Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. Plasma catecholamine and PP levels rose in both groups in response to hypoglycemia and the secretory response of ACTH was lower in the diabetic subjects (p < 0.01). GRP concentrations increased during hypoglycaemia (p < 0.01) while a reduction in AVP occurred at the start of hypoglycaemia (p < 0.001). The plasma AVP concentrations were higher in the diabetic group compared with those in the normal group (p < 0.05). The NPY concentrations were higher in the normal subjects (p < 0.05) but no change in the mean level occurred in either group during hypoglycaemia. No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. These observations support the view that regulatory peptides, if involved in glucose homeostasis, may rather have a modulatory effect than a direct action in restoring normoglycaemia.
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PMID:The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man. 128 60

An impaired pancreatic polypeptide response (PP) after hypoglycemia has been described in type I diabetic patients with overt autonomic neuropathy. Some authors have suggested that PP release might be useful as sensitive indicator of autonomic neuropathy. The meal test is safer and simpler than the insulin infusion test as PP stimulus. The aim of this study was to compare PP response to insulin infusion and protein meal test and to correlate these responses to the presence of measurable neuropathic disturbances. We thus studied 13 IDDM children and adolescents and 6 normal children. In diabetics the PP response to both tests was not different from that of the control subjects, but PP response to insulin infusion was inversely correlated to the duration of illness and was significantly lower in subjects with pathological heart rate response when compared to the control group. PP responses to the two stimuli were not correlated. We suggest that reduced PP response to hypoglycemia is an early sign of autonomic neuropathy as well as impairment of beat-to-beat variation when impaired PP response to meal test is still not evident.
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PMID:Pancreatic polypeptide secretion after insulin infusion and protein meal in juvenile type 1 diabetic subjects. 219 47

The effect of a new octapeptide analogue of somatostatin (SMS 201-995) on blood glucose and gut hormone levels was studied in 10 C-peptide-negative, insulin-dependent diabetic (IDDM) subjects. On separate days, either 50 or 100 micrograms SMS or placebo was s.c. injected simultaneously with an identical insulin dose 30 min before a mixed meal. Postprandial blood glucose decreased after 100 micrograms SMS s.c. within 30 min from 8.9 +/- 0.7 to 7.8 +/- 0.6 mmol/L (P less than 0.001) and remained at similar levels during 180 min. In contrast, postprandial blood glucose concentration increased after placebo from 9.9 +/- 0.8 to 13.8 +/- 0.9 mmol/L (SMS versus placebo P less than 0.001). Plasma glucagon decreased rapidly after SMS to the limit of detection (P less than 0.001) and remained lowered during 180 min; in contrast, glucagon levels increased after the meal during the placebo study (SMS versus placebo P less than 0.001). Plasma growth hormone concentrations were significantly lower after SMS than after placebo (P less than 0.05). SMS abolished completely the postprandial increase in plasma gastrin and pancreatic polypeptide (PP) concentrations. Plasma free fatty acid (FFA) and triglyceride concentrations decreased after SMS, reaching significantly lower levels than after placebo (P less than 0.05 and P less than 0.01), respectively). Plasma SMS concentration increased rapidly after s.c. administration of SMS; its appearance preceded that of plasma free insulin after s.c. insulin injection. Fifty micrograms SMS was similarly effective as 100 micrograms in decreasing blood glucose, triglycerides, glucagon, and gut hormone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced postprandial hyperglycemia after subcutaneous injection of a somatostatin-analogue (SMS 201-995) in insulin-dependent diabetes mellitus. 286 93

