Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methionyl-GH (met-GH) infusions inhibit the GH response to GH-releasing hormone (GHRH). Met-GH infusions induce lipolysis with a rise of plasma FFA that are known to suppress GH release, but the met-GH inhibition of the GH response to GHRH occurs also when lipolysis is pharmacologically blocked by acipimox. In addition, the inhibition of GH release might be due to an enhanced release of hypothalamic somatostatin. The aim of this study was to evaluate the effect of a met-GH infusion on the GH response to GHRH when lipolysis and hypothalamic somatostatin release are pharmacologically blocked. Twelve normal subjects, randomly allocated to two groups (A and B), received GHRH (50 micrograms, iv) at 1300 h after a 4-h saline infusion or met-GH infusion (80 ng/kg.min). To block lipolysis and hypothalamic somatostatin release, subjects in group B received acipimox, an antilipolytic agent (500 mg), and pyridostigmine, an acetylcholinesterase inhibitor (60 mg), during the 6 h before iv GHRH. GHRH induced a clear GH release during saline infusion in both groups, significantly higher in group B (43.6 +/- 4.8 micrograms/L) than in group A (20.1 +/- 6.1 micrograms/L; P less than 0.02 vs. A), and only a slight increase during met-GH infusions (10.4 +/- 4.1 micrograms/L in group A; 16.7 +/- 4.2 micrograms/L in group B; P = NS). These data indicate that the GH response to GHRH is inhibited by met-GH infusions when peripheral lipolysis and hypothalamic somatostatin release are pharmacologically blocked, suggesting the possibility of autoinhibition of GH at the pituitary level.
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PMID:Growth hormone (GH) autofeedback on GH response to GH-releasing hormone. Role of free fatty acids and somatostatin. 167 89

The present study was undertaken in order to evaluate the acute metabolic and hormonal effects of human growth hormone in healthy subjects. Glucose turnover, plasma glucose, FFA, insulin, C-peptide, glucagon, and somatostatin concentrations were determined in the fasting state after a bolus injection of placebo or growth hormone in quantities producing increases in plasma growth hormone levels within the normal physiological range. We found that growth hormone administration resulted in negligible changes in plasma glucose, no significant changes in appearance or disappearance rates of glucose, a moderate increase in FFA and a moderate fall in plasma insulin, C-peptide and glucagon concentrations, while plasma somatostatin levels were unchanged. These findings suggest that rapid changes in plasma growth hormone concentrations, corresponding to the fluctuations seen during normal daily life, may play a role in the short time regulation of blood glucose concentration through an inhibition of insulin and glucagon secretion.
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PMID:Short time effects of growth hormone on glucose metabolism and insulin and glucagon secretion in normal man. 167 25

The effects of bST injection and dietary protein level on blood hormone and metabolite concentrations were examined in four mature Holstein cows in a double crossover design. Cows were assigned at d 5 to 9 postpartum to receive daily injections of either a control (saline) solution or 20.6 mg of bST. Four 3-wk periods were used during which one cow from each group was fed a medium protein diet (17.1% CP), and the other received a high protein diet (23.6% CP). Injections of bST or control solutions began on d 0 of the second period. Intakes of DM were not influenced by dietary protein or bST injection. Milk yield tended to increase with increased CP level but was not affected by bST injection. Based on the rate and extent of decline in milk production after cessation of bST injection, the cows assigned to bST had lower milk production potential than control cows. Thus, the effect of bST injection apparently was to enhance milk yield to levels similar to those of controls. There were no significant CP level or bST injection effects on glucose, FFA, somatostatin, or somatotropin concentrations. Glucagon concentrations were higher in bST-treated cows. Concentrations of insulin-like growth factor-I were increased with increased CP level and also with bST injection. Significant effects of days on bST were observed for insulin, insulin-like growth factor-I, glucose, and FFA. Cows given bST injections and producing equal amounts of milk as control cows did not show major physiological differences in hormones and metabolites with the exception of insulin-like growth factor-I.
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PMID:Hormonal responses to bovine somatotropin and dietary protein in early lactation dairy cows. 191 37

To evaluate the effect of glucagon on regulation of plasma FFA concentration, continuous iv infusions of either somatostatin (S) or somatostatin (S) plus glucagon (G) were administered to 18 individuals with normal glucose tolerance. In 9 of these individuals there was no insulin replacement, whereas in the other 9 individuals enough insulin was infused to restore the insulin concentration to the basal level. Measurements were made of plasma glucose, insulin, G, and FFA concentrations as well as hepatic glucose production (Ra). The results indicated that plasma FFA concentrations were significantly lower when G was infused (S greater than S + G) regardless of whether insulin was infused. However, similar elevations of the plasma G concentration did lead to higher values of Ra and plasma glucose, although the basal concentration of plasma insulin decreased the increases in Ra and plasma glucose caused by G. The ability of a similar amount of insulin to lower plasma FFA concentrations was greater in magnitude than the decrease in Ra. These data indicate that G does not increase plasma FFA concentrations in normal individual, and that insulin plays a role of greater magnitude in suppression of plasma FFA concentrations than in inhibition of Ra.
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PMID:Does glucagon increase plasma free fatty acid concentration in humans with normal glucose tolerance? 196 14

