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)

Somatotrophs in suspensions of anterior pituitary cells from adult male rats can be separated into 2 fractions by density gradient centrifugation. In addition to their different densities, somatotrophs in these 2 fractions can be distinguished morphologically by their staining characteristics and ultrastructure. Somatotrophs of lesser density (type I; approximately 1.068 g/cm3) have fewer secretory granules and a more extensive Golgi apparatus than the somatotrophs of greater density (type II; approximately 1.073 g/cm3). Responsiveness of type I and type II cells to secretory agents (i.e., dibutyryl cyclic adenosine monophosphate, somatostatin, thyroxine, and hydrocortisone) was evaluated by GH radioimmunoassay. Type I cells were consistently more responsive (% GH release) than type II cells. During 7 days in culture, type I cells produced more (approximately 200%) GH than they initially contained, whereas type II cells did not show evidence of increased GH production. Hydrocortisone significantly stimulated GH production in type I, but not type II cells. These results support the hypothesis that at least 2 functionally distinct populations of somatotrophs are present in the anterior pituitary gland of the adult male rat.
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PMID:Functional heterogeneity in somatotrophs isolated from the rat anterior pituitary. 19 32

The main hormones involved in ketone-body metabolism are the anabolic hormone insulin and the primarily catabolic hormones, glucagon, cortisol, catecholamines and growth hormone. These hormones may regulate ketone-body metabolism at three sites: adipose tissue, by regulating fatty acid supply to the liver; the liver itself, by determining the relative activities of the re-esterification and fatty acid oxidation pathways; and the periphery, by influencing the rate of extrahepatic utilization of ketone bodies. The first two are quantitatively the most important. Insulin acts on all three regulatory sites. In adipose tissue lipolysis is inhibited and re-esterification enhanced with consequent decrease of fatty acid release. Both these processes are extremely insulin-sensitive. In the liver insulin increases fatty acid synthesis and esterification. At the same time malonyl-CoA formation is increased, which inhibits the acylcarnitine transferase system and thus decreases the transport of fatty acids into mitochondria and hence fatty acid oxidation and ketogenesis. Insulin also has a small stimulatory effect on extrahepatic ketone-body utilization. The effects of glucagon depend on whether insulin is present. In normal man glucagon stimulates insulin secretion and the predominant effect is that of insulin, i.e. decreased ketogenesis. In insulin deficiency glucagon has a mild stimulatory effect on lipolysis, increasing fatty acid supply to the liver. The main effects of glucagon are, however, on the liver. It activates the carnitine acyltransferase system through inhibition of malonyl-CoA synthesis. Fatty acid oxidation is increased and ketogenesis enhanced. The overall effect on the liver depends on the relative amounts of insulin and glucagon present. Studies with somatostatin show that glucagon can increase ketogenesis acutely when insulin secretion is inhibited in normal man, but the effects are short-lived. Cortisol has similar effects to glucagon. In the presence of insulin there is a small increase in fatty acid mobilization from adipose tissue, secondary to impaired glucose entry, and perhaps a small effect on lipolysis itself. This fatty acid is, however, directed to triacylglycerol in the liver. In insulin deficiency, again demonstrated by somatostatin infusion, the incoming fatty acidstone-body formation. The mechanism remains obscure. Catecholamines, in contrast, have their most potent effects on adipose tissue, stimulating lipolysis and fatty acid release even in the presence of insulin. They thus act mainly by enhancing precursor supply and have only minor effects on liver and no effect on peripheral utilization. Growth hormone, like glucagon, has little effect in the presence of insulin, but can enhance ketogenesis in insulin deficiency, although again the mechanism is unknown. Thus in normally fed man the effects of insulin will be overriding and little ketogenesis occurs because of limited fatty acid availability in the liver...
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PMID:Hormonal regulation of ketone-body metabolism in man. 74 14

