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)

The main intention of this study was to examine the effect of cyclic somatostatin (SRIF) on bovine adrenal cell activity in vitro. beta-Endorphin was applied in another course of experiments. Basal aldosterone secretion when measured was found to be 0.86 +/- 0.33 ng per 10(5) cells and 1.5 h incubation time in the glomerulosa cell fractions. Cortisol production was 1.6 +/- 0.3 ng per 10(5) cells in the fasciculata/reticularis cell incubates respectively. No effect was observed when cyclic somatostatin (SRIF) was added to cell incubates of the bovine adrenal cortex. However, aldosterone secretion was increased 4.5-fold in the presence of 10(-9)M ACTH or 10(-8)M At II. Cortisol production was enhanced similarly after addition of 10(-9)M ACTH.
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PMID:Failure of somatostatin and beta-endorphin to affect bovine adrenal cortex cells in vitro. 611 98

Teleost fish osmoregulation is largely the result of integrated transport activities of the gill, gut and renal system. The basic 'epithelial fabric' in each of these tissues is adapted to provide the appropriate transport mechanisms depending upon whether the fish is in fresh water or sea water. Net NaCl transport by the branchial epithelium reverses direction when euryhaline species migrate between the two media, providing a useful focus in experiments designed to elucidate mechanisms of differentiation and integration of transport function. Isolated opercular membranes and skins from certain seawater-adapted species are good models to study branchial salt extrusion mechanisms. These heterogeneous tissues generate short-circuit currents equal to net chloride secretion. The vibrating probe technique has allowed localization of all current and almost all conductance to the apical crypt of chloride cells. Area-specific surface current and conductance of chloride cells are 18 mA cm-2 and 580 mS cm-2 (1.7 omega cm2), ranking them as one of the most actively transporting and conductive cells known. There is no net sodium transport under short-circuit conditions but the chloride secretion process is sodium-dependent and ouabain and 'loop'-diuretic sensitive. Sodium fluxes through chloride cells are large (PNa = 5.2 X 10(-4) cms-1) nd appear passive and rate-limited by a single barrier. A link may exist between the active transport and leak pathways since sodium fluxes always account for 50% of chloride cell conductance. The sodium pathway is probably the chloride cell-accessory cell tight junction, although this is still unresolved. Chloride secretion can be rapidly modulated by several hormones, including catecholamines, somatostatin, glucagon, vasoactive intestinal polypeptide and urotensins I and II. Regulation by these hormones may be by rapid alterations of cellular cAMP levels. Differentiation of chloride cells and chloride secretion may be controlled by cortisol and prolactin. Cortisol stimulates chloride cell proliferation and differentiation and appears to interact with NaCl to initiate salt secretion. Prolactin appears to cause chloride cell dedifferentiation by reducing both the active-transport and leak pathways proportionately.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chloride cells and the hormonal control of teleost fish osmoregulation. 636 Dec 7

1. Glucose metabolism and changes in the concentrations of several hormones in jugular plasma were measured in growing lambs fed on fresh pasture ad lib. One group of lambs acted as control while the second received a continuous abomasal infusion supplying 44 g sodium caseinate+0.5 g L-methionine/d. 2. Hormone concentrations were determined by radioimmunoassay procedures and glucose irreversible loss measured from continuous infusion of D-[U-14C]glucose. 3. Protein infusion increased plasma concentrations of insulin, glucagon and thyroxine (T4), depressed those of growth hormone, prolactin and somatostatin and had no effect on triiodothyronine (T3) concentrations. Cortisol concentrations also tended to be slightly higher in the plasma of protein-infused lambs. 4. Increases in herbage intake within the ad lib, range were associated with increases in plasma insulin and glucagon concentrations and decreases in growth hormone concentration, and it is suggested that these effects could be mediated in part by the accompanying increases in protein absorption from the intestines. The T4:T3 value also decreased with increasing herbage intake, and it is suggested this was due to conversion of T4 to T3. 5. After correction by covariance to equal herbage intake, rates of irreversible glucose loss for control and protein-infused lambs were 9.2 and 10.0 mg/min per kg body-weight 0.75. It was calculated that respectively 0.12 and 0.19 of the total glucose production in control and protein-infused lambs could be accounted for by net synthesis from protein. 6. It was concluded that changes in the circulating concentration of several hormones in protein-infused compared with control lambs were likely to have been implicated in protein deposition forming a greater proportion of energy retention in the infused lambs (0.41 v. 0.27).
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PMID:Protein metabolism in growing lambs given fresh ryegrass (Lolium perenne)--clover (Trifolium repens) pasture ad lib. 2. Endocrine changes, glucose production, and their relationship to protein deposition and the partition of absorbed nutrients. 706 91