This study was designed to measure plasma gastrin and somatostatin levels in infants and to simultaneously investigate the infants' metabolic status as reflected by the body weight as well as by the blood levels of FFA, D-beta-hydroxybutyrate and glucose. Healthy infants (n = 94) who were born at term were studied cross-sectionally during their first four days of life. We found that the gastrin concentration (mean +/- SD) on the first day of life was 118 +/- 37 pmol/l. Subsequently the concentration decreased and reached its lowest value on the third day; 94 +/- 27 pmol/l (P less than 0.05). On the fourth day the mean concentration increased to the same level as on the first day. There was a significant (P less than 0.01) increase in somatostatin concentrations from 18 +/- 6 pmol/l on the first day to 26 +/- 7 pmol/l on the fourth day and the concentrations were highly related (P less than 0.0001) to postnatal age. We conclude that the decrease in gastrin concentration is probably related to the low volume of breast milk ingested during the first days after delivery, and therefore to the low secretory activity of the gastrin-producing cells. The infants' catabolic condition during that time was evidenced by the reduction in body weight, the decrease in plasma glucose level and the increase in FFA and D-beta-hydroxybutyrate levels. The gastrin increase found on the fourth day reflects most likely, the change in breast milk availability which occurs with the establishment of lactation. The mechanisms controlling the release of somatostatin remains to be established.
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PMID:Plasma gastrin and somatostatin levels in infants during the first four postnatal days. 198 40

In man, continuous infusion of GH-releasing hormone (GHRH) does not sustain GH secretion, unlike prolonged hypoglycemia. To further evaluate this difference in the stimulation of GH release we measured GH concentrations for 3 h during prolonged insulin-induced hypoglycemia and GHRH-(1-29)NH2 (100 micrograms/h) infusion in normal individuals. We also assessed the GH response to combined and separate administration of insulin and GHRH. Plasma GH levels increased during prolonged hypoglycemia and remained elevated for the third hour (22-24 micrograms/L). GH concentrations increased during GHRH infusion, peaked at 60 min (23.5 micrograms/L), and rapidly declined. Thus, our findings confirmed that prolonged hypoglycemia, unlike GHRH infusion, sustained elevated GH levels and that these high levels did not appear to influence GH secretion from the pituitary. Changes in FFA did not account for the sustained GH secretion. FFA levels initially declined during insulin infusion, but after 3 h of hypoglycemia they returned to near-basal values (basal, 0.1 +/- 0.02 g/L; 180 min, 0.09 +/- 0.02). The maximal GH concentration attained during the combined insulin and GHRH test was significantly higher than that with the insulin tolerance test or GHRH test (insulin plus GHRH, 71.9 +/- 13.5; insulin tolerance test, 34.2 +/- 2.9; P less than 0.025; GHRH test, 27.9 +/- 3.2; P less than 0.02), indicating an additive effect on GH secretion. These data suggest that insulin-induced hypoglycemia stimulates GH secretion through a mechanism partly independent of GHRH. The release from somatostatin inhibition and stimulation through other neuropeptides (e.g. galanin) is suggested as possible causes of hypoglycemia-induced GH secretion.
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PMID:Growth hormone does not inhibit its own secretion during prolonged hypoglycemia in man. 211 May 74

We previously reported that GH secretion evoked by GHRH is inhibited after 5 days of treatment with im GH. This impaired pituitary response was associated with a significant increase in the serum concentration of insulin-like growth factor I (IGF-I). To dissociate the possible effects of circulating IGF-I from other effects of GH on the pituitary response to GHRH, we carried out the following study in eight normal men. A bolus injection of GHRH (1 microgram/kg, iv) was administered 2 h after the start of a 4-h continuous iv infusion of GH (180-micrograms bolus dose, then 3 micrograms/min in 150 mmol/L NaCl) or placebo (150 mmol/L NaCl). In addition, a similar injection of GHRH was given 4 h after the start of a 6-h continuous iv GH infusion (180-micrograms bolus dose, then 3 micrograms/min). During the GH infusions, plasma GH levels reached steady state concentrations in the 9-13 micrograms/L range. The mean GHRH-induced GH response was not significantly blunted during the 4-h infusions of GH [724 +/- 163 (+/- SE) vs. 1184 +/- 373 micrograms.min/L during placebo; P = 0.29], but was significantly inhibited during the 6-h GH infusions (226 +/- 105 micrograms.min/L; P = 0.04 vs. control). Serum IGF-I or plasma glucose did not change significantly throughout the GH infusions. During the 6-h GH infusions, plasma FFA increased to levels significantly above basal values during the last 3 h of the 6-h infusion. These results indicate that short term GH infusion inhibits the plasma GH response to GHRH in a time-dependent manner. The inhibition is not due to changes in circulating IGF-I and glucose concentrations. Fluctuations in hypothalamic somatostatin secretion, changes in lipid or other GH-dependent metabolites, paracrine effects of IGF-I, or a direct effect of GH itself may cause the impaired pituitary responsiveness during short term iv GH infusion.
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PMID:Short term continuous intravenous infusion of growth hormone (GH) inhibits GH-releasing hormone-induced GH secretion: a time-dependent effect. 249 83

