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)

We have used a model of experimental protein-energy malnutrition induced in weaned rats by administration of a protein free diet during 2 weeks. Some malnourished rats were then refed with a control diet for 4, 9 or 30 days. Control rats were fed for the same periods with the balanced control diet. Malnourished rats showed a loss in body weight of approximately 25%. After 30 days of refeeding, the animals gained weight reaching values higher than that of control rats. Insulin secreted by perifused pancreatic slices from malnourished rats, was impaired in first and second glucose-induced secretory phases. Basal secretion was also diminished in incubation of pancreatic slices. When malnourished rats were refed for 4 days, basal insulin secretion reached control values. Stimulated insulin secretion was normalized at 9 and 30 days of refeeding. Our result on somatostatin (SRIF) secretion in malnourished rats showed basal hypersecretion and diminished first and second glucose-induced secretory phases. During refeeding basal SRIF secretion was normalized from day 4. On the contrary stimulated secretion was significantly increased at 4 and 9 days of refeeding, and on day 30 values did not differ from controls. In protein energy malnutrition, the disturbed hormonal state can represent adaptative mechanisms to the protein depletion and hormonal changes have also an essential role in refeeding.
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PMID:[The effect of a protein-free diet on insulin and somatostatin secretion in rats]. 136 37

The long-acting somatostatin analogue octreotide is a synthetic cyclic peptide consisting of 8 amino acids. Depending on the organ, it acts either as a hormone or as a neurotransmitter. The effect on various physiological functions in the brain and the gastrointestinal tract is mainly inhibitory. Due to its inhibitory actions, the possibility of intravenous and subcutaneous administration and the lack of serious side-effects, octreotide offers a broad spectrum of possible indications. Today octreotide is recommended in acromegaly patients and for the treatment of hormone dependent symptoms in patients with gastroenteropancreatic tumours. New indications are enterocutaneous and pancreatic fistulas and the prevention of complications in major pancreatic surgery. In patients with dumping and short-bowel syndrome, octreotide may be helpful until dietary regimens are established. In Aids patients with severe diarrhea, octreotide can be used to stabilize patients with severe dehydration and malnutrition. The clinical effectiveness on upper GI-bleeding due to gastric ulcer and oesophageal varices is still controversial. Future studies must prove whether octreotide may be helpful in treating diabetic retino- and nephropathy because of the possibility of suppressing growth hormone and IGF-I. The antiproliferative effect of octreotide also allows its use in patients with somatostatin-receptor-positive, non-endocrine solid tumors (e.g. brain, breast and small-cell lung cancer). A promising area is the scintigraphic visualization of somatostatin-receptor-positive tumors with a radio-labelled octreotide analogue and the possible target irradiation of these tumors by beta-particle emitting isotopes attached to such analogues.
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PMID:[Somatostatin analog (octreotide) in clinical use: current and potential indications]. 162 Oct 78

Two unrelated male infants presented with brittle insulin-dependent diabetes mellitus in the first days of life. Subsequently they each developed severe secretory diarrhea, with stool volumes of more than 100 ml/kg/day. Extensive biochemical and serological investigation failed to reveal the etiology of the diarrhea. The infants, cared for at different institutions, underwent therapeutic trials of various agents including loperamide, cholestyramine, prednisone, indomethacin, and somatostatin analogue, without response. Both infants succumbed to septicemia and malnutrition related to diarrhea and poor control of glycemia. At autopsy, both were found to have absence of islets of Langerhans in the pancreas, and diffuse dysplastic changes in small and large intestinal mucosae. In particular, the entire alimentary tract in each case was lined by epithelia most typical of foregut mucosa: secretory-type glands, absent crypts of Lieberkuhn, and absent villi. These cases are contrasted with previously-reported infants with congenital diabetes mellitus, and the possible interrelation of these two highly unusual findings, congenital diabetes mellitus and diffuse intestinal dysplasia, is examined.
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PMID:Congenital diabetes mellitus and fatal secretory diarrhea in two infants. 177 17

Blood glucose, plasma insulin and glucagon, as well as pancreatic insulin, glucagon and somatostatin contents, were measured in control (C group, 18% casein), deprived (D group, 5% casein) and pair-fed (PF) rats at seven intervals during 23 wk after weaning (wk 0). In C rats, plasma and pancreatic insulin showed parallel variations, in D rats, plasma insulin increased normally until wk 3 after weaning, dropped from wk 3 to 8 and was higher in wk 16 and 23 than in wk 8, while pancreatic insulin increased linearly after a significant drop between wk 0 and 1. Insulin variations in D rats were related to protein deficiency until wk 5, but only to energy deficiency thereafter. Circulating and pancreatic glucagon dropped identically for the three groups until wk 5: its role in adaptation to malnutrition is quite irrelevant, although a dysregulation of its secretion was noted. Protein-energy malnutrition induced an increase of pancreatic somatostatin content that was due to the energy deficiency. On the basis of the insulin-to-glucagon ratio, three phases of adaptation to protein-energy malnutrition appeared. From wk 0 to 3, the metabolic priority was growth, whereas glucose homeostasis was secondary, accounting for the early hypoglycemia. From wk 3 to 8 survival was the main priority. After wk 8, the various biochemical parameters stabilized, and growth was parallel to that of normal animals. Protein-energy malnutrition was responsible for a dissociated adaptation of pancreatic hormones.
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PMID:Progressive adaptation of the endocrine pancreas during long-term protein deficiency in rats: effects on blood glucose homeostasis and on pancreatic insulin, glucagon and somatostatin concentrations. 286 38

