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)

The long-term results of dietary treatment for obesity are often very poor. To predict the effect of a hypocaloric diet, it may be important to consider factors that could influence energy expenditure, especially those altered in obesity. Elevated plasma levels of glucagon are associated with obesity. In this study, the relationship of glucagon to resting metabolic rate (RMR) and glucose-induced thermogenesis (GIT) has been investigated. RMR and GIT, after ingesting 100 g glucose, were measured by indirect calorimetry in 25 obese premenopausal women (body mass index [BMI], 37.2 +/- 4.7 kg.m-2). RMR was significantly related to fat-free mass (FFM) (r = .50, P less than .005). A significant relation could be found between RMR and fasting glucagon levels (r = .36, P less than .05). Plasma glucose and insulin levels were not predictive for RMR. Mean GIT increased with increasing waist-hip circumference ratio (WHR) (r = .71, P less than 0.0001), confirming previous findings of our group. No relation was found between GIT and glucagon levels, neither in the basal state nor after glucose. The only important metabolic determinant was area under the curve (AUC) for glucose (r = .45, P less than .01), suggesting a higher GIT in obese women with impaired glucose intolerance. This suggests that the control of energy metabolism by the concentration of glucagon may be more important in the fasting state than after a meal. Plasma glucagon concentration should be considered in the evaluation of RMR.
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PMID:Importance of glucagon as a determinant of resting metabolic rate and glucose-induced thermogenesis in obese women. 187 Apr 20

Antidiabetic effects of CS-045 were evaluated in 5-month-old C57BL/KsJ-db/db mice (db/db). CS-045 administered for 3 weeks to diabetic db/db mice as a 0.2% food admixture improved hyperglycemia (855 +/- 25 v 298 +/- 62 mg/dL, P less than .01) and glucose intolerance, and lowered plasma triglyceride (299.6 +/- 28.7 v 76.3 +/- 20.7 mg/dL, P less than .01) and free fatty acid (FFA) levels (1.16 +/- 0.14 v 0.57 +/- 0.07 mEq/L, P less than .01). Food intake was not changed, while a small but significant increase in body weight was observed in CS-045-treated mice. Plasma insulin levels gradually increased after 5 days of CS-045 treatment, and a nonsignificant increase was observed in plasma insulin levels after 3 weeks (1.85 +/- 0.50 v 4.54 +/- 1.47 mg/mL). In contrast, the plasma glucagon levels decreased after 3 weeks of CS-045 treatment. Histological examination by aldehyde-fucshin staining demonstrated that pancreatic beta cells in CS-045-treated db/db mice were heavily regranulated, whereas most of the beta cells were extensively degranulated in nontreated db/db mice. The heavily regranulated state of beta cells was also compatible with an increase in pancreatic insulin content in CS-045-treated db/db mice. Electron microscopic analysis showed a well-developed endoplasmic reticulum and the accumulation of much amorphous structural material in the intracisternal space of beta cells from CS-045-treated db/db mice, which were suggestive of an increase in insulin synthesis. Moreover, CS-045 treatment decreased exocrine-containing islets, which was associated with the islets' degeneration process. Immunohistochemical staining of islets showed that CS-045 treatment normalized the distribution pattern of endocrine cells in the islets of db/db mice, reflected by a predominantly peripheral location of alpha and delta cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of CS-045, a new oral antidiabetic agent, II. Effects on glycemic control and pancreatic islet structure at a late stage of the diabetic syndrome in C57BL/KsJ-db/db mice. 194 50

The effects of low-chromium diets containing chromium in the lowest quartile of normal intake on glucose tolerance and related variables in 11 females and 6 male subjects were evaluated. Subjects with glucose concentration greater than 5.56 mmol/L but less than 11.1 mmol/L 90 min after an oral-glucose challenge were designated as the hyperglycemic group and the remainder, the control group. Glucose tolerance and circulating insulin and glucagon of the hyperglycemic group all improved during chromium supplementation (200 micrograms/d) whereas those of the control group were unchanged. Glucose and insulin concentrations 60 min after the oral-glucose challenge and the sum of the 0-90 min and 0-240 min glucose values were all significantly lower after chromium supplementation in the hyperglycemic group. These data demonstrate that consumption of diets in the lowest 25% of normal chromium intake lead to detrimental effects on glucose tolerance, insulin, and glucagon in subjects with mildly impaired glucose tolerance.
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PMID:Supplemental-chromium effects on glucose, insulin, glucagon, and urinary chromium losses in subjects consuming controlled low-chromium diets. 195 Nov 65

