These data demonstrate GH replacement in adult subjects with GHD is effective in changing body composition and restoring IGF-I levels over a 12-month period; however, in our study, these changes were not accompanied by changes in adipokine levels or beneficial effects on plasma lipids or insulin resistance.

Thirteen patients with active acromegaly despite previous surgery were treated with 30 mg lanreotide im twice a month for 9 months. In 10 subjects the treatment continued to 19 months. GH serum levels of all patients decreased significantly from an initial value of 32.0 (29.4) micrograms/l [median (standard error of median)] to 10.0 (3.6) and 19.1 (5.7) after 3 and 9 months of treatment, respectively. In the 10 patients with the treatment longer than one year the decrease in GH was from 46.8 (29.4) micrograms/l to 12.5 (5.0) and 16.1 (5.3) after 13 and 19 months, respectively. IGF-I serum levels decreased significantly from 1193 (73) micrograms/l to 782 (99) and 621 (103) after 3 and 9 months, respectively, and were normalized in 3 patients. In the 10 patients treated for longer than one year, levels decreased significantly from 1318 (74) micrograms/l to 653 (170) and 742 (180) after 13 and 19 months, respectively. IGF BP-3 levels were reduced to the normal range in 6 patients and decreased from 8.7 (1.5) mg/l to 6.4 (0.8) and to 5.4 (1.0) after 3 and 9 months, respectively. In the patients with the 19 months treatment the decrease was from 9.3 (1.6 mg/l to 3.9 (0.9) and 4.8 (0.9) after 13 and 19 months, respectively. The IGF BP-3 to IFG I ratio increased in 7 patients. This elevation significantly correlated with the decrease in bioassayable somatomedin. Prolactin serum levels fell in all patients with increased prolactin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

Ghrelin is a novel peptide hormone which was identified as an endogenous growth hormone secretagogue. It is mainly secreted in the stomach, but important sites of its secretion are other parts of the gastrointestinal tract. Ghrelin is thought to be involved not only in regulation of growth hormone secretion but also in regulation of food intake and nutritional status. This study was aimed to investigate the changes in plasma ghrelin levels in patients with short bowel syndrome. Twenty-four patients with malnutrition due to short bowel syndrome and eleven healthy controls were included in the study. They underwent clinical examination and assessment of plasma or serum levels of ghrelin leptin, soluble leptin receptor, IGF-I, IGFBP-1 and IGFBP-3. Plasma ghrelin levels were decreased in patients with short bowel syndrome (p<0.01). Furthermore, decreased serum levels of IGF-I (p<0.01) and IGFBP-3 (p<0.001) were found in patients with short bowel syndrome. Other laboratory differences between both groups were not significant. No relationship between ghrelin and other determined variables was found. We conclude that plasma ghrelin levels are decreased in the group of patients with short bowel syndrome. It is probably because of a decrease in the tissue mass that is able to secrete ghrelin.

Insulin sensitivity was evaluated in 16 insulinoma patients and in 15 obese persons with Type 2 diabetes mellitus by using hyperinsulinaemic clamps and analysis of insulin receptor characteristics on erythrocytes. Significantly decreased insulin sensitivity index (M/l) was found in both insulinoma and obese Type 2 diabetic patients as compared with healthy non-obese controls (21.2 +/- 2.2 and 19.5 +/- 2.6 vs 40.3 +/- 3.7 mumol.kg-1.min-1 per mU.l-1 x 100, p < 0.001). No difference was observed between both groups of patients. Metabolic clearance rate of glucose was strongly reduced in obese diabetic patients but it was normal in insulinoma patients in comparison with healthy persons (2.7 +/- 0.4 vs 8.7 +/- 0.6 or 7.9 +/- 0.7 ml.kg-1.min-1, p < 0.001). A decreased insulin binding on specific receptors caused by reduced binding capacity was observed only in insulinoma patients but not in obese Type 2 diabetic patients. A significant negative correlation was proved between body mass index (BMI) and insulin sensitivity index (r = -0.82, p < 0.001) indicating that BMI is the main determining factor of insulin resistance in the total cohort of examined patients. We conclude that insulin resistance was caused by postreceptor changes in obese Type 2 diabetes, whereas a decreased insulin binding capacity together with post-receptor defect was present in insulinoma patients.