An insulin-producing cell line, Clone-16, of hamster origin, was characterized for islet hormone production and for reactivity with islet cell surface (ICSA) and islet cell cytoplasmic (ICA) antibodies in sera from children with newly diagnosed insulin-dependent (Type 1) diabetes mellitus (IDDM). The Clone-16 cells have a doubling time of about 50-60 hr. The cells produced 63 +/- 3 ng (mean +/- SD) immunoreactive insulin and 9.4 +/- 0.3 ng immunoreactive glucagon per day per 10(6) cells, while somatostatin (SRIF) and pancreatic polypeptide (PP) were undetectable. The reactivity with autoantibodies in IDDM sera was assessed by indirect immunofluorescence or 125I-protein A binding assay on intact cells to detect islet cell surface antibodies (ICSA) or on frozen sections of cell pellets to detect islet cell cytoplasmic antibodies (ICCA) by indirect immunofluorescence. Although the proportion of the ICSA-positive Clone-16 cells compared favorably with rat islet cells (r = 0.81; p less than 0.01), we found 5/10 IDDM sera to be positive on rat islet cells but 8/10 on the Clone-16 cells. There was also a good correlation in the 125I-protein A binding assay between mouse islet cells and Clone-16 cells (r = 0.91; p less than 0.01). Frozen sections of Clone-16 cells showed a cytoplasmic immunofluorescence in 8/10 of the IDDM sera and this reaction parallelled the results obtained in the standard indirect immunofluorescence assay with a frozen section of human blood group O pancreas. We conclude that the insulin- and glucagon-producing Clone-16 cells are a useful cell line for detecting islet cell autoantibodies.
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PMID:Detection of islet cell autoantibodies in newly diagnosed diabetic patients using insulin-producing Syrian hamster cells. 330 Nov 57

Both basal and postprandial pancreatic polypeptide (PP) concentrations were exaggerated twofold in lean NIDDM patients, whereas they were normal in lean IDDM and obese NIDDM patients who were hyperglycemic as a result of partial insulin withdrawal. Insulin infusion from an artificial endocrine pancreas, which resulted in fasting euglycemia and near-normoglycemia postprandially, had no effect on PP responses in any of the diabetic patients. No postprandial PP responses were observed in totally pancreatectomized (TPX) patients. Excessive basal and postprandial concentrations of PP in diabetes appear to be related to both leanness and residual beta cell function and, therefore, potential markers for lean NIDDM.
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PMID:Pancreatic polypeptide: a marker for lean non-insulin-dependent diabetes mellitus? 404 1

The application of immunofluorescence technique with anti-insulin, anti-glucagon, anti-somatostatin, and anti-pancreatic polypeptide (PP) antisera to sections of precisely sampled regions of the human pancreas allowed the quantitative evaluation of the total content of these four endocrine cell populations in 13 nondiabetics, in 2 insulin-dependent diabetics (IDDM), and in 2 non-insulin-dependent diabetic subjects (NIDDM) of various age and sex. In nondiabetic subjects, PP-cells appear sex-related. Male individuals have a significantly greater volume of PP-cells than female. In diabetic subjects, the only marked difference as compared with nondiabetics is the reduction of insulin cell volume in IDDM. Other small differences between individual endocrine cell volumes are detectable in both IDDM and NIDDM as compared with nondiabetics, but their significance is at present unclear. The qualitative changes of islet structure accompanying insulin cell reduction in IDDM were not considered in the present study.
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PMID:Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans. 613 Oct 2

Pancreases from insulin-dependent diabetics (IDDM), noninsulin-dependent diabetics (NIDDM), and nondiabetic subjects were analyzed by stereological and morphometrical methods in order to determine the weight of the lobe rich in pancreatic polypeptide (PP) cells in relation to the total weight of the pancreas and the volume density of PP cells in both parts of the gland, those rich and poor in PP cells. In control subjects, neither the relative weight of the lobe rich in PP cells, nor the volume density of PP cells varied significantly with aging. In IDDM and NIDDM, the volume density of PP cells was similar to that observed in control subjects. The total weight of the pancreas was markedly decreased in IDD because of an almost selective atrophy of the lobe poor in PP cells; the relative weight of the lobe rich in PP cells was thus much higher than that in control subjects. A less marked atrophy, restricted to the lobe poor in PP cells, was also observed in NIDDM. It is suggested that PP may exert a local trophic role which protects the lobe of the pancreas rich in PP cells from atrophy in diabetic patients. The results further show that the elevated levels of PP in the plasma of elderly or diabetic subjects cannot be ascribed to a hyperplasia of PP cells.
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PMID:The pancreatic polypeptide cells in the human pancreas: the effects of age and diabetes. 633 79

