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 islet amyloid polypeptide (IAPP) was originally identified by chemical analysis of the amyloid component in a human pancreatic islet cell tumor. It consists of 37 amino acids and displays about 50% homology with the neuropeptide calcitonin gene-related peptide (CGRP). In the pancreatic islets the IAPP is confined to the beta-cells, co-stored with insulin in the secretory granules and apparently co-secreted with insulin on glucose stimulation. In beta-cell depletion states such as streptozotocin diabetes in animals and in human type I diabetes mellitus both the IAPP and the insulin levels display reduction or are even absent. Within the mature IAPP molecule the amino acid sequence 23-29 shows considerable amino acid heterogenicity among various mammalian species. The amino acid composition of human IAPP in this specific region promotes the development of pancreatic islet amyloidosis, a phenomenon related to the ability to develop type II diabetes in that particular species. However, as type II diabetes is an inherited disease affecting a subpopulation of humans, not only the gene coding mature IAPP, but also one or several other hereditary factors of unknown origin are needed for the disease to develop. We have established a radioimmunoassay for plasma measurements of IAPP. During screening investigations of a large material of endocrine tumors we found a patient with extremely elevated plasma levels of IAPP, about 20,000 pmol/l. Immunohistochemical investigations confirmed the IAPP content and also revealed amyloid deposits. While performing an oral glucose tolerance test insulin levels remained unchanged whereas there was an increase in the glucose and IAPP levels. It is thus concluded that IAPP can be used as a tumor marker in pancreatic islet cell tumors and that high plasma levels of IAPP can inhibit glucose stimulated insulin secretion.
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PMID:Islet amyloid polypeptide (IAPP). A short review. 185 2

Calcium- and phospholipid-dependent protein kinase (protein kinase C; PKC) may be an important mediator in transduction of some of the cellular actions of insulin. We studied PKC activity in freshly isolated circulating mononuclear cells obtained from healthy subjects and patients with non-insulin-dependent (type II) diabetes mellitus (NIDDM). The kinase activity was measured using a specific nonapeptide substrate, Ala-Ala-Ala-Ser-Phe-Lys-Ala-Lys-Lys-amide. There was negligible calcium- and phospholipid-independent kinase activity in cytosolic and particulate fractions of cells from both control and diabetic subjects. Total (cytosolic and particulate) PKC activity of mononuclear cells from poorly controlled diabetic patients was significantly reduced compared with controls; this reduction was mainly due to a decrease in the cytosolic kinase activity. Tumor-promoting phorbol ester (TPA, 0.1 mumol/L) induced translocation of PKC activity in control cells; in contrast, this subcellular redistribution was not observed in cells from a majority of poorly controlled diabetic subjects. Increased calcium influx into the cells caused by the calcium ionophore A23187-triggered translocation of PKC activity in control cells, while it was ineffective in cells from poorly controlled diabetic patients. Cells from well-controlled diabetic patients demonstrated TPA-induced translocation of the PKC activity approaching that of control cells. The total PKC activity in cells from patients with good glycemic control was normal. Impaired activation of PKC is thus associated with the insulin resistance found in patients with poorly controlled NIDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired translocation of protein kinase C activity in human non-insulin-dependent diabetes mellitus. 186 31

Mice homozygous for the mutation "severe combined immune deficiency" (C.B17-scid/scid) lack functional T and B lymphocytes and readily accept tumor xenografts. Partial lymphohemopoietic scid/human and mouse/rat chimeras have been described, but complete chimerization with thymic engraftment and generation of donor-origin thymocytes has not been achieved. We now report that low-dose irradiation permits the engraftment of BB rat fetal liver stem cells in scid recipients. We observed that BB rat fetal liver cells injected into irradiated scid mice establish a rat hemopoietic system in the scid mouse bone marrow and populate the scid mouse thymus. These stem cells generated rat-origin thymocytes that migrated to the scid mouse spleen, a peripheral lymphoid organ. Finally, we found that xenogeneic chimeras created using fetal liver cells from the abnormal (lymphopenic, diabetes prone) subline of BB rats recapitulated both the quantitative and phenotypic abnormalities of the donor rat. Xenogeneic lymphohemopoietic chimeras established in scid mice may provide a powerful new tool in the study of immune system development and autoimmunity.
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PMID:Recapitulation of normal and abnormal BB rat immune system development in scid mouse/rat lymphohemopoietic chimeras. 186 81

