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)

The effects of an acute injection of synthetic salmon calcitonin (sCT) and human CT (hCT) and of long term (4-month) administration of sCT on serum glucose levels were investigated in eight patients with Paget's disease of bone. The results obtained demonstrate a small but statistically significant rise in serum glucose after a single sc injection of synthetic hCT. However, the serum glucose level was not increased after 4 months of daily administration of synthetic sCT to our pagetic patients. Our results also substantiate the clinical observation that long term administration of CT does not cause clinical diabetes or significantly change fasting blood glucose concentration. Our results are also consistent with the view that the effect of CT administration on glucose metabolism is related to the secondary hypocalcemia.
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PMID:Effect of acute and chronic administration of calcitonin on serum glucose in patients with Paget's disease of bone. 740 Mar

Islet amyloid polypeptide (IAPP) or amylin is a hormone candidate predominantly expressed in insulin cells. A role for IAPP in the regulation of glucose homeostasis and the development of non-insulin-dependent diabetes mellitus has been proposed. IAPP is structurally related to the sensory neuropeptide calcitonin gene-related peptide. In the present study, using in situ hybridization, immunocytochemistry, and immunochemistry, the expression of IAPP in sensory neurons in the rat was investigated. IAPP was expressed in a population of small- to medium-sized nerve cell bodies in dorsal root ganglia from all levels and in the jugular-nodose and trigeminal ganglion; IAPP-expressing nerve cell bodies constituted a subpopulation of those expressing calcitonin gene-related peptide. In addition, IAPP-like immunoreactivity occurred in nerve cell bodies storing substance P and pituitary adenylate cyclase-activating polypeptide. IAPP-immunoreactive nerve fibers were encountered in the dorsal horns of the spinal cord, and to a lesser extent in peripheral tissues receiving sensory innervation; IAPP-immunoreactive fibers constituted a subpopulation of those containing calcitonin gene-related peptide and/or substance P. The immunochemical determinations demonstrated a low level of IAPP-like immunoreactivity in the dorsal root ganglia and spinal cord, which chromatographically coeluted with authentic rat IAPP. We conclude that IAPP is expressed in sensory neurons, thus being a novel sensory neuropeptide candidate for which a physiological role remains to be identified.
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PMID:Islet amyloid polypeptide (amylin) is expressed in sensory neurons. 747 13

Somatostatinoma is one of the rarest tumours of the endocrine pancreas. Cardinal manifestations of a somatostatinoma include gallstones, mild diabetes mellitus, steatorrhoea, diarrhoea and dyspepsia. Like any other pancreatic islet cell carcinoma, a somatostatinoma may also produce several different hormones such as adrenocorticotropic hormone, calcitonin, vasoactive intestinal polypeptide, pancreatic polypeptide, gastrin, insulin, and glucagon. In many cases, the clinical picture is dominated by the effect of these other hormones. We present a patient with somatostatinoma in which an immunocytochemical study of the specimens from pancreas and liver showed a weak positive reaction for gastrin besides a strong positive reaction for somatostatin. Interestingly, this patient also showed the signs of carcinoid syndrome which was successfully treated with octreotide.
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PMID:Carcinoid syndrome due to a malignant somatostatinoma. 749 79

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

Small fiber sensory neuropathy is one of the most common complications of diabetes mellitus. Currently there is no adequate therapy to prevent this often debilitating problem. Nerve growth factor (NGF) is a protein that promotes the survival and integrity of a large percentage of sensory neurons including the small fiber pain transmitting neurons which are often prominently affected in diabetic neuropathy. We report here that exogenously administered NGF is capable of preventing the behavioral and biochemical manifestations of diabetic sensory neuropathy in a streptozocin induced rat model. NGF administration prevented the elevation of tailflick threshold (a measure of the rat's response to a thermal noxious stimulus) which occurred in streptozocin-induced diabetic rats. Further, it prevented the induced reduction in levels of the neuropeptides substance P and calcitonin gene related peptide measured from cervical dorsal root ganglia. Finally, NGF did not ameliorate the prolonged latency of the compound action potentials measured from the caudal nerve of the tail. In view of these results, a clinical trial of NGF in diabetic neuropathy has now commenced.
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PMID:Nerve growth factor administration protects against experimental diabetic sensory neuropathy. 751 29

Rats with streptozotocin-induced diabetes of 4 to 6 weeks duration showed a depletion of both substance P (P < 0.01) and calcitonin gene-related peptide (P < 0.01) in the sciatic nerve. Since expression of both peptides is sensitive to nerve growth factor (NGF) in vitro we examined the effect of treatment of diabetic rats with NGF, which significantly increased the levels of both peptides in treated diabetic animals (P < 0.01 for both). Treatment of non-diabetic rats with a similar NGF regime raised the mean peptide levels to a value similar to that seen in treated diabetic rats but the change was not statistically significant. In vehicle-treated diabetic rats the depletions of sciatic nerve neuropeptides were accompanied by a significant (P < 0.05) reduction in the level of CGRP mRNA in the 4th and 5th lumbar dorsal root ganglia, this was accompanied by an analogous reduction in the mRNA for gamma-preprotachykinin A (gamma-PPT), which did not attain statistical significance. Treatment of diabetic rats with NGF also prevented the deficits in the levels of CGRP and gamma-PPT mRNA in the lumbar dorsal root ganglia (P < 0.05). Treatment of other diabetic rats with the related neurotrophin, brain-derived neurotrophic factor (BDNF), had no effect on the levels of substance P and calcitonin gene-related peptide in the sciatic nerve.
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PMID:Expression of neuropeptides in experimental diabetes; effects of treatment with nerve growth factor or brain-derived neurotrophic factor. 751 41

