Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients suffering from deletions of chromosome 18 (p-, q-) show regularly short stature. Endocrinological investigations were performed to prove if short stature is due to pituitary insufficiency. In three female patients with deletions of chromosome 18 and retarded bone age serum growth hormone was investigated after insulin induced hypoglycemia, after glucagon-propranolol and after stimulation with growth hormone releasing hormone. Thyroid function, gonadal function and adrenal function were investigated too. All three patients showed growth hormone deficiency. In one patient there were found in addition hypothyroidism and gonadotrophine deficiency as well. In conclusion growth failure in some patients with deletions of chromosome 18 seems to due to pituitary insufficiency. In these patients treatment with recombinant growth hormone may increase growth velocity.
 ...
PMID:[Endocrinologic disorders in deletion of chromosome 18]. 161 60

Responses of serum growth hormone (hGH) to glucagon (G), growth hormone releasing hormone (GHRH) and G/GHRH were measured in 8 normal adults and 6 patients with growth hormone deficiency (GHD). In normal adults, serum hGH reached its peak value (12.7 +/- 1.6 ng/ml) at 150 +/- 10 min, as blood glucose declined to its minimum after a transitory hyperglycemia in G test. The normal adults were responsive to GHRH test (GH peak 14.7 +/- 2.3 ng/ml at 30 +/- 0 min). In GHD, the responders to both G and GHRH tests showed a strongly positive response in G/GHRH test, with a serum hGH peak value of 34.6 +/- 4.1 ng/ml at 131 +/- 8 min being much higher than that of either single G or GHRH test (P less than 0.01), but without significant difference to the sum of the two single tests (P greater than 0.10). Among GHD patients, only 2 responded to GHRH and G/GHRH tests with hGH peak values 6.8 +/- 0.7 and 6.9 +/- 0.7 ng/ml at 45 +/- 15 and 90 +/- 0 min, respectively, both peak values being essentially similar (P greater than 0.10). We suggest that the mechanism of stimulation of pituitary hGH secretion in G test might involve inhibition of release of hypothalamic GH release inhibiting factor (GHRIF) caused by hypoglycemia after a transitory hyperglycemia following G injection. These results may further confirm our previous postulation (1986) that insulin hypoglycemia may increase hGH release by inhibiting hypothalamic cell secretion of GH release inhibiting factor.
 ...
PMID:Reduction of the effects of growth hormone release inhibiting factor enhances plasma growth hormone response to GHRH. 256 70

1. Vasoactive intestinal polypeptide (VIP) is present in high concentrations in the hypothalamus and appears to be involved in the modulation of growth hormone (GH) secretion. The effects of VIP on hypothalamic somatostatin (SMS) release are, however, controversial. 2. To further elucidate the mechanism of action of this peptide on GH secretion we studied the effects of VIP on SMS secretion from incubated rat hypothalamic fragments in vitro. 3. At 10(-6) M, VIP induced a significant increase in basal SMS release (P less than 0.01), whereas at 10(-10) M it had an inhibitory effect. 4. We suggest that the increase in GH after in vivo administration of VIP may be modulated, at least in part, by a direct effect of this peptide on SMS neurons, while the stimulatory effect of high doses of VIP on SMS release may represent a pharmacological interaction of this peptide with growth hormone releasing hormone, peptide histidine isoleucine, or glucagon receptors.
 ...
PMID:Dose-dependent effects of vasoactive intestinal polypeptide on somatostatin release from hypothalamic fragments in vitro. 257 24

In the mammalian brain, a major regulatory peptide is vasoactive intestinal peptide (VIP). This 28 amino acid peptide, originally isolated from the porcine duodenum, was later found in the central and peripheral nervous systems and in endocrine cells, where it exhibits neurotransmitter and hormonal roles. Increasing evidence points to VIP's importance as a mediator or a modulator of several basic functions. Thus, VIP is a major factor in brain activity, neuroendocrine functions, cardiac activity, respiration, digestion, and sexual potency. In view of this peptide's importance, the mechanisms controlling its production and the pathways regulating its functions have been reviewed. VIP is a member of a peptide family, including peptides such as glucagon, secretin, and growth hormone releasing hormone. These peptides may have evolved by exon duplication coupled with gene duplication. The human VIP gene contains seven exons, each encoding a distinct functional domain on the protein precursor or the mRNA. VIP gene transcripts are mainly found in neurons or neuron-related cells. VIP gene expression is regulated by neuronal and endocrine signals that contribute to its developmental control. VIP exerts its function via receptor-mediated systems, activating signal transduction pathways, including cAMP. It can act as a neurotransmitter, neuromodulator, and a secretagog. As a growth and developmental regulator, VIP may have a crucial effect as a neuronal survival factor. We shall proceed from the gene to its multiple functions.
 ...
PMID:VIP: molecular biology and neurobiological function. 269 76

