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

Insulin-induced hypoglycemias are a sign of non-sufficient counterregulation, in which different contra-insulinary hormones participate. The aim of the study was to investigate, whether there exists a difference between IDD and non-diabetics regarding secretion of glucagon, cortisol, and growth hormone during an insulin-induced hypoglycemia and further on pointing out, expecially, the importance of glucagon. Insulin-induced hypoglycemias are counterregulated in non-diabetics, not in IDD. The missing glucagon secretion during insulin-induced hypoglycemia in IDD seems to be independent from an autonomic neuropathy. Only after high doses of exogenous glucagon can one see a counterregulating increase of glucose. The STH secretion is similar in non-diabetics and IDD during an insulin-induced hypoglycemia and has evidently only a secondary effect in hypoglycemic counterregulation. The STH secretion may be the expression of a diencephal-triggered stress situation. The cortisol secretion is the same in both groups. The gluconeogenetic effect of cortisol is not sufficient to accomplish a fast compensation of hypoglycemia. This does not exclude long-term effects. When inhibiting the secretion of insulin and different contra-insulinary hormones with somatostatin, one is able to demonstrate that glucagon alone is a sufficiently counterregulatory hormone in insulin-induced hypoglycemias.
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PMID:[Glucagon, growth hormone, and cortisol response to insulin-induced hypoglycemia in insulin-dependent diabetics (IDD) without autonomic neuropathy (author's transl)]. 700 32

The secretion of hormones stimulating and inhibiting gastric secretory activity was studied in 85 patients with postvagotomy syndromes. The somatropin level was found to increase significantly in gastrostasis. The lower values of the blood insulin and C-peptide content in patients with recurrent ulcers was evidently associated either with insufficiency of the pancreatic insular apparatus or with partial vagal denervation, increased STH level, and plausible inhibiting effect of glucagon. Increased somatostatin secretion in the dumping syndrome, gastrostasis, and peptic ulcers may be due to the encountered hypergastrinemia.
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PMID:[Neurohumoral regulation of gastric secretion in postvagotomy syndromes]. 793 83

Blood levels of STH, ACTH, somatostatin, bombesin, gastrin, hydrocortisone, aldosterone, testosterone, estradiol, progesterone and gastric juice levels of gastrin and somatostatin were measured in remission and exacerbation of gastric and duodenal ulcer (GU), (DU) using radioimmunoassay. The study included 250 DU, 200 GU and 5O control subjects. As a result, two forms of DU were identified. DU type 1 is characterized by basal and stimulated hypergastrinemia, paradoxical D-cell response to stimulation, high blood concentrations of STH, ACTH, testosterone. Type 2 DU exhibits basal hypogastrinemia, elevated gastrin concentration in response to stimulation, adequate reaction of D-cells, low levels of estradiol and progesterone. In GU there were low concentrations of STH, bombesin, hydrocortisone, estradiol, testosterone, progesterone, somatostatin. D-cell response to loading was adequate. It is concluded that DU and GU pathogeneses are different, that DU is a heterogeneous disease.
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PMID:[The hormonal characteristics of the pathogenesis of gastric peptic ulcer and duodenal peptic ulcer]. 877 96

Long-lasting problem on the differentiation of adenohypophyseal cell, which prepares them for their specific tasks (somatotropic, lactotropic ect.), becomes elucidated after recognition of the differentiational effect of transcription factor Pit-1. Expression of that factor in somatotrops results in STH secretion, contrary to lactotrops producing prolactin. Subclinical hypothyreosis (increased TSH with normal T3 and T4) endangers vessel not because of hypercholesterolemia, but because of changes in the dynamics of the blood flow. The idea of cardiotropic effect of thyroidal hormones is supported by the finding that administration of trijodthyronine to children after the surgical correction of heart malformations (cardiopulmonary bypass) improves myocardial function--it elevates cardiac output and decreases requirements on the intensive care. Receptors for hormones in tissues are flexible, they can be "heterooligomers" for dopamine and somatostatin. Mutations of mineralocorticoid receptor may cause hypertension in pregnancy and progesterone receptors have several isoforms. Receptors can be also activated by short exposition to a hormone. Glucocorticoids have probably also membrane receptors. Diabetes mellitus "type I" needn't to be immunogenic and DM type II not only results from down-regulation of receptors and subsequent insulin resistance, but it can be also caused by defects in insulin secretion. Insulin has receptors in the brain and participates in the appetite regulation. The attempt to use "desensibilisation" by peroraly administered insulin in patients with immunogenic DM had no effect. Stress affects memory mechanisms, heavy emotional stress during gravidity can bring congenital malformations. The decrease of mental functions in aged women depends on the level of free estradiol (the fraction, which is not bound to plasma proteins). Activation of dopaminergic neurons can be achieved by neurotropic growth factors. Nesiritide is a recombinant brain natriuretic hormone successfully tested in heart failure. The role of leptin in the appetite regulation in man is still not clear, other signalling molecules may have also an effect, e.g., ghrelin, which primarily stimulates STH secretion and brings about weight gain. Sildenafil influences nitrergic neurons elsewhere than in penis, for example it has positive effects in patients with oesophageal achalasia.
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PMID:[Endocrinology 1999-2000]. 1128 21


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