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)

Maximal dynamic exercise results in a postexercise hyperglycemia in healthy young subjects. We investigated the influence of maximal exercise on glucoregulation in non-insulin-dependent diabetic subjects (NIDDM). Seven NIDDM and seven healthy control males bicycled 7 min at 60% of their maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. In both groups, glucose production (Ra) increased more with exercise than did glucose uptake (Rd) and, accordingly, plasma glucose increased. However, in NIDDM subjects the increase in Ra was hastened and Rd inhibited compared with controls, so the increase in glucose occurred earlier and was greater [147 +/- 21 to 169 +/- 19 (30 min postexercise) vs. 90 +/- 4 to 100 +/- 5 (SE) mg/dl (10 min postexercise), P less than 0.05]. Glucose levels remained elevated for greater than 60 min postexercise in both groups. Glucose clearance increased during exercise but decreased postexercise to or below (NIDDM, P less than 0.05) basal levels, despite increased insulin levels (P less than 0.05). Plasma epinephrine and glucagon responses to exercise were higher in NIDDM than in control subjects (P less than 0.05). By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. It is concluded that, because of exaggerated counter-regulatory hormonal responses, maximal dynamic exercise results in a 60-min period of postexercise hyperglycemia and hyperinsulinemia in NIDDM. However, this event is followed by a period of increased insulin effect on Rd that is present 24 h after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes. 219 7

We measured C-peptide after glucagon and breakfast tests to compare the effectiveness of both tests in evaluating residual beta cell function in normal and diabetic subjects. A significantly higher C-peptide response was elicited after standard breakfast in patients with insulin-dependent diabetes mellitus of less than two years' evolution, ranging from 0.12 +/- 0.07 to 0.83 +/- 0.18 ng/ml (P less than 0.05). In nonobese noninsulin-dependent diabetes mellitus the response ranged from 0.86 +/- 0.02 to 1.89 +/- 0.48 ng/ml (P less than 0.0025); in obese NIDDM from 1.02 +/- 0.37 to 1.55 +/- 0.46 ng/ml (P less than 0.05), and in normal subjects from 0.77 +/- 0.23 to 2.11 +/- 1.22 ng/ml (P less than 0.0025). We conclude that the standard breakfast test is a useful and practical approach to the study of residual beta cell function.
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PMID:Standard breakfast test: an alternative to glucagon testing for C-peptide reserve? 219 64

Ninety-eight patients with diabetes mellitus (52 women and 46 men) underwent a glucagon stimulated C-peptide test. Treatment was instigated on the basis of classical criteria, independent of the test results, and remained unchanged during a 2-yr test period. The type of treatment and metabolic control were then related to the test results. Fasting C-peptide concentrations do not discriminate between insulin dependent and non-insulin dependent diabetes mellitus. C-peptide concentrations 10 min after intravenous injection of 1 mg of glucagon, however, correctly classified the patients. With the help of this test, the correct model of treatment for patients with diabetes mellitus can be chosen.
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PMID:The glucagon-stimulated C-peptide test: an aid in classification of patients with diabetes mellitus. 235 96

Knowledge of the metabolic changes that occur in insulin-resistant type 2 diabetes is relatively lacking compared to insulin-deficient type 1 diabetes. This paper summarizes the importance of the C57BL/KsJ-db/db mouse as a model of type 2 diabetes, and illustrates the effects that insulin-deficient and insulin-resistant states have on hepatic glycogen metabolism. A longitudinal study of db/db mice of ages 2-15 weeks revealed that significant changes in certain parameters of hepatic glycogen metabolism occur during this period. The liver glycogen levels were similar between diabetic and control mice. However, glycogen particles from db/db mice were on average smaller in mass and had shorter exterior and interior chain lengths. Total phosphorylase and phosphorylase a activities were elevated in the genetically diabetic mice. This was primarily due to an increase in the amount of enzymic protein apparently the result of a decreased rate of degradation. It was not possible to find a consistent alteration in glycogen activity in the db/db mice. Glycogen synthase and phosphorylase from diabetic liver revealed some changes in kinetic properties in the form of a decrease in Vmax and altered sensitivity to inhibitors like ATP. The altered glycogen structure in db/db mice may have contributed to changes in the activities and properties of glycogen synthase and phosphorylase. The exact role played by hormones (insulin and glucagon) in these changes is not clear but further studies should reveal their contributions. The db/db mouse provides a good model for type 2 diabetes and for fluctuating insulin and glucagon ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatic glycogen metabolism in the db/db mouse. 240 41

