Showing papers by "Omar Serri published in 1989"
TL;DR: Weight loss and blood glucose, triglycerides, FFA, amino acids, insulin, and T3 changes were similar in both groups and Nitrogen balance was determined daily throughout the study.
Abstract: The response of serum growth hormone (GH) to a test bolus of growth hormone-releasing factor (GRF) (1 μg/kg, IV) was examined in eight obese subjects (166% ± 8% ideal body weight [IBW]) during a weight-maintaining control period and after 2 weeks of hypocaloric feeding (750 kcal). During the period of hypocaloric feeding subjects received either repetitive GRF 1 μg/kg, IV (GRF group, n = 6) at 9 am, 1 pm, and 5 pm three times a week, or saline injections (placebo group, n = 6) at the same intervals. Four subjects were studied twice, several months apart, each receiving GRF and placebo treatments. Nitrogen balance was determined daily throughout the study. We also examined GH response to the GRF test in seven normal-weight subjects (106% ± 6% IBW). During the control period, obese subjects demonstrated a blunted GH response to GRF expressed as peak height or GH area under the curve (0 to 120 minutes) compared with normal subjects (P < .005). At the end of the hypocaloric feeding, mean GH peak height after the GRF test was unchanged in the placebo group compared with the control period. GH release was significantly increased only during the second hour of testing (P < .025). However, the GRF group demonstrated an increase in both mean GH peak height (P < .025) and GH release during the first and second hours of testing (P < .025) compared with the control period. Weight loss and blood glucose, triglycerides, FFA, amino acids, insulin, and T3 changes were similar in both groups. Nitrogen balance was also similar in both groups, indicating that neither the peak nor the total GH release increase demonstrated by the GRF group was sufficient to induce a significant nitrogen retention during hypocaloric feeding. Repeated GRF injections during hypocaloric feeding can enhance both the peak and integrated GH response to GRF in obese subjects. This suggests that at least during a hypocaloric regimen, somatotrophs may be primed by GRF in some obese subjects.
16 citations
TL;DR: C cessation of SMS 201-995 may be followed in some acromegalic patients by a rebound of plasma GH levels, which suggests that SMS201-995 decreases GH levels by an inhibition of its release from the pituitary.
Abstract: We studied a 42-year-old woman who had persistent active acromegaly despite conventional therapies. She was treated for 6 months with SMS 201-995. Her mean plasma growth hormone GH values decreased during treatment from 9.1 +/- 1.2 to 6.6 +/- 1.2 micrograms/L. One month after the withdrawal of SMS 201-995, the plasma GH level increased to 24.4 micrograms/L (P less than 0.001). This elevation was clinically silent and transitory, as GH levels decreased 8 months later to 6.9 +/- 1.3 micrograms/L. Furthermore, at the beginning of therapy, her intractable headache was completely relieved; however, it progressively resumed under therapy. In conclusion, cessation of SMS 201-995 may be followed in some acromegalic patients by a rebound of plasma GH levels. This rebound suggests that SMS 201-995 decreases GH levels by an inhibition of its release from the pituitary. Furthermore, SMS 201-995 may relieve intractable headache in some acromegalic patients, but tolerance to the analgesic effect may develop.
7 citations
TL;DR: The results suggest that GRF can stimulate PRL release by actions on the normal pituitary and on pituitaries, including microprolactinomas, including acromegalic patients, and that in acromegaly there is a relative functional deficiency of hypothalamic somatostatin.
Abstract: We have examined the serum growth hormone (GH) and prolactin (PRL) response to growth hormone releasing factor (hGRF-(1-44)NH2 (GRF) 1 microgram/kg i.v. bolus) in 16 acromegalic patients (eight of whom were hyperprolactinaemic), 13 patients with microprolactinoma, and 14 healthy subjects. The GH responses to TRH and to the somatostatin analogue SMS 201-995 were also studied in acromegalic patients. In these, and in patients with microprolactinoma, GH responses after GRF (P less than 0.001 vs saline) were variable. The absolute GH increase (calculated as area under the curve) in acromegalic patients (2489 +/- 920 micrograms/l min), or in patients with microprolactinoma (1322 +/- 279 micrograms/l min) was not different from that in controls (2238 +/- 633 micrograms/l min). In addition, a significant increase in PRL release was observed after GRF in comparison to saline in acromegalic patients (P less than 0.01), in patients with microprolactinoma and in normal subjects (P less than 0.001). The PRL increase was significantly correlated with basal PRL levels in acromegalic patients (r = 0.99, P less than 0.001) and in patients with microprolactinomas (r = 0.61, P less than 0.05). Furthermore, a significant correlation was found between GH rise after GRF and basal GH, and between GH rise after GRF and GH decrement after SMS in patients with acromegaly. These results suggest that GRF can stimulate PRL release by actions on the normal pituitary and on pituitary adenomas, including microprolactinomas. Moreover, the data suggest that in acromegaly there is a relative functional deficiency of hypothalamic somatostatin.
4 citations