Dairy cows in early lactation were reported to secrete growth hormone in response to declining glucose concentrations at day 5 but not day 30 post-partum, whereas GH responses to TRH were reported to be enhanced after day 30 post partum. The present study examined GH response following glucose infusion and the effect of GHRH as well as effects of SRIH on GHRH-stimulated GH release. Declining plasma glucose concentrations after glucose infusion stimulated GH release at day 5 post partum but not in nonpregnant, nonlactating cows or in cows at days 30 and 90 post partum. GHRH stimulated GH release on all days tested, but the response was highest at day 30 post partum when compared to other days. Somatostatin infusion inhibited GHRH effects on GH concentrations only at day 30 post partum and in nonpregnant, nonlactating cows. Thus, a differential response of the GH regulatory system could be demonstrated between days 5 and 30 post partum utilizing different stimuli. Evaluation of plasma glucose and free fatty acid concentrations on days 5, 10, 20, and 30 post partum revealed a progressive decrease in FFA but not glucose as lactation progressed. Decreased plasma FFA concentrations were paralleled by a decrease in basal GH, somatomedin-C and epinephrine. Thus, a decline in FFA may be responsible for the disparity between effects of GHRH and glucose on GH release between days 5 and 30 post partum.
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PMID:Differential growth hormone responses to glucose and growth hormone releasing hormone in lactating dairy cows. 256 12

GH release is controlled by hypothalamic hormones and insulin-like growth factor I, synthesized under the influence of GH, and perhaps also by GH itself. The availability of recombinant Met-GH was the basis for studies aimed at 1) obtaining constant serum GH levels by means of constant Met-GH infusions (40 and 80 ng/kg.min for 6 h), and 2) evaluating the metabolic effects of constant GH levels and, in particular, their effects on the serum GH response to GHRH. In six normal men, both Met-GH infusions increased plasma FFA levels, but did not alter the circulating levels of somatostatin, insulin-like growth factor I, insulin, glucose, cholesterol, and triglycerides. The Met-GH infusions did cause a dose-related inhibition of GHRH-induced GH release. These data indicate that it is possible to maintain constant serum GH levels by means of constant Met-GH infusions at different infusion rates, and that GH inhibits its own release.
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PMID:Inhibition of the growth hormone (GH) response to GH-releasing hormone by constant Met-GH infusions. 256 14

The role of elevated plasma epinephrine concentrations in the regulation of plasma leucine kinetics and the contribution of beta-receptors were assessed in man. Epinephrine (50 ng/kg per min) was infused either alone or combined with propranolol (beta-blockade) into groups of six subjects fasted overnight; leucine flux, oxidation, and net plasma leucine forearm balance were determined during 180 min. Constant plasma insulin and glucagon concentrations were maintained in all studies by infusing somatostatin combined with insulin and glucagon replacements. Plasma leucine concentrations decreased from baseline during epinephrine infusion by 27 +/- 5 mumol/liter (P less than 0.02) due to a 22 +/- 6% decrease in leucine flux (P less than 0.05 vs. controls receiving saline) and to an increase in the metabolic clearance rate of leucine (P less than 0.02). Leucine oxidation decreased by 36 +/- 8% (P less than 0.01 vs. controls). beta-Blockade abolished the effect of epinephrine on leucine flux and oxidation. Net forearm release of leucine increased during epinephrine (P less than 0.01), suggesting increased muscle proteolysis; the fall of total body leucine flux was therefore due to diminished proteolysis in nonmuscle tissues, such as splanchnic organs. Nonoxidative leucine disappearance as a parameter of protein synthesis was not significantly influenced by epinephrine. Plasma glucose and FFA concentrations increased via beta-adrenergic mechanisms (P less than 0.001). The results suggest that elevation of plasma epinephrine concentrations similar to those observed in severe stress results in redistribution of body proteins and exerts a whole body protein-sparing effect; this may counteract catabolic effects of other hormones during severe stress.
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PMID:Elevation of plasma epinephrine concentrations inhibits proteolysis and leucine oxidation in man via beta-adrenergic mechanisms. 256 73


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