Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcitonin concentration (CT) was measured in 52 children with insulin-dependent diabetes (IDDM). All the patients studied were divided into three groups. The first group consisted of children with freshly diagnosed diabetes remaining in the condition of ketonemic acidosis. The second group was composed of children with the well controlled diabetes during the first two years od duration of the disease. The third group included the patients with poorly controlled diabetes of the duration longer than ten years having the accompanying vascular complications. The control values were determined in children without metabolic disturbances of either diabetic or other origin. CT concentration was significantly elevated both in the patients of the first group and those of the third group. In the second group the concentration of this hormone was close to normal. It is known that calcitonin participates in the homeostasis of calcium and is an important regulator of insulin secretion. The results obtained suggest that calcitonin may play a role both in the pathogenesis of diabetes and in developing of diabetic osteopenia.
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PMID:[Level of calcitonin in blood serum of children with insulin dependent diabetes]. 136 94

Calcitonin gene-related peptide (CGRP) is an intrapancreatic neuropeptide that is known to inhibit glucose-stimulated insulin secretion in rats. To study if this inhibition is a direct islet effect, isolated, overnight cultured, rat islets were incubated together with glucose (3.3 or 8.3 mM) and CGRP (10(-11) to 10(-6) M). It was found that insulin secretion stimulated by glucose (8.3 mM) was inhibited by 77% by CGRP at 10(-6) M (p less than 0.001) and by 48% by the peptide at 10(-7) M (p less than 0.05). To study the possible mechanism(s) behind this inhibition, we investigated the effects of CGRP (10(-6) M) on the efflux of 45Ca2+ and 86Rb+ (reflecting Ca2+ and K+ ion movements, respectively) from isolated, perifused, rat islets. Furthermore, we examined the influence of CGRP on the content of cyclic AMP in overnight cultured isolated rat islets. We found that the initial, immediate 2-8 min peak of glucose (16.7 mM)-stimulated 45Ca(2+)-efflux was not affected by CGRP. In contrast, when the peptide was added at min 20 after glucose introduction, i.e., when the peak 45Ca(2+)-efflux had vanished, a small decrease in 45Ca(2+)-efflux was observed (p less than 0.001). CGRP did not alter the 86Rb(+)-efflux at 8.3 mM glucose neither in the presence nor in the absence of extracellular Ca2+. The islet content of cyclic AMP after 30 min incubation was 19.1 +/- 3.1 fmol/islet at 3.3 mM glucose and increased to 36.0 +/- 5.7 fmol/islet at 16.7 mM glucose (p less than 0.05). CGRP (10(-6) M) completely abolished this increase.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1990 Sep
PMID:Calcitonin gene-related peptide inhibits insulin secretion studies on ion fluxes and cyclic AMP in isolated rat islets. 196 31

Calcitonin is known to inhibit secretion of gastrin and insulin in vivo. The objective of this study was to determine whether calcitonin can act directly on pancreatic islets in vitro to inhibit insulin release. Isolated islets were obtained from collagenase-treated rat pancreas, and three peptides (gastrin-releasing peptide, cholecystokinin-8, bombesin) and glucose were used to stimulate insulin release. All agents caused a significant increase in insulin secretion and calcitonin inhibited these responses, but had no consistent effect on basal release. This study provides evidence that calcitonin is an effective inhibitor of insulin secretion and acts directly on islet tissue.
Diabetes 1986 Jan
PMID:Calcitonin inhibition of insulin release from isolated rat pancreatic islets. 351 Jan 39

In eight normal pregnant women and in eighteen women with a family history of diabetes, plasma calcitonin (CT), parathyroid hormone (PTH), insulin and glucagon variations and total plasma calcium levels were investigated. Calcitonin, parathyroid hormone and glucagon were all increased during the 2nd and 3rd trimester of pregnancy in normal women (N.W.) and in women with a family history of diabetes (W.F.H.D.). Plasma calcitonin levels were statistically significantly different between the two groups only in the 3rd trimester (118 +/- 4.9 vs 139 +/- 3.6 pg/ml p less than 0.01 in N.W. and W.F.H.D. respectively). Total plasma calcium levels were decreased significantly in the 3rd trimester in both groups: 3rd vs 1st trimester p less than 0.005 and p less than 0.001 in N.W. and W.F.H.D. respectively. Statistically significant difference between the two groups in total insulinemic area (p less than 0.001), in the rapid phase area (p less than 0.01) and insulinogenic index (p less than 0.05) were observed in the 3rd trimester.
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PMID:Plasma calcitonin variations in normal women and in women with family history of diabetes during pregnancy. 354 28

