Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study examines the endocrine function of duct-obliterated canine segmental autografts for periods up to 5 years posttransplant. Overall the response profile of autografted animals was subnormal. After intravenous glucose tolerance tests K-values in transplanted animals (2.8 +/- 0.9%/min) were significantly lower than normal (4.6 +/- 1.2% min, p less than 0.001). After oral glucose stimulation, blood glucose in the autografted dogs reached a mean peak of 10.6 +/- 2.8 mmol/L whereas in normal dogs the peak value was 6.0 +/- 1.0 mmol/L (p less than 0.002). The mean insulin response in autografted dogs showed lower insulin concentrations in the early stages of the test, whereas insulin secretion after glucagon stimulation was significantly reduced in autografted dogs. Intravenous glucose tolerance tests were analyzed by calculating K value or measuring a single blood glucose concentration 40 min after glucose injection. This value had a high correlation with the K value (r = 0.967). No progressive deterioration of graft function up to 5 years was found. Glycosylated hemoglobin levels were measured in autografted (646 +/- 59 pmol/mg) and normal dogs (620 +/- 85 pmol/mg) and no significant difference was found. In conclusion, duct-occluded segmental pancreatic autografts were shown to have a reduced functional capacity but there was no deterioration of function up to 5 years after duct-occlusion and grafting. The degree of metabolic control may be sufficient to prevent diabetic complications.
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PMID:Long-term canine duct-occluded segmental pancreatic autografts: endocrine function. 306 74

Glycemic control and glucose metabolism were examined in 5 patients with insulin-dependent diabetes mellitus (IDDM) and 8 insulin-treated non-insulin-dependent diabetes mellitus (NIDDM) patients before and after 2 mo of therapy with glyburide (20 mg/day). Glycemic control was assessed by daily insulin requirement, 24-h plasma glucose profile, glucosuria, and glycosylated hemoglobin. Insulin secretion was evaluated by glucagon stimulation of C-peptide secretion, and insulin sensitivity was determined by a two-step euglycemic insulin clamp (1 and 10 mU X kg-1. X min-1) performed with indirect calorimetry and [3-3H]glucose. In the IDDM patients, the addition of glyburide produced no change in daily insulin dose (54 +/- 8 vs. 53 +/- 7 U/day), mean 24-h glucose level (177 +/- 20 vs. 174 +/- 29 mg/dl), glucosuria (20 +/- 6 vs. 35 +/- 12 g/day) or glycosylated hemoglobin (10.1 +/- 1.0 vs. 9.5 +/- 0.7%). Furthermore, there was no improvement in basal hepatic glucose production (2.1 +/- 0.2 vs. 2.4 +/- 0.1 mg X kg-1 X min-1), suppression of hepatic glucose production by low- and high-dose insulin infusion, or in any measure of total, oxidative, or nonoxidative glucose metabolism in the basal state or during insulin infusion. C-peptide levels were undetectable (less than 0.01 pmol/ml) in the basal state and after glucagon infusion and remained undetectable after glyburide therapy. In contrast to the IDDM patients, the insulin-treated NIDDM subjects exhibited significant reductions in daily insulin requirement (72 +/- 6 vs. 58 +/- 9 U/day), mean 24-h plasma glucose concentration (153 +/- 10 vs. 131 +/- 5 mg/dl), glucosuria (14 +/- 5 vs. 4 +/- 1 g/day), and glycosylated hemoglobin (10.3 +/- 0.7 vs. 8.0 +/- 0.4%) after glyburide treatment (all P less than or equal to .05). However, there was no change in basal hepatic glucose production (1.7 +/- 0.1 vs. 1.7 +/- 0.1 mg X kg-1 X min-1), suppression of hepatic glucose production by insulin, or insulin sensitivity during the two-step insulin-clamp study. Both basal (0.14 +/- 0.05 vs. 0.32 +/- 0.05 pmol/ml, P less than .05) and glucagon-stimulated (0.24 +/- 0.07 vs. 0.44 +/- 0.09 pmol/ml) C-peptide levels rose after 2 mo of glyburide therapy and both were correlated with the decrease in insulin requirement (basal: r = .65, P = .08; glucagon stimulated: r = .93, P less than .001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of glyburide on glycemic control, insulin requirement, and glucose metabolism in insulin-treated diabetic patients. 310 Mar 65