We have proposed that chronic hyperglycemia causes the abnormal glucose influence on arginine-stimulated insulin secretion in the neonatal streptozocin (STZ) rat model of NIDDM and therefore studied the effect of 24 h of mild insulin-induced hypoglycemia on this defect. Ultralente insulin, 20 U/kg, was given at 9 a.m. and 10 U/kg at 5 p.m., and insulin and glucagon secretion were then studied the next morning using the in vitro isolated, perfused pancreas. The fed plasma glucose concentrations decreased in the STZ rats from 191 +/- 13 to 101 +/- 9 mg/dl and from 133 +/- 4 to 99 +/- 8 mg/dl in the controls. As expected, 10 mM arginine caused a trivial insulin response at 2.8 mM glucose in the treated and untreated control groups compared with the marked one at 16.7 mM. The response to arginine at 2.8 mM glucose in the untreated STZ rats, however, was strikingly elevated (7.65 +/- 2.29 versus 0.41 +/- 0.16 ng/ml in the untreated controls) and it was not potentiated by the high glucose background, but the result at 2.8 mM glucose in the treated STZ rats was similar to that of the treated controls (0.46 +/- 0.12 versus 0.16 +/- 0.03 ng/ml). A return of glucose influence on IBMX-stimulated insulin secretion was also noted. Glucose-induced insulin release, however, was not restored in the treated STZ rats, but it was markedly suppressed in the controls by the insulin treatment. Glucose influence on the glucagon response to arginine was maintained in the STZ model even though the glucagon release to a lowered glucose concentration was lost.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal insulin secretion in a streptozocin model of diabetes. Effects of insulin treatment. 240 48

The spontaneous diabetic Cohen-rat is one of the few animal models of the diabetes mellitus Type II (NIDDM). A spontaneous diabetic animal line and a diabetes-resistant line originated from a parental lineage by genetic selection with regard to the glucose tolerance on condition of feeding of a saccharose-rich and copper-poor diet. In each case 1000 islets of the diabetes-resistant line were transplanted in 28 animals of the diabetic line. Body weight, blood-sugar concentration, glucosuria, glucose tolerance, and the HbA1 were normalized after the transplantation. The serum levels of insulin and glucagon increased. These results emphasize etiopathogenetic importance of the islets of Langerhans in this animal model.
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PMID:[Islet transplantation in type II diabetes mellitus--model of the spontaneous diabetic Cohen rat]. 250 51

A study was made of the effect of natural (vegetable dish) and refined (food methylcellulose--MC-100 and citrus pectin) vegetable fibers and Arfazetin (antidiabetic species, USSR) on the level of glucose, immunoreactive insulin (IRI), C-peptide, glucagon and gastrin in the blood of 41 patients with type II diabetes mellitus. These parameters were investigated on an empty stomach, 1, 2 and 4 h after breakfast I with a standard set of foodstuffs and minimum content of nutritive fibers. Similar investigations were conducted after intake of the same breakfast I in combination with various vegetable components. All the vegetable factors under study were shown to contribute to a decrease in a value of a glycemic rise noted after food intake. A vegetable dish and Arfazetin equally caused a significant rise of IRI secretion and C-peptide 60-90 min. after breakfast. MC-100 and particularly pectin decreased IRI and C-peptide secretion. There was a significant rise of gastrin secretion 1, 2 and 4 h when pectin was added to breakfast. When Arfazetin, a vegetable dish and MC-100 were added to breakfast I, a tendency to a rise of serum gastrin was observed 1 h after breakfast. The level of IRG during investigations with vegetable components did not differ from the results of investigations without these components.
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PMID:[The importance of food and drug plant factors in the combined treatment of patients with type-II diabetes mellitus]. 256 Jan 85