Modulation of feeding by opiates, putative satiety peptides, and dopamine was explored in the Chinese hamster, an animal that develops diabetes mellitus in certain inbred strains. Diabetic hamsters were hyperphagic relative to their nondiabetic controls, but both groups exhibited natural circadian variation in feeding. Starvation provoked hyperphagia of about 1-h duration in both groups. Naloxone and butorphanol had no effects on Chinese hamster feeding. Opiate receptor binding on Chinese hamster brains demonstrated no specific binding of naloxone or ethylketocyclazocine, but IR-dynorphin concentrations were comparable with that in rats. N-allylnormetazocine, a sigma-opiate receptor agonist, appeared to stimulate diabetic hamster feeding. Peptides reputed to have satiety effects in rats were without effect in Chinese hamsters: cholecystokinin, bombesin, somatostatin, and pancreatic polypeptide. Calcitonin limited feeding in both groups but may be nonspecific. Dopaminergic blockade by haloperidol also limited feeding, and diabetic hamsters were more sensitive to this. Although Chinese hamsters clearly can modulate their food intake when diabetic, we conclude that the opiatergic and peptidergic influences on feeding are very different from those in rats and may be of little importance.
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PMID:Feeding systems in Chinese hamsters. 614 21

The present study was aimed at investigating the effect of calcitonin on plasma glucose, C-peptide, glucagon and growth hormone (GH) responses to arginine in insulin-dependent diabetic subjects. For this purpose, 6 insulin-requiring diabetics were submitted to an arginine tolerance test twice, in basal conditions and during the simultaneous infusion of salmon calcitonin (100 MRC) plus arginine in random order. Calcitonin caused a clear inhibition of the plasma glucose rise triggered by the amino acid, without significant modifications of the plasma C-peptide and glucagon responses. A significant rebound of plasma glucose was seen after calcitonin was stopped. Plasma GH rise following arginine administration was significantly inhibited by calcitonin. These findings suggest some positive interferences of calcitonin with the arginine-induced plasma glucose increase in insulin-dependent diabetes.
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PMID:Effect of Calcitonin on plasma glucose, C-peptide, glucagon and growth hormone responses to arginine in insulin-dependent diabetic subjects. 702 89

Endoneurial hypoxia of ischaemic origin is believed to cause the reduction in sciatic nerve substance P levels in experimentally diabetic rats. The first part of this study was designed to determine whether the changes seen extended to another neuropeptide, calcitonin gene-related peptide, and to reveal any correlation between substance P and calcitonin gene-related peptide levels in the sciatic nerve of both diabetic and centrally hypoxaemic rats. Comparison of streptozotocin diabetic rats (four-week duration) with their control group showed clear reductions in both substance P-like immunoreactivity (control = 225 +/- 20 pg/mg protein, diabetic = 139 +/- 19; P < 0.01) and calcitonin gene-related peptide-like immunoreactivity (control = 9.08 +/- 0.65 ng/mg protein, diabetic = 4.43 +/- 0.44; P < 0.001). A similar pattern was seen with the comparison of five-week centrally hypoxaemic rats (housed in 10% O2) with their controls for both substance P-like immunoreactivity (control = 222 +/- 10 pg/mg protein, hypoxic = 148 +/- 13; P < 0.001) and calcitonin gene-related peptide-like immunoreactivity (control = 6.58 +/- 0.42 ng/mg protein, hypoxic = 3.01 +/- 0.45; P < 0.001). Calcitonin gene-related peptide levels correlated closely with substance P levels in both the diabetes and central hypoxaemia studies (r2 = 0.69 and 0.62, respectively). The second part of this study measured the messenger RNA levels of the substance P precursor, preprotachykinin-A, and calcitonin gene-related peptide messenger RNA in the L4 and L5 dorsal root ganglia of control, diabetic and centrally hypoxaemic rats. There was no change in preprotachykinin-A or calcitonin gene-related peptide messenger RNA levels between any of the groups, suggesting that the sciatic nerve decreases in substance P and calcitonin gene-related peptide described above are post-transcriptional in origin.
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PMID:Reduced sciatic nerve substance P and calcitonin gene-related peptide in rats with short-term diabetes or central hypoxaemia co-exist with normal messenger RNA levels in the lumbar dorsal root ganglia. 751 37