To test the possibility that insulitis might play an etiological role in the pathogenesis of insulin dependent diabetes, functions of 3 kinds of islet constituting cells (A, B and PP cells) were estimated by quantifying secretory responses of glucagon-, C-peptide-and pancreatic polypeptide-producing cells to hyperglycemia and hypoglycemia. In insulin dependent diabetes, all 3 hormonal responses were severely impaired to the same extent. On the other hand, 3 islet cell functions were uniformly but less severely impaired in insulin independent diabetics without a diabetic family history. These results suggest that A, B, and PP cells of islet of Langerhans are evenly destroyed in parallel fashion at least in insulin dependent diabetes and in some insulin independent diabetes, suggesting insulitis as a possible cause of these types of diabetes.
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PMID:Parallel dysfunctions of pancreatic A, B and PP cells in insulin dependent diabetes. 701 3

Disturbed hemodynamic reactions to insulin-induced hypoglycemia have been documented in diabetic patients and considered related to hyperinsulinemia and impairment of autonomic nervous functions. In the present study we investigated the effect on skin microcirculation of insulin-induced hypoglycemia obtained during moderate hyperinsulinemia, in 7 men with type 1 diabetes and in 8 healthy age- and sex-matched controls. The patients had all normal cardiovascular reflexes as assessed by respiratory sinus arrhythmia and Valsalva ratio. The skin microcirculation of the left fourth finger nailfold was investigated by laser Doppler fluxmetry, and the skin temperature within the same area was measured by a thermistor. Hypoglycemia was induced by a constant insulin infusion of Actrapid Human, 0.034 U kg-1 h-1 during 120 min. Plasma adrenaline, noradrenaline and pancreatic polypeptide increased significantly in both groups during hypoglycemia and the insulin levels never exceeded 50 mUl-1. A close to identical arterial hypoglycemia was obtained in the two groups 60 min after onset of insulin infusion. During hypoglycemia the control subjects revealed a significant decrease in laser Doppler flux (p < 0.025), while it was unchanged in the diabetic patients. Simultaneously, the skin temperature decreased (p < 0.05) in the controls, but was unchanged in the diabetic patients. The present study indicates that type 1 diabetic patients with normal cardiovascular reflexes have an abolished vasoconstrictor response in skin microcirculation of fingers during insulin-induced hypoglycemia, despite the fact that neurogenic and neuroglucopenic symptoms developed in these patients during hypoglycemia.
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PMID:Patients with type 1 diabetes lack vasoconstrictor response in skin microcirculation during insulin-induced hypoglycemia. 770 86

Children with IDDM have diminished glucagon responses to hypoglycemia. We evaluated possible mechanisms in 60 children and adolescents with IDDM (age 15.4 +/- 2.6 years, duration 7.8 +/- 3.5 years [mean +/- SD]) and without diabetic complications. These were: 1) suppression by hyperinsulinism, 2) autonomic neuropathy, 3) a pan-islet cell defect, and 4) a glucotoxic effect. Glucagon and pancreatic polypeptide responses to hypoglycemia (insulin bolus 0.15-0.75 U/kg) were studied after insulin withdrawal and 3 days of intensive insulin therapy. Responses to arginine and mixed meal were also studied. The control group consisted of children with non-growth hormone deficient short stature. IDDM children had lower glucagon responses to hypoglycemia than controls (p < 0.001), the response to arginine did not differ from controls, and was greater than the response to hypoglycemia (p < 0.001). Responses to hypoglycemia after insulin withdrawal and intensive therapy did not differ. Basal pancreatic polypeptide levels were lower in IDDM than in controls (p < 0.05) but responses to hypoglycemia did not differ between groups. Thus the diminished glucagon response to hypoglycemia reflects a defect in hypoglycemic recognition or response by the alpha cells.
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PMID:Abnormal alpha cell hypoglycemic recognition in children with insulin dependent diabetes mellitus (IDDM). 782 Feb 17


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