In healthy subjects intravenous glucagon administration induces a prompt (at 1 h) fall in serum T3 concentration and a later (at 4 h) rise in biologically inactive rT3. Since high levels of plasma glucagon have frequently been found in some patients with severe chronic illnesses, together with an anomalous thyroid condition (low serum T3, high serum rT3), it has been supposed that hyperglucagonemia could play a pathogenetic role in causing selective T3 deficiency. In the present study fasting plasma glucagon concentration was measured in 48 patients with low T3 and severe nonthyroidal illnesses: hepatic cirrhosis in 16 cases, chronic non-A non-B hepatitis in 4 cases, uncontrolled type II diabetes mellitus in 5 cases, renal failure in 12 cases, congestive heart failure in 5 cases, tumor in 16 cases. In comparison with a group of 21 healthy controls fasting plasma glucagon concentration was significantly higher in the patients (198.75 +/- 13.20 pg/ml vs. 127 +/- 6.80 pg/ml; p less than 0.001). However, only 29 patients (60.4%) had elevated plasma glucagon levels, whereas 19 (39.5%) had abnormal plasma glucagon levels. Furthermore, no significant difference was found between the thyroid hormone pattern of the patients with hyperglucagonemia and of the patients with normal glucagonemia. On the other hand, a significant correlation between plasma glucagon concentrations and serum T3 and rT3 concentrations was not found. All these findings indicate that in patients with severe chronic illnesses the fall in circulating T3 cannot be due to hyperglucagonemia only which, therefore, might simply be a contributory factor together with other as yet unidentified disorders.
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PMID:[Role of high blood glucagon in the reduction of serum levels of triiodothyronine in severe non-thyroid diseases]. 263 98

The frequency of secondary failure to oral hypoglycaemic agents (OHA) in patients with non-insulin dependent diabetes (NIDDM) is still unknown, despite more than 30 years of use of OHA. The term secondary failure should be limited to patients who, despite maximal dosages of OHA and despite full compliance with diet and therapy, are no longer controlled and require insulin to obtain an acceptable glucose metabolism. We evaluated 248 out-patients, either on OHA, or on insulin because of poor metabolic control with OHA, in order to assess duration of treatment with OHA since diagnosis, by means of actuarial curves (Mantel-Cox test). Patients with low relative body weight (RBW less than or equal to 100) experienced secondary failure earlier and more often than obese patients (RBW greater than 120) or overweight (RBW 101-120) patients. In 66 of the above out-patients, 33 OHA-treated and 33 insulin-treated, matched for age at onset and duration of disease, islet-cell-antibodies (ICA) and C-peptide release at fasting, 6 min after i.v. glucagon and post prandially were evaluated. Only among lean and overweight patients, was C-peptide release significantly lower in insulin-treated than in OHA-treated patients; differences disappeared in obese patients. ICA were found in only 7 patients (10.6%). HLA phenotype was different from that of healthy blood donors for the loci HLA B5, B13, CW4, with no differences between OHA-treated and insulin-treated patients. These data indicate that secondary failure is more frequent in lean patients with NIDDM, and is related to reduced insulin release.
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PMID:Secondary failure to oral hypoglycaemic agents in non-obese patients with non-insulin-dependent diabetes is related to reduced insulin release. 266 Dec 81

Substrate utilisation and glucose homoeostasis during exercise is controlled by the effects of precise changes in insulin, glucagon and the catecholamines. The important role these hormones play is clearly seen in people with diabetes, as the normal endocrine response is often lost. In individuals with insulin-dependent diabetes (IDDM), there can be an increased risk of hypoglycaemia during or after exercise or, conversely, there can be a worsening of the diabetic state if insulin deficiency is present. In contrast, it appears that people with non-insulin-dependent diabetes (NIDDM) can generally exercise without fear of a deleterious metabolic response. The exercise response both in healthy subjects and in those with diabetes is dependent on many factors such as age, nutritional status and the duration and intensity of exercise. Since there are so many variables which govern individual response to exercise, an exact exercise prescription for all people with diabetes cannot be made. There are many adjustments to the therapeutic regimen which an individual with IDDM can make in order to avoid hypoglycaemia during or after exercise. In general, a reduction in insulin dosage and the added ingestion and continual availability of carbohydrates are wise precautions. On the other hand, exercise should be postponed if blood glucose is greater than 2500 mg/L and ketones are present in the urine. As more is understood about the regulation of substrate metabolism during exercise, more refined therapeutic strategies can be defined. An understanding of the metabolic response to exercise is critical for generating an effective and safe training programme for all diabetic individuals who wish to be physically active.
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PMID:Physiological bases for the treatment of the physically active individual with diabetes. 266 24


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