The present study was undertaken to determine whether an acute physiological increase in plasma cortisol level had significant effects on alanine metabolism and gluconeogenesis within 3 hours in conscious, overnight-fasted dogs. Each experiment consisted of an 80-minute tracer and dye equilibration period, a 40-minute basal period, and a 3-hour experimental period. A primed, continuous infusion of [3-3H]glucose and continuous infusions of [U-14C]alanine and indocyanine green dye were initiated at the start of the equilibration period and continued throughout the experiment. Dogs were studied with (1) a hydrocortisone infusion ([CORT] 3.0 micrograms.kg-1.min-1, n = 5), (2) hydrocortisone infused as in CORT, but with pancreatic hormones clamped using somatostatin and basal intraportal replacement of insulin and glucagon (CLAMP+CORT, n = 5), or (3) saline infusion during a pancreatic clamp (CLAMP, n = 5). Glucose production and gluconeogenesis were determined using tracer and arteriovenous difference techniques. During CLAMP, all parameters were stable except for a modest 67% +/- 6% increase in gluconeogenic conversion of alanine to glucose and a 53% +/- 26% increase in gluconeogenic efficiency. When plasma cortisol levels were increased fourfold during CLAMP+CORT, there was no change in the concentration, production, or clearance of glucose. Gluconeogenic conversion of alanine to glucose increased 10% +/- 34% and gluconeogenic efficiency increased 65% +/- 43%, while net hepatic alanine uptake (NHAU) increased 60% +/- 19% and hepatic fractional extraction of alanine increased 38% +/- 12%. Cortisol did not cause an increase in the arterial glycerol level or net hepatic glycerol uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of acute elevations in plasma cortisol levels on alanine metabolism in the conscious dog. 146 Nov 35

Some pituitary hormones secrete hormones while others do not. Nonsecreting tumors can interfere with normal pituitary hormone secretion and produce tumor symptoms and signs like headaches and visual field defects. The most frequent hormone-secreting tumors are prolactinomas. Growth hormone or ACTH or gonadotropin or gonadotropin-alpha and beta chain-producing tumors are less frequent, TSH producing tumors are extremely rare. The most important elements of the diagnostic work-up are clinical signs and symptoms, assessment of pituitary function (measurement of TSH, free T4, LH, FSH, oestradiol/free testosteron, growth hormone, IGF-1, prolactin, ACTH, Cortisol, serum and urine osmolality), CT and/or MRI and, in patients with large tumors, a visual field exam. The treatment of choice of pituitary tumors is often surgery. Alternative therapies are radiation treatment (in nonoperable patients or when hormone levels are persistently elevated after pituitary surgery) and drug treatment (dopamine agonists in hyperprolactinemia, somatostatin analogues in acromegaly). Pituitary hormone deficiencies are treated depending on the specific deficiency with thyroxine, cortisone, oestrogen/gestagen/testosterone gonadotropines or ADH analogues.
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PMID:[Hypophyseal dysfunction and tumors]. 158 68

Sixteen Yorkshire pigs (49 +/- 2 kg BW at 17 weeks) were immunized against somatostatin (SRIF; 4 males, 4 females) or its conjugated protein, bovine serum albumin (BSA; controls; 4 males, 4 females). Immunizations were done at 10, 12 and 14 weeks of age. Jugular vein cannulae were surgically inserted at 17 weeks of age. Five d later, half of each sex from the control and SRIF-immunized groups were stressed. The other half were subjected to the same stress 48 hr later. On both days, remaining animals were used as unstressed controls. The stress consisted of 5 min of snare restraint. Blood samples were collected from all pigs on both days at -20, -15, -10, -5, 0 (beginning of stress), 2, 6, 10, 15, 20, 30, 40, 60, 90, 120, 150, 180 and 240 min. Samples were radioimmunoassayed for cortisol, growth hormone (GH), prolactin (Prl), insulin, triiodothyronine (T3), thyroxine (T4) and insulin-like growth factor I (IGF-I). Mean antibody titers against SRIF (1:150 dilution) at 15 weeks were 0.49 +/- .09% and 54.5 +/- 4.9% for control and SRIF immunized pigs, respectively. Gender and immunization against SRIF had no effect on any of the variables measured (P greater than 0.05), except for T3 levels which were greater in females than in males (P less than 0.05). The stress by time of sampling interaction was significant (P less than 0.01) for all hormones measured. Cortisol values almost tripled within 15 min of stress, reaching concentrations above 100 ng/mL. Maximal increases were seen at 2 min for T4 (14%), at 6 min for T3 (36%), at 15 min for Prl (46%) and at 10 min for insulin (141%). An increase of 129% in GH concentration was present at 20 min in stressed pigs; however, an increase of 97% was also seen at 120 min in control pigs. Concentrations of IGF-I decreased (21%) by 60 min in the stressed pigs and remained depressed for up to 150 min. Stress associated with snare restraint, therefore, induces major changes in the concentrations of a series of hormones in growing pigs. On the other hand, immunization against SRIF did not alter any of the hormonal profiles measured. Since snare restraint is widely used to handle pigs during jugular puncture, any study of hormonal secretion in this species should be carried out under carefully controlled conditions in terms of blood sampling technique.
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PMID:Hormonal changes following an acute stress in control and somatostatin-immunized pigs. 168 21