Vasoactive intestinal peptide (VIP) is a highly basic 28 amino-acid peptide which was first isolated from porcine small intestine (Said & Mutt, 1970). It is related to several other peptides including PHI (peptide with N-terminal histidine and C-terminal isoleucine amide), secretin, glucagon, and has some sequences similar to those of growth hormone releasing hormone (Fig. 1). The amino-acid sequence of human VIP is identical with that of the porcine form (Itoh et al., 1983). It has been shown that human VIP is cosynthesized with PHM (peptide with N-terminal histidine and C-terminal methionine amide, the human analogue of PHI) from the same large precursor protein (Itoh et al., 1983).
 ...
PMID:Vasoactive intestinal peptide and anterior pituitary function. 307 50

Medullary thyroid carcinoma (MTC) can be important for gastroenterologists because 20-30% of patients with MTC suffer from chronic diarrhea and the tumor is capable of producing--besides other bioactive substances--a multitude of gastroenteropancreatic hormones. Gastrointestinal hormone profiles of 5 patients with MTC were determined both basally and after intravenous stimulation with secretin and calcium respectively. Diagnosis of MTC was confirmed histologically or cytologically and by demonstration of elevated serum concentration of calcitonin both basally and after calcium stimulation. 4/5 patients had chronic diarrhea. Normal values or only borderline increases were found for the following hormones: vasoactive intestinal polypeptide (VIP), neurotensin, substance P, growth hormone releasing hormone (GRH), glucagon, neurokinin A, peptide YY, and pancreatic polypeptide. Somatostatin was elevated after calcium stimulation in 1/5 patients only. The main findings were increased basal concentrations for GAWK in 5/5 patients and elevated concentrations for gastrin-releasing peptide (GRP, human bombesin) after calcium stimulation in 4/5. Probably as a consequence of the GRP increase, an increase in gastrin occurred in parallel, indicating bioactivity of the GRP released from the tumor. Besides calcitonin as the main tumor marker for MTC, determination of GAWK and GRP seems to provide helpful additional markers in laboratory diagnosis of MTC. GRP determination after i.v. calcium infusion allowed identification of patients with normal basal plasma GRP concentration.
 ...
PMID:[Gastrointestinal hormone profile in medullary thyroid carcinoma]. 801 6

A cDNA encoding a pituitary adenylate cyclase-activating polypeptide (PACAP) receptor was cloned from a bovine brain cDNA library using a synthetic oligonucleotide probe corresponding to the partial N-terminal amino acid sequence of the PACAP receptor purified from the bovine brain. The cloned cDNA encoded a polypeptide of 513 amino acid residues with seven putative transmembrane domains. The deduced amino acid sequence exactly matched the N-terminal amino acid sequence of the purified PACAP receptor. It also shared an apparent similarity with the vasoactive intestinal peptide (VIP), secretin, growth hormone releasing hormone, calcitonin, and glucagon receptors, suggesting that the PACAP receptor is a member of the secretin receptor subfamily of the guanine nucleotide-binding regulatory protein-coupled receptor family. Northern blot analysis showed that the size of the major mRNA band which hybridized with the cDNA was about 7 kb in the bovine cerebral-cortex and hippocampus. An expression vector containing the cloned cDNA for the PACAP receptor was introduced into Chinese hamster ovary (CHO) cells. The affinity of PACAP receptors expressed on the transfected CHO cells was quite similar to that of natural PACAP receptors on the bovine brain membranes. Competitive binding experiments showed that PACAP38 displaced the binding of 125I-labeled PACAP27 to the receptors on the CHO cells more efficiently than PACAP27, while VIP was less effective. In addition, both of PACAP27 and PACAP38 elevated the levels of cAMP and inositol phosphates in the transformed CHO cells. These results indicate that the PACAP receptors encoded by the cloned cDNA are identical to the purified PACAP receptors, and that they can stimulate dual signaling cascades.
 ...
PMID:Cloning and expression of a complementary DNA encoding the bovine receptor for pituitary adenylate cyclase-activating polypeptide (PACAP). 804 55

