Abstract. In order to determine the influence of thyroid function on the pineal gland in humans, the circadian rhythm of the serum melatonin concentration was estimated in 16 women with thyroid disorders: 8 with hypothyroidism and 8 with hyperthyroidism, as well as in 5 healthy controls. A significant melatonin circadian rhythm was observed in all the three groups studied. The melatonin rhythm parameters derived from cosinor analysis: mesor (controls: 0.163 ± 0.03 nmol/l (± sem), hypothyroid patients: 0.176 ± 0.22 nmol/l, and hyperthyroid patients: 0.167 ± 0.04 nmol), amplitude (0.155, 0.145 and 0.138 nmol/l, respectively), acrophase (1:38, 2:22 and 1:51 h, respectively) did not differ significantly in the three groups studied. Integrated 24-h melatonin secretion was also similar in patients and controls. The melatonin concentrations were positively correlated with TSH levels in hypothyroidism, and negatively correlated with T3 in hyperthyroidism. In conclusion: in patients with hypo- and hyperthyroidism the circadian rhythm of melatonin secretion is not altered.

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Although volume and vasoconstriction have been considered polar elements in a useful pathogenetic hypertension model, many observations suggest that vasoconstriction is involved in volume-dependent hypertension, reflecting the effect of a digitalis-like factor. To examine that possibility, we assessed the depressor responses to Digibind, an antibody Fab directed against digoxin, in a volume-dependent model--DOCA-salt-induced hypertension in rats. Digibind (10 mg/kg, intravenously) induced a gradual blood pressure fall over 2 h that was sustained for 4 h (P < .001). Blood pressure did not fall with Digibind when DOCA was administered without salt or a high-salt intake was provided without DOCA. The intracellular sodium content of the rat aorta, measured by atomic absorption spectroscopy after cold choline wash, was increased in the DOCA-high-salt rats (23.3 +/- 2.7 mEq/L) compared to control rats (12.1 +/- 0.8 mEq/L; P < .001). Aorta sodium content, in parallel with blood pressure, was not increased either by dietary salt supplementation without DOCA, or by DOCA with a low-salt diet. Sodium pump activity was measured as 86Rb uptake into vascular smooth muscle (VSM). Both ouabain-sensitive and ouabain-resistant 86Rb uptake were significantly higher in VSM from DOCA-high-salt animals (P < .01). Despite its effectiveness in reducing blood pressure in this model, Digibind influenced neither VSM sodium content nor 86Rb uptake. The results are consistent with a role for a circulating digitalis-like factor in this volume-dependent model, but events at the VSM level are complex.

Ethanol administration decreases GH secretion in humans and experimental animals. The mechanism of these inhibitory effects was investigated by evaluating the spontaneous secretory pattern of GH in chronically cannulated unanesthetized rats, plasma insulin-like growth factor-I (IGF-I) concentrations, and hypothalamic GH-releasing hormone (GHRH) and somatostatin, and pituitary GH mRNA levels. Body weight gain was reduced in ethanol (5%)-liquid diet-fed rats (n = 6) for 6 days compared to that in both isocalorically pair-fed controls (n = 6) and ad libitum-fed animals (n = 6). Spontaneous GH secretion was markedly decreased (by 75-90%) in ethanol-fed rats compared to that in pair-fed and ad libitum-fed groups, while pulsatile pattern of GH release was preserved, with secretory bursts occurring every 180-220 min in all groups. Mean 6-h plasma GH levels in ethanol-, pair-, and ad libitum-fed animals were: 18.8 +/- 4.5, 113.3 +/- 14.9, and 179.6 +/- 30.1 ng/ml, respectively (P < 0.01, ethanol vs. each control). Plasma IGF-I concentrations were decreased in the ethanol-fed rats (338 +/- 16 ng/ml) compared to those in pair-fed (427 +/- 39 ng/ml; P < 0.05) and ad libitum-fed (769 +/- 25 ng/ml; P < 0.01) rats. Ethanol treatment decreased GHRH mRNA levels to 9% of those in ad libitum-fed (P < 0.01) and 20% of those in pair-fed (P < 0.05) animals, whereas it did not significantly alter somatostatin or GH mRNA levels. The results indicate that the effects of ethanol inhibit GH secretion primarily at the hypothalamic level, resulting in impaired GHRH gene expression. Since the GHRH-GH-IGF-I axis has an important role in growth regulation, the growth retardation seen in experimental models of alcohol abuse may be a consequence at least in part of the suppressive effects of ethanol on this axis.

In order to establish the role of insulin in the pathogenesis of lipid abnormalities in hyperandrogenic women with the polycystic ovary syndrome (PCO) 49 women aged 18 to 35 yr with a normal glucose tolerance test were studied. They were divided into two groups: 27 women with PCO (9 obese and 18 nonobese), and 22 healthy women (12 with simple obesity and 10 with normal body weight). In the PCO group, the fasting insulin levels and the insulin response to oral glucose load were higher than in the matched controls. Significantly lower levels of HDL2-cholesterol and higher levels of apolipoprotein B were observed in obese and non nonobese PCO patients. In obese women with PCO this was associated with lower levels of HDL-cholesterol and apolipoprotein A-I (Apo A-I), whereas the levels of total triglycerides and VLDL-triglycerides (VLDL-TG) were increased. Multiple regression analysis in PCO women, after adjustment for age, body mass index and the levels of insulin and sex hormones, showed a strong positive correlation between the fasting insulin levels and total triglycerides and VLDL-TG, while a negative correlation was found between fasting insulin levels and apo A-I. These results indicate that hyperinsulinemia may play a role in the development of lipid disturbances in women with the PCO.