We have recently shown that hypersomatostatinemia is a feature of cystic fibrosis (CF) when these patients have CF-associated pancreatogenic diabetes mellitus (CFDM). To address the possibility that patients with CFDM might have suppressed pituitary growth hormone (GH) release as a result of increased plasma somatostatin, GH secretion in 8 CFDM patients and 8 normal male controls was studied using a standard arginine infusion stimulus. Concentrations of the GH-dependent peptides, insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein 3 (IGFBP-3) were also measured. We found that mean GH concentrations in the CFDM group were significantly increased (p < 0.05) rather than decreased at the 30-min (12.3 +/- 3.6 vs. 3.8 +/- 1.9 ng/ml), 45-min (15.4 +/- 2.9 vs. 6.1 +/- 2.3 ng/ml) and 60-min (13.2 +/- 2.3 vs. 6.2 +/- 2.2 ng/ml) time points of study. Mean GH area under the curve (633 +/- 128 vs. 249 +/- 107 ng/ml) was also significantly greater (p < 0.05) in the CFDM group. Despite higher GH levels in the CFDM patients, their IGF-I and IGFBP-3 concentrations were low. We conclude that plasma somatostatin elevations in the CFDM group are not of sufficient magnitude to suppress pituitary GH release. Decreased levels of growth mediating peptides in the relatively malnourished CF subjects suggest a pattern of malnutrition-induced GH resistance which may contribute to poor weight and height gain.
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PMID:Effect of hypersomatostatinemia on growth hormone secretion in cystic fibrosis patients with diabetes. 750 19

Chronic renal insufficiency (CRI) is associated with growth failure in children and laboratory rats and is considered to be due, in part, to co-existent malnutrition. Alterations in hypothalamic control of growth hormone (GH) secretion have been suggested in uremic patients. We sought to determine whether factors unique to CRI play a role in this disturbance of GH regulation. Using in situ hybridization histochemistry, we compared messenger RNA (mRNA) levels for the hypothalamic neurohormones GH-releasing hormone (GHRH) and somatostatin (SRIH) in three groups: rats with CRI induced by 5/6 nephrectomy (NPX, N = 4); sham-operated, ad libitum fed rats (SAL, N = 5); and sham-operated, pair-fed rats (SPF, N = 5). We also measured plasma GH at 10 minute intervals for a six hour period via intra-atrial cannulae. The NPX group had significantly lower hypothalamic GHRH mRNA concentrations than both other groups; in addition, these levels were significantly lower in the SPF than in the SAL group. Concentrations of hypothalamic SRIH mRNA did not differ significantly among the three experimental groups. Six-hour mean plasma GH concentrations were significantly lower in the SPF (18.3 +/- 1.8 micrograms/liter) than in either the SAL (27.0 +/- 3.3 micrograms/liter) or the NPX groups (36.8 +/- 7.2 micrograms/liter); the difference in the mean plasma GH levels in the NPX vs. the SAL group did not attain statistical significance. This study provides evidence for an effect of CRI on the neuroendocrine control of GH secretion not related to caloric intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in the neuroendocrine control of growth hormone secretion in the uremic rat. 809 33

The effect of stressful stimulation and protein malnutrition on the gonadotrophic and somatotrophic axis of sheep is discussed with special references to the relationship between these stimuli and the GnRH and somatostatin neuronal systems in the hypothalamus. Generally, long-term stimulation and chronic underfeeding reduce gonadal functions in the sheep. There is evidence for the GnRH-dependent pathway for the mechanism of these phenomena in female sheep. GnRH neurons respond to long-term stress in diminishing of neuropeptide release from the nerve terminals due to the depression of its axonal transport. Chronic restriction of dietary proteins in lambs reduces the plasma LH concentrations but does not impair the development of GnRH neurons nor the synthesis and processing of GnRH. It is suggested that malnutrition delays the first ovulation probably due to the neural mechanism responsible for the preovulatory GnRH/LH output. Stress has rather unclear effect on growth hormone (GH) secretion in the sheep. Prolonged, but not short stressful stimulation provokes the rapid release of somatostatin, which is sustained during long-term stimulation. These results suggest that effect of stress on somatotrophic axis depends on the period of stressful stimulation. Chronic malnutrition enhances secretion of GH by an increase in amplitude of GH pulses and reduces the secretory activity of somatostatin neurons. It is postulated that nutrients can influence GH secretion in the sheep by mechanism dependent on the hypothalamic somatostatin.
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PMID:Stress and nutritional influences on GnRH and somatostatin neuronal systems in the ewe. 891 8