Excess production or long-term administration of glucocorticoids is detrimental to longitudinal growth in people and rats. A portion of this effect is attributed to cortisol inhibition of growth hormone (GH). Glucocorticoid effects are usually studied in subjects under long-term treatment with synthetic, more potent glucocorticoids, and, to the authors' knowledge, have not been examined in domestic animals. We sought to examine the effects of cortisol infusion on GH release in sheep. Cortisol infusion into castrated, male Suffolk sheep (1 to 1.5 years old) caused a significant (P < 0.0001) increase in cortisol concentration. Basal GH release was not affected over the 4-hour period of infusion. Growth hormone-releasing hormone administration stimulated GH release in both groups (P < 0.001); however, the control group had a greater response to growth hormone-releasing hormone than did the cortisol infused group (P < 0.0001). These results were duplicated in cultured sheep pituitary cells. Cortisol inhibition of GH release may be mediated via enhanced somatostatin release, owing to a direct inhibition of somatotrope function, or a combination of both mechanisms. Because of effects of stress and disease in increasing cortisol concentration, additional study of the mechanisms for cortisol inhibition of GH release in sheep needs to be performed.
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PMID:Effects of short-term cortisol infusion on growth hormone-releasing hormone stimulation of growth hormone release in sheep. 748 4

Reduced O2 availability, as might occur under some physiological and pathological conditions, stimulates insulin and glucagon release and increases glucose fluxes and muscle carbohydrate metabolism. The aim of this study was to determine the role of reduced PO2, independent of changes in glucagon and insulin. In six dogs, in paired studies separated by 2 wk, glucagon and insulin levels were fixed throughout by infusion of somatostatin with basal intraportal glucagon and insulin replacement. A control period was followed by 90 min of breathing 21% (NO) or 8% (LO) O2. Isotopic and arteriovenous methods were used to assess carbohydrate metabolism. Measured variables were constant over time in NO. Arterial PO2 (Pao2) was approximately 100 mmHg in NO and approximately 30 mmHg in LO, resulting in a 50% fall in O2 content. Insulin, glucagon, and catecholamine levels were similar in NO and LO. Cortisol was significantly increased in LO. Arterial glucose was unchanged in both groups. In the last 45 min of the experimental period in LO, 1) glucose production (14 +/- 1 to 18 +/- 1 mumol.kg-1.min-1), glucose disappearance (15 +/- 1 to 17 +/- 1 mumol.kg-1.min-1), and net hepatic glucose output (11 +/- 1 to 15 +/- 1 mumol.kg-1.min-1) rose, 2) limb pyruvate oxidation (11 +/- 2 to 24 +/- 5 mumol/min) and estimated glycogenolysis (9 +/- 3 to 42 +/- 9 mumol/min) increased, 3) percentages of CO2 from limb pyruvate and glucose increased, and percentage of lactate from blood glucose decreased, and 4) arterial blood lactate was approximately 100% more, although net limb and hepatic lactate balances were unaltered, which suggests that neither liver nor muscle is the source of increased blood lactate. Comparison of these results with our previous study [Zinker et al. Am. J. Physiol. 266 (Endocrinol. Metab. 29): E921-E929, 1994] shows that the response to reduced PaO2, although present, is reduced when glucagon and insulin levels are fixed at basal. The majority of stimulation of glucose production by decreased PaO2 is still present when pancreatic hormones are clamped at basal, while the response by the hindlimb tissues is greatly reduced.
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PMID:Contribution of pancreatic hormone responses to the elevation in carbohydrate metabolism with reduced PaO2. 761 94