Glucagon-like peptide-1 (GLP-1) is promptly released from endocrine cells of the distal part of the gut after oral ingestion of a meal. To test the possibility that hormones produced by the proximal small intestine or transmitters of the enteric nervous system may be involved in the early phase of meal-induced GLP-1 secretion, various intestinal regulatory peptides and neurotransmitters of the gut were administered intraarterially in the isolated vascularly perfused rat colon preparation. The release of GLP-1 in the portal effluent was measured by a specific RIA. Intraarterial infusion of glucose-dependent insulinotropic peptide (GIP) over the concentration range 0.25-1 nM evoked a dose-dependent release of GLP-1, with a maximal response of 350% of the basal value. Tetrodotoxin did not modify the GIP-induced release of GLP-1. Secretin or cholecystokinin did not stimulate the secretion of GLP-1. Bombesin (10(-9)-10(-7) M) provoked a dose-dependent release of GLP-1, consisting of an early peak, followed by a sustained response. Calcitonin gene-related peptide (5 x 10(-8) M) induced a dramatic rise of GLP-1 immunoreactivity in the portal effluent (peak at 800% of the basal value 10 min after the start of infusion). Similarly, the beta-adrenergic agonist isoproterenol at concentrations of 10(-7) and 10(-6) M provoked a pronounced release of GLP-1 (peak at 500% of the basal value with 10(-6) M isoproterenol). Finally, the muscarinic cholinergic agonist bethanechol at a concentration of 10(-4) M evoked a gradual increase in GLP-1 immunoreactivity, which reached a maximal value (900% over basal) at the end of the 30-min infusion period. The lowest concentration of bethanechol used in the present study (10(-5) M) did not increase portal GLP-1 immunoreactivity over the basal value. Tetrodotoxin did not modify the bethanechol-, isoproterenol-, calcitonin gene-related peptide-, or bombesin-induced GLP-1 release. In conclusion, the present study conducted with the isolated vascularly perfused rat colon shows that there are interactions between the two most potent incretins, GIP and GLP-1, probably through an enteroendocrine pathway. Additionally, several transmitters of the gut are potent stimulants of GLP-1 release and, therefore, represent potential tools in the treatment of the noninsulin-dependent diabetes mellitus.
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PMID:Regulation of glucagon-like peptide-1-(7-36) amide secretion by intestinal neurotransmitters and hormones in the isolated vascularly perfused rat colon. 798 23

A case of a 36-year patient with persistent diabetes mellitus of type I and gangrene of the foot is presented. Calcitonin has been used to treat osteitis and inflammation of the adjacent soft tissues. Despite performed surgery and conservative treatment, destruction of the bones has been progressing, and could lead to the high amputation of the extremity. Calcitonin produced an increase in bone, massive calcification around bone stumps, and anastomosis within one year. An acceleration of the wound healing has also been noted. Taking calcitonin mechanism of action and the clinical course of this case into consideration, it seems justified to use calcitonin in the treatment of gangrene of the foot in diabetes.
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PMID:[Calcitonin in treatment of diabetic foot syndrome]. 800 72

Calcitonin gene-related peptide (CGRP), a widespread neuropeptide with multiple actions, has substantial homology with amylin, a peptide implicated in insulin-resistant diabetes, and adrenomedullin, a recently discovered potent vasodilator. There is controversy over the existence of CGRP receptor subtypes, and whether independent receptors exist for amylin and adrenomedullin. In this article, the current status of CGRP receptor classification is reviewed by David Poyner, taking particular account of species differences, and evidence is presented supporting the existence of multiple receptors for CGRP, as well as independent binding sites for amylin.
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PMID:Pharmacology of receptors for calcitonin gene-related peptide and amylin. 857 16


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