnaire containing Sexual Health Inventory for Men was obtained from 792 subjects with type 2 diabetes at our institution. Clinical data were obtained through chart review. Main Outcome Measures The contribution of glycemic control assessed by glycated hemoglobin (HbA1c) level as well as age, duration of diabetes, hypertension (HT), dyslipidemia, and cigarette smoking to risk of ED was evaluated. Results Of 792 subjects, 83.6% reported having ED and 43.2% had severe ED. HbA1c level (%) adjusted for age and duration of diabetes was significantly associated with ED (OR 1.12, 95% CI: 1.01–1.25). None of HT, dyslipidemia, and cigarette smoking was a significant risk factor for ED after adjusted for age and duration of diabetes. HbA1c level, age, and duration of diabetes were significant independent risk factors for ED among the younger group (age ≤ 60 years), and only age and duration of diabetes were independent risk factors among the older group (age > 60 years). For the risk of severe ED, compared with no and mild to moderate ED, HbA1c level, duration of diabetes, and HT were independent risk factors among the younger group, and only age was an independent factor among the older group. Conclusions Better glycemic control probably would reduce the prevalence of ED and its severity among the younger men with type 2 diabetes. For the older group, aging was the major determinant for ED risk among this population with type 2 diabetes.

The acute effects of thyroid hormones on glucocorticoid secretion were studied. Venous blood samples were collected from male rats after they received intravenous 3,5,3′-triiodothyronine (T3) or thyroxine (T4). Zona fasciculata-reticularis (ZFR) cells were treated with adrenocorticotropic hormone (ACTH), T3, T4, ACTH plus T3, or ACTH plus T4 at 37°C for 2 h. Corticosterone concentrations in plasma and cell media, and also adenosine 3′,5′-cyclic monophosphate (cAMP) production in ZFR cells in the presence of 3-isobutyl-1-methylxanthine, were determined. The effects of thyroid hormones on the activities of steroidogenic enzymes of ZFR cells were measured by the amounts of intermediate steroidal products separated by thin-layer chromatography. Administration of T3 and T4 suppressed the basal and the ACTH-stimulated levels of plasma corticosterone. In ZFR cells, both thyroid hormones inhibited ACTH-stimulated corticosterone secretion, but the basal corticosterone was inhibited only with T3>10−10 M or T4>10−8 M. Likewise, T3 or T4 at 10−7 M inhibited the basal- and ACTH-stimulated levels of intracellular cAMP. Physiological doses of T3 and T4 decreased the activities of 3β-hydroxysteroid dehydrogenase, 21-hydroxylase, and 11β-hydroxylase. These results suggest that thyroid hormones counteract ACTH in adrenal steroidogenesis through their inhibition of cAMP production in ZFR cells.

1 The effect of amphetamine on the secretion of testosterone and the production of testicular adenosine 3':5'-cyclic monophosphate (cyclic AMP) in rats was studied. 2 A single intravenous injection of amphetamine decreased the basal and human chorionic gonadotropin (hCG)-stimulated levels of plasma testosterone. Plasma LH levels were not altered by the injection of amphetamine. 3 Administration of amphetamine in vitro resulted in a dose-dependent inhibition of both basal and hCG-stimulated release of testosterone. 4 Amphetamine enhanced the basal and hCG-increased levels of cyclic AMP accumulation in vitro in rat testes. 5 These results suggest that amphetamine inhibits the spontaneous and hCG-stimulated secretion of testosterone from the testes through a mechanism involving an increase in cyclic AMP production.

1 The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory e ect on testicular interstitial cells of male rats. 2 Administration of amphetamine (10 712 ± 10 76 M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml 71 )-stimulated release of testosterone. 3 Amphetamine (10 79 M) enhanced the basal and hCG-increased levels of adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in vitro (P50.05) in rat testicular interstitial cells. 4 Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P50.05) of testosterone in vitro and abolished the inhibitory e ect of amphetamine. 5 Nifedipine (10 76 M) alone decreased the secretion of testosterone (P50.01) but it failed to modify the inhibitory action of amphetamine (10 710 ± 10 76 M). 6 Amphetamine (10 710 ± 10 76 M) signi®cantly (P50.05 or P50.01) decreased the activities of 3b-hydroxysteroid dehydrogenase (3b-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography (t.l.c.). 7 These results suggest that increased cyclic AMP production, decreased Ca 2+ channel activity and decreased activities of 3b-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.