Hydrocortisone was infused overnight into nine normal healthy adults on three occasions at 0, 80, and 200 micrograms.kg-1.h-1, producing plasma cortisol concentrations of 10.6 +/- 1.2, 34.0 +/- 2.0, and 64.9 +/- 4.3 micrograms/dl, respectively. L-[1-13C]leucine, L-[phenyl-2H5]phenylalanine, and L-[2-15N]glutamine were infused during the last 7 h of hypercortisolemia to measure amino acid kinetics. During the last 3.5 h, somatostatin, glucagon, and insulin were infused to reduce the cortisol-induced elevation in plasma insulin to basal. Hypercortisolemia increased plasma glucose, free fatty acid (FFA), and insulin concentrations. Institution of the somatostatin clamp returned insulin to basal but increased glucose and FFA. Acute hypercortisolemia increased protein breakdown 5-20%, as measured by increases in leucine and phenylalanine appearance rates. Normalizing insulin during hypercortisolemia did not alter phenylalanine flux but enhanced leucine appearance rate, the latter result indicating that insulin was affecting leucine metabolism during hypercortisolemia. The fraction of the leucine flux that was oxidized was not significantly increased with hypercortisolemia, but disposal by the nonoxidative route of leucine uptake for protein synthesis was increased. Hypercortisolemia increased cycling of amino acids by increasing protein breakdown and synthesis, but the increase in this process could have increased resting energy expenditure (REE) only 1-2%. Hypercortisolemia increased glutamine flux in a dose-dependent fashion through an increase in de novo synthesis, which presumably reflects increased release from skeletal muscle. Hypercortisolemia increased REE 9-15% at the 80 and 200 micrograms.kg-1.h-1 infusion rates. Respiratory quotient did not rise with cortisol infusion but tended to decrease, suggesting that the increase in REE was fueled by increased oxidation of fat. These data demonstrate that hypercortisolemia increases metabolic rate and may be in part responsible for the hypermetabolic state in injury.
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PMID:Effect of cortisol on energy expenditure and amino acid metabolism in humans. 790 Jul 96

Cortisol is known to influence growth hormone release probably by modulating somatostatin tone. We examined the effect of metyrapone (the 11 beta-hydroxylase inhibitor) treatment on growth hormone response to growth hormone releasing hormone (1 microgram kg-1 body wt). Six healthy male subjects were tested on two occasions 1 wk apart. On one occasion they received metyrapone followed by growth hormone releasing hormone and on the other placebo followed by growth hormone releasing hormone. In all subjects metyrapone produced a significant drop in cortisol levels. Together with this drop there was a significant enhancement of growth hormone response to growth hormone releasing hormone. The GH response was negatively correlated with the cortisol level. Growth hormone release in response to growth hormone releasing hormone challenge is thus seen to be heavily influenced by cortisol levels.
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PMID:Lowering cortisol enhances growth hormone response to growth hormone releasing hormone in healthy subjects. 797 13

The effect of the long-acting somatostatin analog octreotide (SMS 201-995) on adrenocorticotropin (ACTH) secretion was studied in five patients with untreated Cushing's disease in vivo and in six human corticotropic adenoma cell cultures in vitro. For the in vivo study, 100 micrograms of octreotide sc was given 30 and 180 min after cannulation of the cubital vein and 100 micrograms of corticotropin-releasing hormone (CRH) was injected iv at 210 min. Serum ACTH and cortisol levels were measured for 390 min. In vivo, octreotide had no significant effect either on basal or CRH-stimulated ACTH levels and did not influence cortisol levels. The in vitro studies were conducted with corticotropic adenoma cell cultures derived from adenoma tissue obtained from six patients with Cushing's disease. In four of six cell cultures, octreotide (1 nmol/l-1 mumol/l) inhibited basal ACTH secretion in a dose-dependent manner. The inhibition ranged from 70 to 92% for 1 nmol/l octreotide to 14-46% for 1 mumol/l octreotide as compared to controls (100%). In three of three octreotide-responsive adenoma cell cultures investigated. CRH-stimulated ACTH secretion was suppressed by octreotide. Hydrocortisone pretreatment in vitro abolished the inhibitory effect of octreotide on ACTH secretion in one octreotide-responsive corticotropic adenoma cell culture. In conclusion, we showed that octreotide in most cases could inhibit the ACTH release from human corticotropic adenoma cells in vitro but had no suppressive effect on ACTH levels of patients with Cushing's disease in vivo. This discrepancy could be due to a somatostatin receptor down-regulation by cortisol at the hypercortisolemic state in vivo.
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PMID:Octreotide exerts different effects in vivo and in vitro in Cushing's disease. 813 Aug 85