We evaluated the hospital records of 412 patients with isolated or combined ocular nerve palsies in a retrospective study. Palsies of the oculomotor nerve (n = 172) and of the abducens nerve (n = 165) were more frequent than those of the trochlear nerve (n = 25). Combined ocular nerve palsies (n = 50) were generally combinations of the 3rd and 6th cranial nerves (n = 21) or pareses of all three ocular nerves (n = 17). 165 ocular nerve palsies were due to vascular causes: in 135 of these cases diabetes mellitus and hypertension were present. The oculomotor nerve was most frequently affected; in 63% there was no involvement of the pupil. In inflammatory disease and brain tumor the abducens nerve was most frequently affected, with aneurysm of the oculomotor nerve. The origin of ophthalmoplegia was unclear in 73 patients. Ocular nerve paralysis was most common with tumors, aneurysm, and vascular processes and in 206 cases was only partial. Pain was associated with tumor, trauma and aneurysm. In trochlear nerve palsies concomitant pain was much less frequent than in palsies of the other two ocular nerves. The clinical course was followed for 3 weeks in 352 patients; in 191 patients there was a complete regression of the pareses and in 59 only a partial recovery. The most favorable prognosis was with inflammatory and vascular lesions; in the latter the outcome was improved by the administration of non-steroidal anti-inflammatory drugs.
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PMID:Isolated and combined pareses of cranial nerves III, IV and VI. A retrospective study of 412 patients. 186 22

Examined were 27 patients with pancreatic cancer and concomitant diabetes mellitus. It was established that in women, the likelihood of pancreatic cancer development increases with the age. Obesity and cholelithiasis are also the risk factors for development of cancer of the given location. In pancreatic cancer and diabetes mellitus lasting more than 2 years which is an independent disease with a tumor developed against its background, the mutual aggravation syndrome occurs: a severe course of diabetes and increased growth of a neoplasm.
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PMID:[The mutual aggravation syndrome in pancreatic cancer and diabetes mellitus]. 187 8

Hip disarticulation, especially in patients with peripheral vascular disease, has been associated with high morbidity and mortality rates. This report describes patient characteristics that influence the clinical outcome of hip disarticulation. The medical records of all patients undergoing hip disarticulation from 1966 to 1989 were reviewed for surgical indication, perioperative wound complications, and postoperative deaths. Fifty-three patients underwent hip disarticulation for limb ischemia (10), infection (12), infection and ischemia (14), or tumor (17). The overall incidence of wound complications was 60%, and no significant differences were found among the groups. Prior above-knee amputation and urgent/emergent operations were significantly associated with increased wound complications (p less than 0.05). The overall mortality rate was 21%, ranging from 0% (tumor) to 50% (ischemia) and differed significantly among the groups (p less than 0.02). Mortality was significantly associated with urgent/emergent operations (p less than 0.01). Age, diabetes mellitus, and previous inflow procedures did not influence mortality rates. The presence of limb ischemia influenced mortality rates to a greater extent than did infection, and a history of cardiac disease was statistically predictive of death. Wound complications frequently accompanied hip disarticulation, regardless of operative indication, and were significantly increased by urgent/emergent operations and prior above-knee amputation. Hip disarticulation can be performed with low mortality rates in selected patients. Both limb ischemia and infection substantially increase operative mortality rates.
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PMID:Hip disarticulation: factors affecting outcome. 188 Aug 49

We hypothesized that differential housing, shown to influence emotionality and health in infectious and neoplastic disease, would influence onset/incidence of diabetes in an autoimmune animal model of insulin-dependent diabetes mellitus (IDDM). Non-obese diabetic mice were assigned to same-sex groups of one, five, or eight animals/cage, counterbalanced across shelf level by sex and group. During weekly urine glucose testing, presence of behaviors indicating emotional arousal was recorded. Sex, group, and shelf level affected emotionality: males, animals housed alone, and those on the top of the rack exhibited higher emotionality. Emotionality and shelf level predicted IDDM in females only. Delayed onset of IDDM was associated with high emotionality and with being housed on the top of the rack. Group size had no significant effect on IDDM. Emotionality may be a mediating factor in animals genetically predisposed to develop IDDM. This variable and cage shelf level should be incorporated into the design of studies in which IDDM is the outcome.
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PMID:Group size, cage shelf level, and emotionality in non-obese diabetic mice: impact on onset and incidence of IDDM. 188 12