Dorsal root ganglion neurons from streptozotocin (STZ)-induced diabetic, genetic diabetic and normal mice were cultured in serum-containing media with or without nerve growth factor (NGF). The immunocytochemical analysis carried out after 1 week in culture revealed that the ratios of neurons immunoreactive to calcitonin gene-related peptide (CGRP) in NGF-free medium in the STZ-diabetic mice (average 23.2%) were significantly lower than those in the normal mice (45.1%). The ratios of neurons immunoreactive to CGRP and substance P (SP) in the NGF-free medium were also lower in the genetic diabetic mice (23.6% and 21.8%) than those in the normal ones (40.7% and 34.2%). However, treatment with NGF restored these reduced immunoreactivities in the diabetic groups in a dose-dependent manner. These results show that NGF can be effective for the diabetes-induced depletion of CGRP and SP in sensory neurons, and suggest its possible role in the prevention and improvement of diabetic sensory neuropathy.
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PMID:Nerve growth factor (NGF) restores depletions of calcitonin gene-related peptide and substance P in sensory neurons from diabetic mice in vitro. 753 Jul 67

This study examined the expression of the sensory neuropeptides, calcitonin gene-related peptide (CGRP) and substance P (SP), in the lumbar 4 and 5 dorsal root ganglion (DRG) and spinal cord of spontaneously diabetic BB rats and non-diabetic controls using quantitative immunohistochemical analysis. In both animal groups immunoreactivities for CGRP and SP were widely distributed within the neurons of DRG and in nerve fibres of the dorsal spinal cord. Image analysis of each neuropeptide subpopulation in the DRG showed that in diabetic rats the cell diameter of immunostained CGRP neurons was significantly decreased compared with controls, while no difference could be found for SP-immunoreactive (IR) neurons. The decrease in the CGRP-IR cell diameter appeared to occur mainly in medium to large neurons (30-50 microns diameter; 2.2% controls, < 1% diabetes), this change being parallel to an increased frequency of small-size neurons (< 20 microns diameter) in diabetic rats (62% controls, 69% diabetes; P < 0.05). However, there was no statistical difference in the total number of cells immunostained for either CGRP or SP between control and diabetic rats. The ratio of CGRP or SP neurons compared to total cells in the ganglion was similar in control and diabetic groups. No difference could be observed for peptide immunoreactivity in the dorsal and ventral horns of either control or diabetic animals. The observed changes of perikaryal size in diabetic rats might relate to the reduced axonal calibre and conduction velocity observed in these animals, and indicate that subpopulations of sensory neurons are affected differently by diabetes.
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PMID:Changes in sensory neuropeptides in dorsal root ganglion and spinal cord of spontaneously diabetic BB rats. A quantitative immunohistochemical study. 753 45

Complications of diabetes include sensory and autonomic neuropathy. The aim of the present paper was to study the degree of sensory and autonomic neuropathy and correlate these findings with the distribution and density of neuropeptidergic nerve fibers in the skin of the forearm of diabetic patients and healthy controls. We investigated 30 diabetics (24 type 1 and 6 type 2) and compared them with 13 healthy controls. There were no differences between the groups with respect to density and distribution of nerve fibers displaying immunoreactivity to the pan-neuronal marker PGP 9.5 and sensory and parasympathetic neuropeptides (substance P, calcitonin gene-related peptide and vasoactive intestinal peptide). By contrast, nerve fibers containing neuropeptide Y, a marker of sympathetic neurons, were reduced in number in the diabetic patients. C-fiber function (measured as the axon-reflex-evoked flare response) became impaired with increasing age in all subjects. The diabetic patients, however, showed a reduced flare compared to age-matched healthy controls. The reduction was particularly prominent in the younger patients (20-50 years). There was a greater reduction of the flare in neuropathic patients than in non-neuropathic patients, but there was no correlation between the degree of functional impairment and the duration of the disease.
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PMID:Innervation of the skin of the forearm in diabetic patients: relation to nerve function. 753 56

ODU Plaque-susceptible rats (ODUS/Odu) exhibit markedly heavy plaque formation in the lower incisors and develop both periodontal pockets and gingivitis after being fed a commercially available powder diet. These rats have been established as an inbred strain. We have demonstrated that the ODUS/Odu are a very suitable experimental model for studying periodontitis. We already reported about the allelic distribution, changes of plaque formation and body weight, biochemical nature, toxic activity, vascular permeability factor and bradykinin inactivating factor of the plaque, histological and immunological studies, the pH in the periodontal pocket, amount of saliva, IgA in the saliva, salivary kallikrein, the relationship between sialic acid in the saliva and the serum, leukocyte functions (chemotaxis and superoxide anion) in ODUS/Odu, histamine, mast cell, free radicals, superoxide dismutase activities in gingiva and gingival nerve fibers with substance P or calcitonin gene-related peptide, and effect of diabetes. Streptozotocin-induced diabetic ODUS/Odu may be a useful tool for studying the pathological mechanisms in the development of periodontal tissue breakdown in diabetes. ODUS/Odu should help to further establish the utility of this strain as a model for experimental periodontal disease.
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PMID:[Experimental periodontitis in rats]. 762 82


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