Both exogenous and endogenous hypercortisolism result in reduced GH secretion and decreased somatic growth. However, little is known about the relation between endogenous cortisol and GH secretion under physiological or slightly disturbed conditions. To examine this, we measured and evaluated the pulsatility and circadian rhythmicity, and we cross-correlated the secretory patterns of cortisol and GH in six prepubertal patients with nonclassic 21-hydroxylase deficiency (NCCAH) and seven age-matched short-normal children. Cortisol and GH were secreted in a pulsatile fashion in both the NCCAH and control groups. The nocturnal peak cortisol increment and time-integrated area were lower in the NCCAH patients than in controls, whereas there was no difference in the total 24-h cortisol secretion between the two groups. The nocturnal increase of GH in NCCAH children, on the other hand, was associated with a significant augmentation of the pulse amplitude, whereas in control children there was an elevation of the baseline component. The cross-correlation analysis of the 24-h raw data showed that cortisol and GH were negatively correlated at brief lag times of 0-30 min, and positively correlated at long lag times of 12-12.5 h in both groups, with cortisol leading GH. The negative correlation might reflect either the negative effect of glucocorticoids on the adrenergic system, which stimulates GH secretion through GH-releasing hormone (GHRH) elevations and somatostatin (SRIH) decreases, or the absence of an inhibitory effect of CRH on SRIH. The positive correlation may reflect the positive effect of glucocorticoids on the GH gene. In conclusion, NCCAH children have a mild nocturnal cortisol deficiency compared with control children, as previously reported, and a distinct circadian pattern of pulsatile GH secretion. The hypothalamic-pituitary-adrenal (HPA) axis exerts both negative and positive influences on GH secretion, with mild disturbances in cortisol biosynthesis associated with slight alterations of GH secretion.
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PMID:Spontaneous cortisol and growth hormone secretion interactions in patients with nonclassic 21-hydroxylase deficiency (NCCAH) and control children. 863 54

Octreotide (OCT) is a somatostatin analog used for its inhibitory action on multiple GI functions. Although octreotide has numerous clinical benefits, it has also been shown to inhibit postresectional hyperplasia of small bowel and hepatic regeneration. Because octreotide inhibits both trophic and anabolic hormones, we hypothesize that the use of octreotide may be detrimental in patients with a recent bowel anastomosis. To test this hypothesis, 60 male rats were randomized to four equal groups following small bowel anastomosis. Group I = control; Group II = 10 mg/day of hydrocortisone succinate; Group III = 2.5 micrograms/kg/day octreotide (equivalent of a clinical dose); Group IV = 25 micrograms/kg/day octreotide. Hydrocortisone was used as a negative control because it is known to have inhibitory effects on small bowel anastomotic healing. On postoperative Day 7, bursting pressures were measured. Serum T-kininogen levels, as a marker for systemic inflammation, and hydroxyproline content from the anastomotic segments were obtained. These results indicate that in the rat small bowel model, octreotide did not have any deleterious effect on anastomotic strength, systemic inflammation, and collagen content, even at high doses. Hydrocortisone, as expected, showed significant detrimental effects on bursting strength, as well as decreasing systemic inflammation. These findings have significant clinical implications, as octreotide could be used without jeopardizing the intestinal anastomosis.
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PMID:The effects of octreotide on healing of small bowel anastomosis. 875 64


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