CA 19-9 is a monoclonal antibody-defined tumor marker expressed by exocrine pancreas. It has been shown that exocrine atrophy was associated with deficiency. Hyperamylasemia has been described during ketoacidosis. Our study aimed at investigating the relationships between CA 19-9 and metabolic control of diabetes. Study was performed on 51 adult consecutive diabetic patients (21 type 1 and 30 type 2), with ketoacidosis or hyperosmolarity (group A, n = 15), poor glycaemic control (group B, n = 19), or good control (group C, n = 17). Serum CA 19-9 and metabolic parameters were evaluated on day 1 and day 30. Analysis of variance showed a very significant global difference between groups for CA 19-9 (p less than 0.0001); group A (66.1 +/- 11.4 u/ml) significantly differed from group B (36.4 +/- 4 u/ml) (p less than 0.01) and group C (22.4 +/- 2.8 u/ml) (p less than 0.001). Simple regression showed a significant correlation between CA 19-9 and fasting blood glucose (r = 0.6, p less than 0.001), plasma creatinine level (r = 0.37, p = 0.01), bicarbonate (r = 0.47, p = 0.001) and HbA 1c (r = 0.33, p = 0.032). The Ca 19-9 decrease on day 30 paralleled the improvement of glycaemic control. We conclude that CA 19-9 in diabetic patients is raised in acute metabolic situations and correlated very well with blood glucose concentration. A careful interpretation of this tumor marker assay is required when screening for pancreatic carcinoma among diabetic patients. CA 19-9 could be a useful and sensitive marker for the severity of exocrine damage and functional cellular disorders following metabolic disturbances in diabetes.
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PMID:Influence of metabolic disturbances of diabetes mellitus on serum CA 19-9 tumor marker. 190 32

Diabetes mellitus is associated with high levels of adenosine 3',5'-cyclic monophosphate in tissue and plasma. Diabetes inhibits and insulin stimulates and restores low Km adenosine 3',5'-cyclic monophosphate phosphodiesterase activity. We recently reported that phorbol ester, a tumor promoting agent known to act through protein kinase C also stimulates phosphodiesterase. Here, we address the issue of whether or not the activation of phosphodiesterase by insulin and phorbol ester is different in streptozotocin diabetic adipose tissue. Rat adipose tissue was incubated with insulin, phorbol ester or other known components or effectors of the protein kinase C pathway, i.e. 1,2 dioleoyl-glycerol, 1- oleoyl, 2- acetylglycerol, Ca(++)-Ionophore A 23187, and nifedipine. After incubation, preparation and assay of adenosine 3',5'-cyclic monophosphate phosphodiesterase was made. As in previous data streptozotocin-diabetes inhibits basal phosphodiesterase by about 50% (P less than .02); insulin and phorbol ester each stimulate phosphodiesterase, in streptozotocin-diabetes less than normal (P less than .025); nifedipine inhibits phorbol stimulated phosphodiesterase in streptozotocin-diabetes but not normal (P less than .001); and nifedipine inhibits insulin stimulated phosphodiesterase in normal (84%) and diabetic (97%) (P less than .005). In normal and diabetic tissue, diacyl glycerol and oleoyl-acyl glycerol stimulate phosphodiesterase, are augmented by ionophore and inhibited by nifedipine. In addition 32P incorporation studies and measurements of tyrosine kinase activity are presented which support these differences between normal and diabetic. In summary then, these data suggest common pathways of activation for low Km adenosine 3',5'-cyclic monophosphate phosphodiesterase by insulin and phorbol ester; imply a relationship between two second messenger systems, phosphoinositides and adenosine 3',5'-cyclic monophosphate; and demonstrate a difference in activation of phosphodiesterase between normal and diabetic adipose tissue.
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PMID:Activation of cyclic AMP phosphodiesterase by phorbol and protein kinase C pathway: differences in normal and diabetic tissue. 196 4

A 56-year-old man underwent distal pancreatectomy, splenectomy, and partial resection of the splenic flexure of the colon because of tumor in the tail of pancreas and the splenic hilus. The patient presented with symptoms of general malaise, anorexia, weight loss, mild diarrhea, and borderline diabetes mellitus, although there was no cholelithiasis. The diagnosis remained unclear until immunohistochemical studies of the resected specimen revealed somatostatin and synaptophysin, suggesting a somatostatinoma. Twenty-three reported cases of pancreatic somatostatinoma are reviewed and their clinical features discussed. The role of immunohistochemical studies in the diagnosis of somatostatinoma is described.
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PMID:Pancreatic somatostatinoma: a case report and review of the literature. 196 77


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