The concentration of extracellular calcium rightly regulates calcitonin secretion by calcium influx through dihydropyridine-sensitive voltage-dependent calcium channels; the result is an increase in intracellular calcium. There also exists a cAMP-dependent pathway of calcitonin release activated by glucagon or growth hormone releasing hormone. In thyroid C-cells, as in all cells, there is dual regulation of adenylate cyclase, mediated by inhibitory or stimulatory G proteins; glucagon stimulated cAMP production can be inhibited by somatostatin via pertussis toxin sensitive inhibitory G proteins. Somatostatin inhibits not only cAMP dependent but also calcium-dependent calcitonin secretion. Furthermore, somatostatin inhibits voltage dependent calcium channel currents thereby lowering cytosolic calcium. These actions also involve a pertussis toxin-sensitive inhibitory G protein but they occur independently of changes in the cytosolic cAMP concentration. Thus multiple interactions between second messenger systems at different cellular levels modulate calcitonin secretion.
 ...
PMID:Regulation of calcitonin secretion in vitro. 822

We have recently cloned CTRs from cDNA libraries prepared from porcine renal and human ovarian cell lines. In situ hybridization and Northern analysis confirm the widespread distribution of CTR mRNA in numerous tissues. Hydropathy plots of the predicted amino acid sequence of the receptors demonstrate multiple hydrophobic regions that could generate 7 transmembrane spanning domains, similar to other G protein-coupled receptors. Searches of databanks for proteins with related amino acid sequences reveals that the CTRs are closely related to the receptors for parathyroid hormone/parathyroid hormone related peptide, secretin, vasoactive intestinal peptide, growth hormone releasing hormone, glucagon-like peptide-1 and glucagon. These receptors have no significant sequence homology to other G protein-coupled receptors, and therefore, appear to comprise a distinct receptor family. Expression of the hCTR or pCTR in COS cells results in expression of high affinity CTRs which are coupled to adenylate cyclase (AC). The hCTR, however, demonstrates higher affinity for human and salmon CT compared to the pCTR. Both CTRs demonstrate low affinity binding and AC activation in response to calcitonin gene related peptide, amylin or secretin, providing a possible explanation for the cross-reactivity among these peptides in vivo. Stable transfectants expressing the pCTR increase cAMP levels and increases in cytosolic free Ca2+ concentration consistent with dual coupling to AC and phospholipase C. Additional studies will help to establish the structural basis for this functional property as well as the evolutionary relationship of the members of this newly identified family of receptors.
 ...
PMID:Characterization of the structural and functional properties of cloned calcitonin receptor cDNAs. 822 1

Food intake can be increased or decreased after either central or peripheral administration of peptides. Galanin, neuropeptide Y, opioid peptides, growth hormone releasing hormone and desacetyl-MSH increase food intake whereas insulin, glucagon, cholecystokinin, anorectin, corticotropin releasing hormone, neurotensin, bombesin, enterostatin, cyclo-his-pro and thyrotropin-releasing hormone reduce food intake. A number of these peptides also affect the activity of the sympathetic nervous system. The peptides which have been tested have a reciprocal effect on food intake and sympathetic activity. Opioids, NPY and GHRH, which increase food intake, decrease sympathetic activity. Conversely, peptides which reduce food intake, increase sympathetic activity, with glucagon, cholecystokinin, corticotropin releasing hormone, calcitonin, neurotensin and bombesin being examples, Several of these peptides also affect the intake of specific nutrients. Insulin reduces food intake in animals fed a high carbohydrate diet, but not when fed a high fat diet. Neuropeptide Y increases carbohydrate intake. Galanin and opioid peptides increase fat intake. Enterostatin and cyclo-His-Pro, on the other hand reduce fat intake. Glucagon decreases protein intake. The effect of peptides on the intake of specific nutrients suggests that peptides may work in part by modulating basic feeding mechanisms to lead to the selection of specific nutrients from the diet. This hypothesis might be called a nutrient specific model of peptide-induced food intake.
 ...
PMID:The nutrient balance hypothesis: peptides, sympathetic activity, and food intake. 848 34


1 2 Next >>