The appetite-regulating hormones leptin and ghrelin are altered in alcoholism and influence the hypothalamic-pituitary-adrenal system. We investigated whether acute ethanol ingestion and stress exposure affect ghrelin secretion. Nine healthy male volunteers were exposed to a standardized laboratory stressor involving public speaking on 2 days. On the first day they ingested 0.6 g/kg ethanol and on the second a placebo drink 50 minutes before the stressor. Plasma ghrelin, cortisol, glucose, and insulin were measured at baseline and in eight subsequent samples obtained up to 120 minutes after drinking (75 minutes after stress onset). The stress test induced a transient and significant rise in cortisol, which was not altered by prior alcohol administration. No significant change of ghrelin, insulin or glucose levels was observed after the stressor. Ghrelin declined significantly within 15 minutes after alcohol drinking, fell to a minimum of 66% of baseline at 75 minutes and remained at that level until the last sample at 120 minutes. No significant ghrelin changes were observed during placebo experiments. Insulin and glucose were not significantly influenced by stress or by alcohol. We conclude that alcohol drinking acutely attenuates circulating ghrelin levels. This effect is more pronounced than would be expected from the calories ingested with alcohol, as compared with a prior report where liquid meals of different caloric content were administered. We could not observe a stress effect on ghrelin, which does not support a role for ghrelin in stress-induced anorexia.
Acromegaly is associated with an increased prevalence and a specific pattern of affective disorders. Greater emphasis on diagnosing and treatment of mental disorders in acromegalic patients might improve the disease management.
Object: Treatment with somatostatin analogues (SA) not only inhibits GH secretion but may also impair insulin secretion. In order to evaluate the influence of SA on glucose metabolism, we investigated insulin resistance (IR) and b-cell function, using the recommended combination of homeostatic model assessment of IR (HOMA-IR) and b-cell function (HOMA-b). Design and methods: This is a prospective, cross-sectional study. We measured fasting insulin, blood glucose and IGF-I. Insulin and blood glucose measurements were taken 120 min after an oral glucose tolerance test with 75 g glucose. We studied 51 patients (27 female/24 male, age 54 years (20-75)). Eighteen patients were on Lanreotide Autogel (LA) treatment, 33 had no medical treatment. GH-levels of more than 2.5 ng/ml was reached by 59% of the patients, 74.5% had normal IGF-I levels. Results: We found no significant influence of disease activity on HOMA-IR and HOMA-b. In the 33 of 51 subjects without any drug treatment, median HOMA-b was 170.4% (36.0-624.0%). In contrast, in the 18 patients on LA treatment, median HOMA-b was found to be significantly lower (84.2% (36.5-346.2%); PZ0.001). Despite this, there was no difference in HOMA-IR in both groups (2.4 (0.7-8.4) vs 2.3 (0.7-6.1); P!0.001) despite similar insulin values. Conclusion: In conclusion, we found that LA decreases b-cell function significantly without affecting IR. Therefore, we think that insulin secretagogues are probably more effective in the treatment of diabetes mellitus in acromegalic patients on LA therapy than insulin sensitizers. European Journal of Endocrinology 155 73-78
Lanreotide Autogel (Ipsen) is a long-acting somatostatin analogue (SA) in a new galenic formulation suitable for subcutaneous (s.c.) injection. In our department, 11 patients with therapy-resistant acromegaly were treated with Lanreotide Autogel for 48 months. 10/11 patients had previously undergone transsphenoidal surgery. For a median duration of 1.4 years prior to Lanreotide Autogel, the patients received Lanreotide PR 30 mg every 7, 10, or 14 days. 60, 90, or 120 mg of Lanreotide Autogel was administered by deep s.c. injection every 28 days, with the higher dosage being given to those with the previously shortest injection interval under Lanreotide PR. Dose was adjusted on the basis of Growth Hormone (GH) level after 4, 8, and 12 months with a minimum dose of 60 mg and a maximum dose of 120 mg. The efficacy of Lanreotide Autogel treatment was evaluated by measuring GH concentrations (4 hour profiles) and IGF-I levels. Before switching to Lanreotide Autogel, the multiple of the upper limit of normal (xULN) of IGF-I levels was 1.2 (median) and the median GH level was 1.3 microg/l. 3 out of 11 patients had an IGF-I within the age- and sex-adjusted normal range. After 48 months of treatment with Lanreotide Autogel, six patients had an IGF-I within the normal range. Median GH levels were at 1.3 microg/l and xULN of IGF-I was at 1.0 compared to Lanreotide PR 30 mg treatment (p < 0.001). At the end of the study, 8 patients received 120 mg Lanreotide Autogel, 2 patients 90 mg and 1 patient 60 mg, respectively. There was slight but significant deterioration of glucose metabolism with an increase of HbA1c. In conclusion, the new galenic formulation of Lanreotide improves not only the control of biochemical markers of acromegaly compared to the conventional PR formulation, but is also easier to administer given its deep s.c. method of administration. Glucose metabolism has to be followed carefully in patients on high-dose Lanreotide Autogel.
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