To improve criteria for entry into future trials of immunosuppression, we enrolled 40 children with recent-onset Type I insulin-dependent diabetes in a pilot trial of cyclosporine. Twenty-seven patients were able to discontinue insulin therapy 48 +/- 5 days after the start of immunosuppression. At four months, their fasting and postprandial blood glucose concentrations averaged 110 and 160 mg per deciliter (6.1 and 8.9 mmol per liter) with a mean hemoglobin A1c level of 6.15 percent. Seventy-five percent of these patients with early remission still did not need insulin at 12 months, and their glycemic control was similar to that at 4 months. The major differences between the 27 patients with remission and the 13 without remission were the duration of symptoms before diagnosis (26.8 vs. 48.0 days, P less than 0.01), the degree of weight loss (3.2 vs. 10 percent of body weight, P less than 0.001), the initial hemoglobin A1c level (10.7 vs. 13.2 percent, P less than 0.001), and the frequency of ketoacidosis (11 vs. 61.5 percent, P less than 0.001). The lesser degree of weight loss was the strongest independent predictor of remission. The response of C-peptide to intravenous glucagon (0.50 vs. 0.17 pmol per milliliter, P less than 0.05) was also an independent predictor. No differences were observed between the two groups of patients in age, sex, HLA phenotype, autoantibodies to insulin or islet-cell antigens, or doses or trough levels of cyclosporine. Only minimal manifestations of toxicity were detected over the period of observation. We conclude that early treatment with cyclosporine in children with recent-onset Type I diabetes can induce remission from insulin dependence, with half the patients not requiring insulin after a full year.
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PMID:Factors associated with early remission of type I diabetes in children treated with cyclosporine. 312 34

The counterregulatory hormone responses of cortisol, growth hormone, glucagon, epinephrine, norepinephrine, and dopamine to a fixed hypoglycemic stimulus (50 mg/dl for 1 h) were studied in five type I (insulin-dependent) diabetic subjects during conventional insulin therapy (CT), after 3 mo of continuous subcutaneous insulin infusion (SC), and after 3 mo of continuous intravenous insulin infusion (IV). During the two infusion periods, the overall mean levels of preprandial blood glucose (116 +/- 6 SC vs. 114 +/- 5 mg/dl IV) and glycosylated hemoglobin (6.1 +/- 2 SC vs. 5.9 +/- 2% IV) were virtually identical, but there were more hypoglycemic episodes and greater variability of preprandial blood glucose levels during SC than with IV. During the last 30 min of the hypoglycemic clamps, the mean levels of epinephrine and cortisol were significantly lower after 3 mo of SC (epinephrine, 268 +/- 80 pg/ml; cortisol, 14 +/- 1 microgram/dl) than with both CT (epinephrine 485 +/- 80 pg/ml; cortisol, 20 +/- 2 micrograms/dl) and IV (epinephrine, 443 +/- 62 pg/ml; cortisol, 19 +/- 2 micrograms/dl)(P less than .05). The mean growth hormone level was significantly (P less than .05) lower after SC (37 +/- 9 ng/ml) than after IV (79 +/- 12 ng/ml), but it did not reach statistical significance compared with CT (66 +/- 12 ng/ml). The mean glucagon, dopamine, and norepinephrine levels during the same period of hypoglycemia were not different when all treatment regimens were compared. We conclude that intensified insulin therapy with SC leads to significant blunting of the counterregulatory hormone response to hypoglycemia, whereas IV does not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Counterregulatory hormone responses preserved after long-term intravenous insulin infusion compared to continuous subcutaneous insulin infusion. 328 43

