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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty patients with diabetes mellitus and a reference group of forty-five healthy controls have been studied. Significantly increased serum concentrations of parathyroid hormone and calcitonin were found in the diabetics as well as increased levels of alkaline phosphatase activity and phosphate independent of the duration of the diabetic state. No difference was found in serum calcium levels when compared with the healthy controls. Since these results cannot be explained by diabetes nephropathy an altered balance between parathyroid hormone and calcitonin in diabetes mellitus is postulated.
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PMID:Parathyroid hormone and calcitonin in diabetes mellitus. 371 26

Antibodies to calcitonin appear in blood of rats with experimental alloxan diabetes. This phenomenon is observed only under high blood sugar. At the stage of latent diabetes, i.e. during alloxan administration to the body and low blood sugar no antibodies to calcitonin are detected. It is possible that appearance of autoantibodies to calcitonin is one of pathogenetic factors of hyperglycemia development in rats with alloxan diabetes.
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PMID:[Calcitonin antibodies in experimental diabetes mellitus]. 388 41

The effect of mild, non-insulin-dependent diabetes (NIDDM) on bone calcification and calcium (Ca) homeostasis was studied in growing rats (males and females). The diabetic state was characterized by mild insulin deficiency, plasma levels being 73% of controls, and mild hyperglycemia, with nonfasting plasma glucose levels of 1.5 times normal. There was no difference in plasma levels of Ca, phosphate (Pi), magnesium (Mg), alkaline phosphatase, immunoreactive parathyroid hormone (iPTH), calcitonin, 25-(OH)vitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2D), and 24,25-dihydroxyvitamin D (24,25[OH]2D) between the NIDDM rats and their controls of either sex. Metabolic Ca and Pi balance studies revealed that the experimental animals of both sexes were in positive Ca and Pi balance similar to that of their controls. Histologic studies of the kidney and intestinal slices from the experimental group were normal. Ca and Pi bone content calculated per gram bone ash of the femur, mandible, and second and fourth caudal vertebrae, and the organic content in the bones of the NIDDM animals showed no difference from their controls. Femur bone density and tibial epiphyseal growth plate width and morphology were similar histologically in the experimental and control rats. No decreased osteoid content in the tibial bone was found in the diabetic rats compared with controls. Physiologic sex differences, consisting of lower plasma Pi, higher plasma calcitonin levels, increased ratio of femur dry bone weight to total body weight, and increased percentage of mineralized and total bone volume at the tibial metaphysis seen in female compared with male control rats were also seen in the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Apr
PMID:Bone calcification and calcium homeostasis in rats with non-insulin-dependent diabetes induced by streptozocin. 397 85

A pancreatic somatostatinoma metastatized to the liver was detected in a 70-yr-old woman presenting with chronic diarrhea, steatorrhea, pancreatic insufficiency, diabetes mellitus, and achlorhydria. At immunocytochemistry, most tumor cells stored both somatostatin and calcitoninlike substances. Chromatography of acid extracts of the tumor on G50 Sephadex gave two distinct peaks coeluting with cyclic ovine somatostatin and human calcitonin, respectively, thus ruling out the hypothesis of a single cross-reacting molecule synthetized by the neoplastic cells. When the tumor was extracted at neutral pH, larger molecular forms of the above components were found, which accounted for less than 20% of the total immunoreactivity. Gel permeation of plasma showed that the circulating calcitonin- and somatostatinlike components consisted of three and four different forms, respectively, including components of molecular weights similar to those of the reference peptides. Inhibition curves and immunoadsorption experiments indicated that the large forms were immunologically similar, if not identical, to the corresponding standard preparations. The present case illustrates the occasional ability of neoplastic somatostatin cells of pancreas to synthetize simultaneously components immunologically related to somatostatin and calcitonin. These two inappropriate secretions could account for the symptoms displayed by this patient.
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PMID:Calcitonin-producing pancreatic somatostatinoma. 610 50

We report here 2 patients with somatostatin-secreting tumours and hypersomatostatinaemia. One subject, a 36 year old woman with diabetes, flushing, labile blood pressure and diarrhea, had elevated basal plasma levels of somatostatin-like immunoreactivity (SLIR) and calcitonin. Plasma SLIR increased further following tolbutamide administration. Plasma levels of prostaglandin E2 (PGE2) and pancreatic polypeptide (PP), normal in the basal state, showed exaggerated responses to pentagastrin and secretin, respectively. Immunocytochemistry of the tumour tissue revealed cells containing somatostatin-, calcitonin-, PGE2- and PP-like immunoreactivity. The other patient, a 52 year old male, had an SLIR-secreting tumour of the proximal duodenum and elevated basal and post-tolbutamide SLIR levels but no signs or symptoms suggestive of increased SLIR production. Tumour tissue revealed cells containing somatostatin- and calcitonin-like immunoreactivity. We conclude that patients with somatostatinomas do not always exhibit a predictable syndrome. Patients with these tumours may exhibit a range of clinical, biochemical and immunocytochemical features typical of endocrine tumours of mixed-cell origin, such that the dominant signs and symptoms associated with these neoplasms cannot readily be ascribed to overproduction of any single hormone.
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PMID:Somatostatinoma syndrome: does a clinical entity exist? 629 17