Purified rat peritoneal mast cells were incubated overnight with or without hydrocortisone (3 X 10(-6) M) and then stimulated with anti-IgE, somatostatin or a phorbol ester-ionophore combination, i.e., 12-O-tetradecanoyl-phorbol-13-acetate and A23187. The release of both histamine and [1-14C]arachidonic acid and its metabolites was determined. Hydrocortisone treatment markedly inhibited both anti-IgE and TPA-A23187 stimulated release, but not release stimulated by somatostatin. These results suggest that anti-inflammatory steroids may alter histamine release through an action involving the activation of the phosphatidylserine-calcium dependent protein kinase or its substrates.
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PMID:Hydrocortisone inhibits phorbol ester stimulated release of histamine and arachidonic acid from rat mast cells. 241 Dec 63

The dog pituitary pars intermedia (PI) appears to consist of relative large numbers of ACTH-containing cells in addition to the more abundant alpha MSH-containing cells. Since regulation of PI secretion probably varies across mammalian species, this study was undertaken to identify substances potentially involved in the control of dog PI POMC peptide secretion and to determine if these substances altered the secretion of immunoreactive (IR) ACTH and IR-alpha MSH in a parallel fashion. Pituitary neurointermediate lobes from dogs were collected and dispersed, and the PI cells obtained were perifused. For comparison, rat PI and pars distalis (PD) cells as well as dog PD cells were similarly collected and perifused. Dog PI cells secreted IR-alpha MSH at a basal rate of 125 +/- 59 (mean +/- SD) pg/min.10(5) cells and IR-ACTH at a rate of 40 +/- 9 pg/min.10(5) cells (molar IR-alpha MSH/IR-ACTH = 10). In contrast, secretion rates for IR-alpha MSH and IR-ACTH from perifused rat PI cells were 171 +/- 108 and 3 +/- 2 pg/min.10(5) cells, respectively (molar IR-alpha MSH/IR-ACTH = 179). Using Sephadex G-50 gel filtration chromatography, virtually all of the IR-beta-endorphin secreted by dog PI cells eluted near beta-endorphin (1-31). In addition, all of the IR-alpha MSH secreted by dog PI cells coeluted with synthetic alpha MSH on the G-50 column, but IR-ACTH appeared in two peaks, one eluting near porcine ACTH-(1-39) and another, apparently larger mol wt species. Dopamine and somatostatin were found to inhibit the secretion of IR-alpha MSH and IR-ACTH from perifused dog PI cells in a parallel and dose-dependent fashion. Norepinephrine and epinephrine similarly inhibited POMC peptide secretion, but this effect was blocked by haloperidol, suggesting that it was mediated through a dopamine receptor. CRF stimulated the secretion of both hormones from dog PI, and this effect was abolished by treatment of the cells with either dopamine or somatostatin. Cortisol had no effect on either basal or CRF-stimulated secretion of IR-alpha MSH or IR-ACTH from dog PI cells, but it did inhibit CRF-stimulated IR-ACTH from perifused dog PD. These results suggest that 1) dog PI secretes considerably more IR-ACTH than that in the rat; 2) the probable separate cell sources of IR-alpha MSH and IR-ACTH in dog PI are regulated in an identical fashion; and 3) dopamine, somatostatin, and CRF may function in the physiological or pathophysiological regulation of dog PI.
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PMID:Regulation and secretion of proopiomelanocortin peptides from isolated perifused dog pituitary pars intermedia cells. 253 71