Changes in blood glucose, glucagon and insulin as well as changes in insulin binding by specific receptors on blood erythrocytes, were studied in 45 rats on various days of adaptation to high altitude. By the 14th day the levels of blood insulin and glucagon were steadily decreasing, whereas glucose homeostasis remained on the same level. Insulin binding by receptors on erythrocytes increased on the 3rd and particularly on the 14th day. The importance of the said reaction is discussed in connection with its compensatory nature in maintaining increased glycolysis in erythrocytes and 2,3-DFG levels in them which in its turn leads to changes in hemoglobin affinity to oxygen and correction of tissue hypoxia.
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PMID:[Hormonal function of the insular apparatus and erythrocyte insulin-binding capacity during adaptation of the rat to high altitude]. 330 19

Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .01), and glycosylated hemoglobin and fasting level of glucose were lower (P less than .01 to .05) in the 31 patients with pancreatogenic diabetes than than in 35 otherwise comparable patients with type I (insulin-dependent) diabetes, yet daily insulin dose was similar in the two groups. Glucagon stimulated C-peptide was inversely correlated to glycosylated hemoglobin in insulin-dependent patients with pancreatogenic diabetes and in type I diabetes. Since body mass indices were identical in the two groups, better glucoregulation was not due to reduced food intake or malabsorption in pancreatogenic diabetes. Rather residual B cell function and/or different secretion of other pancreatic hormones in pancreatogenic diabetes may account for different metabolic control in type I IDDM compared with insulin-dependent pancreatogenic diabetes.
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PMID:Metabolic control and B cell function in patients with insulin-dependent diabetes mellitus secondary to chronic pancreatitis. 330 47

Production of and response to interleukin 2 (IL-2) were studied using peripheral blood mononuclear cells (PBMC) from 23 patients with type 1 diabetes. When compared to PBMC from 18 control subjects, mean PHA-stimulated IL-2 synthesis in the diabetic group was found unimpaired (1.2 +/- 0.1 vs 1.5 +/- 0.2 U/ml). However, 3 subgroups could be distinguished with regard to IL-2 synthesis: IL-2 production was significantly increased in 5 patients and decreased in 2 patients, while the remaining 16 diabetics produced normal levels of IL-2. The diabetic group displayed a curve of PBMC proliferation in response to a range of recombinant IL-2 which was not significantly altered. However, an abnormally high blastogenic response was detected in 5 patients, correlating to an increased percentage of Ia-bearing T lymphocytes, while a markedly low response was seen in 2 other patients. These alterations of the IL-2 system could be related duration of diabetes. Indeed, high synthesis of IL-2 was more frequent in patients with long-standing disease than in recent onset diabetics: 44% and 7%, respectively. Conversely, increased response to IL-2 was found more often in the latter group than in the former (28% vs 11%) while decreased sensitivity was seen only in the latter group (14%). No correlations were found between these results and basal or glucagon-stimulated C peptide levels, percent of glycosylated hemoglobin, presence of autoantibodies, lymphocyte subsets, or HLA typing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Production of and response to interleukin 2 by blood mononuclear cells from some type 1 diabetic patients. 349 40

One hundred fifty-four selected patients with nonketotic diabetes diagnosed between the ages of 35 and 75 yr and treated with diet or oral hypoglycemic agents for at least 1 yr were investigated for parameters of glycemic control (weight loss, blood glucose, and glycosylated hemoglobin), islet cell function (fasting and glucagon-stimulated C-peptide responses), and immunologic markers of insulitis (total ICA and CF-ICA) or autoimmunity (thyroid and gastric antibodies). These parameters were all repeated in 9 of 22 ICA-positive patients after a 2-yr follow-up and correlated with secondary drug failure. The antibody tests were also done on 51 nondiabetic controls matched for age and body weight. The 22 (14%) diabetic subjects having positive islet cell antibodies (ICA) included more women than men with a shorter duration of symptoms, lower body weight, more associated thyroid autoimmunity, and a tendency to have more type I diabetes in their families, although glycemic control, age at onset, and family history of type II diabetes were the same as in the 132 ICA-negative cases. Patients with ICA had lower initial C-peptide levels and showed little rise after glucagon stimulation. Beta cell function deteriorated significantly during the 2-yr follow-up in 9 of 22 positive patients and more ICA-positive patients required insulin. It is suggested that these latent type I diabetic patients are characterized by persistent ICA, progressive loss of beta cells, and a high frequency of thyrogastric autoimmunity. The determination of ICA may be of clinical value in the diagnosis and treatment of nonketotic diabetes with onset in later life.
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PMID:Islet cell antibodies identify latent type I diabetes in patients aged 35-75 years at diagnosis. 351 Sep 30