A 56-year-old woman with many unusual manifestations of von Hippel-Lindau syndrome is described. In addition to retinal hemangioblastomas, pheochromocytoma, renal cell carcinoma, and multiple organ cysts, she had a cerebellar astrocytoma, pancreatic exocrine insufficiency, diabetes mellitus, thyrotoxicosis, and a metastatic calcitonin-secreting islet cell carcinoma. This case report documents the first example of a metastatic islet cell tumor in a patient with von Hippel-Lindau disease. The possible relationship between this disorder, the other neurocutaneous syndromes, and the multiple endocrine neoplasia syndromes is discussed.
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PMID:Metastatic islet cell tumor in von Hippel-Lindau disease. 633 Nov 59

Calcium metabolism was studied in hemodialyzed patients with diabetes mellitus nephropathy (HD/DM) and in hemodialyzed nondiabetic patients with chronic glomerulonephritis (HD/non-DM). Incidence of bone changes visible in X-ray films, assessed by changes in the lamina dura and trabecular patterns of mandibulae, was less in HD/DM than in HD/non-DM patients. Serum c-terminal parathyroid hormone was significantly lower in HD/DM than that in HD/non-DM. Serum calcitonin was higher in HD/DM than that in HD/non-DM. The lower level of c-terminal parathyroid hormone would be a reason that bone changes were less in HD/DM than in HD/non-DM patients.
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PMID:Abnormal calcium metabolism in hemodialyzed patients with diabetic nephropathy. 647 29

Filtered proteins including insulin are absorbed in the proximal tubule by means of pinocytosis. The first step in this process is binding of the protein to brush border membrane. As it is not known whether absorption exhibits specificity, we set out to determine whether specific binding sites for insulin are present in brush border membranes. Rabbit-isolated brush border membranes were incubated with 125I-insulin and varying concentrations of cold insulin or other peptide hormones. Binding and degradation of 125I-insulin occurred in a time- and temperature-dependent manner. Native insulin competitively inhibited 125I-insulin binding, but calcitonin, arginine vasopressin, glucagon, and growth hormone (10(-6) M) were relatively ineffective. Nonspecific binding averaged one-third of the total radioactivity bound. Scatchard analysis of binding data revealed two classes of insulin receptors: high affinity, low capacity receptors and low affinity, high capacity receptors. Gel filtration analysis of 125I-insulin exposed to brush border membrane revealed the formation of low-molecular-weight products similar to that produced by intact kidneys. The degrading process exhibited some specificity, for cold insulin (10(-6) M) was more effective than calcitonin, vasopressin, glucagon, or growth hormone in inhibiting degradation (32% versus less than 13% inhibition; P less than 0.01). Whether this reflects inhibition of insulin specific binding before exposure to degradation or inhibition of specific enzymes is unclear. In summary, it appears that renal brush border membranes have a major insulin-specific receptor component that could potentially mediate tubular insulin absorption. In addition, there is a smaller nonspecific component that may also have the potential to mediate insulin absorption. Finally, it appears that brush border membranes have the ability to degrade insulin to low-molecular-weight products by a process that exhibits some specificity for insulin.
Diabetes 1982 Jul
PMID:Binding and degradation of insulin by isolated renal brush border membranes. 676 Dec

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

The characteristic hyperphagia of the genetically obese diabetic (C57Bl/Ks-db+/db+) mouse (db/db) is thought to be due to defect in the satiety circuitry with a secondary overproduction of a circulating satiety factor to which they are insensitive. Recent studies have suggested that calcitonin may be a potent hormonal mediator of the satiety reflex. In this study it was shown that db/db mice were eight fold more sensitive to calcitonin than their heterozygote littermate controls. Mice with streptozotocin-induced diabetes were ten-fold more sensitive to calcitonin than their littermate controls. These results show that diabetes increases the sensitivity to the satiety effects of calcitonin.
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PMID:The effect of calcitonin on food intake in diabetic mice. 707 91


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