The in vitro effects of several factors, including cortisol, somatostatin (SRIF), and medium osmotic pressure, on growth hormone (GH) release from the tilapia pituitary were examined in relation to fish size. Spontaneous GH release from the proximal pars distalis (PPD) of approximately 60-g fish was significantly less than that from tissue of fish weighing either approximately 120 or approximately 280 g when incubated in 340 m phi smolal medium. While GH content of the PPD cultures (tissue + medium measured by densitometry) increased consistently with fish size, GH concentration (per microgram of tissue protein) was variable, being highest in 120-g fish and lowest in 280-g fish. Moreover, GH concentration was not related to GH release. Fish size also appeared to be important in the responsiveness of GH cells to stimulation by cortisol (Nishioka et al., 1985) and by increased osmotic pressure. In cultures of PPD from approximately 60-g fish, in which spontaneous release was relatively low, cortisol and increased medium osmotic pressure significantly enhanced release. Cortisol and hyperosmotic medium were without significant effect, however, on GH release from PPD of approximately 120-g fish, which showed high spontaneous release. In contrast, SRIF, a potent inhibitor of GH secretion, was effective in lowering GH release regardless of fish size. Nevertheless, SRIF was apparently more effective in inhibiting GH release from tissue of 60-g fish than from tissue of 120-g fish. Our data suggest that GH secretion may be augmented when smaller tilapia (approximately 60 g) are transferred to seawater, a situation in which blood cortisol and osmotic pressure would presumably be elevated.
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PMID:Studies on the regulation of growth hormone release from the proximal pars distalis of male tilapia, Oreochromis mossambicus, in vitro. 287 68

Altogether 54 male patients with insulin-dependent diabetes mellitus participated in the studies. The impact of insulin-induced hypoglycemia on posthypoglycemic insulin sensitivity was evaluated for up to 12 hours following nadir hypoglycemia. The effect on glucose homeostasis following transient elevation of counterregulatory hormones was studied by exogenous administration of adrenaline, adreno-corticotropic hormone and growth hormone and by suppression of the endogenous release of growth hormone in connection with hypoglycemia. The studies were performed in the fasting state preceded by a 24 hour intravenous insulin infusion in order to avoid interference of subcutaneous insulin. Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. This test seemed appropriate for the evaluation of total insulin resistance, and its reproducibility was acceptable. By using this method it was demonstrated that insulin resistance occurred for at least 12 hours after a hypoglycemic event in patients with IDDM, and that adrenaline caused immediate insulin resistance which, however, faded out within four to six hours, while GH exerted no immediate effect on insulin sensitivity but caused marked and sustained insulin resistance after a lag period of about four hours. Cortisol had no apparent effect within six hours but enhanced the effect of GH. The magnitude of these diabetogenic effects of hypoglycemia and GH was less pronounced in patients who already were more insulin resistant. These results are compatible with the idea that adrenaline is of major importance for the counterregulation and restoration of blood glucose during the first few hours following hypoglycemia, while GH is responsible for the induction of a long-lasting state of insulin resistance. It is possible that such prolonged insulin resistance may cause posthypoglycemic hyperglycemia in patients with IDDM. These studies therefore indicate that the GH suppressing hormone somatostatin may be of clinical value as an adjunct to insulin in the treatment of patients with insulin-dependent diabetes mellitus and labile blood glucose control.
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PMID:Studies on posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. 290 16

The hormonal regulation of thyroglobulin synthesis has been studied using two independent clones of the OVNIS 6H cell line. Insulin, hydrocortisone and TSH were able to stimulate thyroglobulin synthesis, whereas transferrin, somatostatin and glycyl-histidyl-lysine were without effect. Insulin stimulated thyroglobulin synthesis without affecting cAMP production. Hydrocortisone, when combined with insulin was a stimulator too; this stimulation was not accompanied by an increase in cAMP. TSH alone was unable to stimulate either cAMP or thyroglobulin synthesis. The stimulatory effect of TSH on thyroglobulin synthesis took place only when combined with insulin or insulin plus hydrocortisone, and was mediated by cAMP. Consequently, insulin and hydrocortisone stimulated thyroglobulin synthesis by cAMP-independent mechanisms, whereas TSH acted via the cAMP system. Forskolin mimicked TSH effects on cAMP and thyroglobulin synthesis. Calf serum inhibited cAMP and thyroglobulin production. Optimal cAMP and thyroglobulin synthesis as well as TSH responsiveness were obtained in serum-free medium supplemented with 5 micrograms/ml insulin, 100 nM hydrocortisone and 1 mU/ml TSH.
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PMID:cAMP dependent and independent regulation of thyroglobulin synthesis by two clones of the OVNIS 6H thyroid cell line. 304 Apr 95


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