Six gastrointestinal hormones were measured in the plasma of six healthy controls and long-term changes were evaluated in six patients 2-20 years after upper gastrointestinal surgery. In a metabolic unit study we determined fasting hormonal levels, the time to peak hormonal response, and a 135-minute hormonal response to the meal. Test meals were isocaloric, 500 kcal, and isonitrogenous, consisting either of natural breakfast components or of complete liquid diets with intact protein (Ensure) or hydrolyzed protein (Vital). Postsurgical subjects were in good health and had no postcibal complaints. Nevertheless, their hemoglobin and serum albumin were significantly lower than in controls. Postsurgical subjects had higher fasting gastrin (121.3 +/- 11.6 vs 65.4 +/- 6.6 pg/ml, P less than .01) and motilin (148.7 +/- 32.9 vs 70.4 +/- 13.1 pg/ml, P less than .05) than controls. In postsurgical patients the peak gastrin and pancreatic glucagon responses to meals were obtained in significantly shorter time. Their total response to motilin and secretin to meals was significantly lower than in controls. Fasting glucose and the meal-induced responses of insulin and vasoactive intestinal polypeptide were not different from controls. The nature of dietary protein did not significantly affect hormonal responses to feeding. We conclude that gastrointestinal hormonal changes persist many years after surgery. These changes are probably related to faster transit of meals with a generally weaker total hormonal response to feeding. Although these differences from normal may be nutritionally well compensated, they may become important in periods of metabolic stress.
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PMID:Hormonal responses to complete or hydrolyzed protein diets in patients after upper gastrointestinal surgery. 353 46

We evaluated the serum glucose/insulin/C-peptide dynamics and C-peptide/insulin molar ratios during sequential standard meal and intravenous (IV) glucagon testing for 240 minutes in eight genetically predisposed but nondiabetic female offsprings of type II diabetic patients and seven weight-matched, normal female controls. Glucose turnover rates and metabolic clearance rates of glucose (MCRG) were also determined isotopically by the D-[3-3H]glucose infusion technique. All the subjects had normal fasting serum glucose and glycosylated hemoglobin (HbA1) values. After meal ingestion, mean serum glucose concentrations were not different except for 120 to 180 minute values, which were significantly higher in the offsprings v controls. After intravenous glucagon infusion, percent maximum increments of glucose were no different. Mean basal immunoreactive insulin (IRI) levels were significantly (P less than 0.02) higher in the nondiabetic offsprings v controls. Following meal ingestion, mean IRI rose to a peak at 40 minutes in both groups, but values were significantly (P less than 0.001) higher in the offsprings v controls. After glucagon administration, the percent maximum increment was significantly (P less than 0.05) lower in the offsprings v controls. Despite exaggerated IRI levels in the offsprings, the mean fasting and stimulated C-peptide levels were identical in both groups throughout the study period. Basal and stimulated C-peptide/IRI molar ratios were quantitatively lower but qualitatively no different in the nondiabetic offsprings v controls throughout the study period. Mean basal hepatic glucose output (HGO) was higher but not statistically different in the offsprings compared with the controls (2.10 +/- 0.28 v 1.65 +/- 0.15 mg/kg X min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered C-peptide/insulin molar ratios and glucose turnover rates after stimulation in nondiabetic offsprings of type II diabetic patients. 354 13


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