Neuroendocrine mechanisms governing growth hormone (GH) secretion are sensitive to nutritional status since the normal pulsatile pattern of GH release is disrupted during conditions of food deprivation or malnutrition. A reasonable hypothesis for this occurrence is the alteration of somatostatin and GH-releasing hormone (GHRH) synthesis, storage and secretion. In this study, we investigated the effects of food deprivation on GH, GHRH, hypothalamic and pituitary galanin (GAL), and somatostatin through immunocytochemical and mRNA analysis. Adult male rats were subjected to 72 h of food deprivation, during which an average of 18% total body weight was lost. ICC studies were performed on brain sections from the rostral, middle and caudal regions of the median eminence of the hypothalamus using the avidin-biotin-peroxidase method. Immunocytochemical results were generated for the percent area and optical density (intensity) of immunostaining in the median eminence. Messenger RNA analyses were performed using sense and antisense riboprobes produced from cDNA clones for GH, GHRH, somatostatin and GAL. Food deprivation decreased somatostatin immunostaining in middle and caudal regions of the median eminence; similarly, food deprivation resulted in decreased GHRH immunostaining in rostral and middle sections of the median eminence of the hypothalamus. mRNA levels for somatostatin, GHRH and GH and GAL were also reduced by food deprivation. Our data suggest that suppressed GH secretion in food-deprived rats may reflect a general downregulation of the neuroendocrine and pituitary GH axis.
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PMID:Effects of food deprivation on the GH axis: immunocytochemical and molecular analysis. 906 90

Male Wistar rats, (2 months old), randomly divided according to the diet offered to four groups (C-control; A- alcoholized, PD-protein-deprived, A-PD- alcoholized protein-deprived). In group A and A-PD rats, the number of gastrin producing G-cells was significantly lower. The volume density of G-cells was significantly decreased in alcoholic rats. Fasting serum gastrin level (FSGL) significantly raised due to combined effect of alcohol consumption and protein malnutrition. In group A rats, the profile area of G-cells and their nuclei increased. In PD rats, the profile area of G cells also increased. There were no differences in nucleus/cell ratio due to alcohol ingestion alone, but it decreased significantly in PD and A-PD rats. Pale and lucent types of granules were predominantly seen in G-cells of animals of group A and A-PD. Mean diameter of granules increased in A, PD and A-PD rats. Other endocrine cells (ECL, D, EC) also decreased in number in A rats. Somatostatin producing D-cells decreased significantly in A-PD rats, both in fundic and pyloric mucosa.
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PMID:Gastrin producing G-cells after chronic ethanol and low protein nutrition. 1008 78

In the majority of patients suffering from chronic pancreatitis an endocrine pancreatic insufficiency is correlated with exocrine dysfunction. The prevalence of impaired or diabetic glucose tolerance is 40-70%, half of these patients suffer from an insulin-dependent diabetes mellitus. In general the probability of endocrine insufficiency progressively increases within the ten years following diagnosis of chronic pancreatitis. Onset and severity of the endocrine dysfunction depend on parenchymal destruction of the pancreas but are also influenced by ongoing alcohol consumption. Pathological findings in the endocrine pancreas are a loss of B-cells with decrease in secretion of insulin but also a loss of B-cell responsiveness to glucose by impaired perisinusoidal diffusion. Disturbances of the enteroinsulinar axis with diminished levels of incretins due to an exocrine insufficiency are also discussed. In addition, an impaired A-cell function may be important, that is characterized by diminished levels of stimulated glucagon. Increased plasma levels of somatostatin were found, the source of which is unknown. The susceptibility to severe hypoglycemia in patients with diabetes mellitus secondary to chronic pancreatitis is higher than in Type I diabetics. This is mainly caused by the impaired glucagon secretion but also influenced by malnutrition and concomitant hepatic dysfunction due to the toxic affect of alcohol. Diagnostic procedures are the measurement of C-peptide-concentrations and profiles of blood glucose after fasting and stimulation with L-arginine or glucose. Especially in the beginning of the endocrine insufficiency the determination of basal levels of blood glucose or C-peptide are not useful. Unless treatment by diet is effective, the therapy of diabetes secondary to chronic pancreatitis should be done by insulin replacement. A certain degree of hyperglycemia may be tolerated due to the risk of hypoglycemia and the persistent alcohol consumption in these patients. Intensified insulin therapy should only be done in selected patients with good compliance. Long-term complications in patients with pancreatogenic diabetes are comparable to diabetes Type I and largely depend on the duration of the diabetes. Life expectancy is reduced, death in these patients is mainly due to persistent alcohol and nicotine abuse (cardiovascular disease, malignant tumors, etc.), in only a minority pancreatitis or diabetes (mainly hypoglycaemia) are relevant risk factors.
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PMID:[Secondary diabetes in chronic pancreatitis]. 1044 9


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