The effects of four different diets, a balanced (BD), a high protein (HP), a high fat (HF), and a high carbohydrate (HC) diet on glucose tolerance and pancreatic hormone secretion were compared during the ten-week period immediately after weaning in rats having glucose intolerance induced by streptozocin in the neonatal period (NSZ). Feeding HF or HC produced decrease in calorie intake and a delay in body weight increase. All NSZ rats showed glucose intolerance as adults; the HF rats showed a further deterioration of glucose tolerance and a decreased insulinogenic index after oral glucose loading. Plasma insulin levels of HC rats were lowest. The glucose-induced insulin and somatostatin secretion from the isolated perfused pancreas was almost identical in all four groups. The arginine-induced insulin and glucagon secretion was decreased in HF and HC rats, compared to both HP and BD rats, but somatostatin secretion was not. These results indicate that a high fat or high carbohydrate dietary environment is an important factor in the development of glucose intolerance and in the impairment of pancreatic hormone responsiveness to stimulation.
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PMID:Effect of dietary environment on the development of impaired glucose tolerance and pancreatic hormone secretion in neonatal streptozocin-treated (NSZ) rats. 197 2

A study was made of glucose tolerance and insulin secretion in 33 persons who later developed insulin-dependent diabetes (aged 4-24 years) and observation continued further in the first years after manifestation. Patients who developed the typical labile type of diabetes were of normal weight and had either normal glucose tolerance tests before diagnosis or had impaired glucose tolerance (IGT) for a short interval of 2-16 months. Subjects with IGT over a significantly (p less than 0.01) longer period of 32.30 +/- 6.25 (normal body weight) or 94.71 +/- 20.62 (obese) months developed a milder form of diabetes with retarded insulin dependency in obese subjects. The severe and mild form of IDDM are distinct with respect to insulin requirement (0.75 +/- 0.03 or 0.28 +/- 0.04 U/kg b.w., P less than 0.01) and glucagon stimulated C-peptide (0.18 +/- 0.05 or 1.41 +/- 0.27, P less than 0.01) in the first 2.5-3.5 years after onset. The two forms were not different regarding HLA-DR antigens. Islet cell surface antibodies investigated in 15 probands at 27 occasions before diabetes onset had no prognostic value. The development of a mild form of IDDM may be expected in cases with pre-existing IGT for more than one year. The insulin secretion is of low predictive value under these conditions. The observation is of practical use and theoretical interest.
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PMID:Glucose tolerance behaviour before the onset of type I (insulin-dependent) diabetes in young people as a predictor of the further course of the disease: a retrospective analysis of 33 cases. 202 75

We have studied the endocrine-metabolic status of patients in non-insulin-receiving (NIR) remission of insulin-dependent diabetes mellitus (IDDM) within 6-60 mo of diagnosis during administration of cyclosporine, in comparison with nondiabetic subjects. IDDM patients in NIR remission were recognized when target glycemic control (plasma glucose and mean capillary blood glucose levels less than 7.8 mM before meals) was maintained without administration of insulin for at least 2 wk. In so-called isoglycemic tests, 50 g glucose was administered orally, and the glycemic curve was simulated in a subsequent study by programmed intravenous infusion of glucose. Under these conditions, the subjects with diabetes exhibited obvious glucose intolerance: acute beta-cell responses to intravenous glucose were virtually absent but significant, although subnormal responses were present after oral glucose. The responses of plasma immunoreactive gastric inhibitory polypeptide to oral glucose were normal. After bolus intravenous injections of glucose, the patients with diabetes again exhibited glucose intolerance; acute responses of immunoreactive insulin (IRI) and C-peptide were present, although grossly obtunded. On intravenous infusion of arginine (30 g in 30 min), the patients with diabetes showed substantial but subnormal increases in plasma IRI and C-peptide. Intravenous infusion of arginine elicited increments of plasma immunoreactive glucagon (IRGI) in both groups, and this response was slightly exaggerated in the patients with diabetes. On ingestion of a standard mixed meal (Sustacal) delivering 600 cal, there was a modest but significantly greater increase in plasma glucose levels in the diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrine-metabolic function in remission-phase IDDM during administration of cyclosporine. 202 4

As a result of the improvement in life-expectancy in cystic fibrosis patients, simultaneous presence of cystic fibrosis and diabetes mellitus is no longer exceptional. In teenagers and young adults with cystic fibrosis, the prevalence of insulin-dependent diabetes mellitus (IDDM) is 7 to 10%. Fifty percent of cystic fibrosis patients have impaired glucose tolerance. These prevalences increase with advancing age. Insulin deficiency is a consistent feature. An endocrine pancreatic deficiency thus exists in addition to the exocrine pancreatic deficiency, as demonstrated by the fall in glucagon and pancreatic polypeptide productions. Development of insulin dependency is associated with deterioration in clinical status and indicates an adverse prognosis. Although in cystic fibrosis patients diabetes mellitus seems to occur as a result of different pathophysiologic mechanisms than those involved in autoimmune IDDM, the risk of degenerative complications is similar in both conditions. It follows that early detection of diabetes mellitus and appropriate insulin treatment are warranted in cystic fibrosis patients.
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PMID:[Glucose intolerance and diabetes during cystic fibrosis]. 206 59

In six patients with pheochromocytoma oral glucose tolerance test (OGTT) and arginine test were carried out. Blood insulin and glucagon response were investigated. In subjects with adrenal tumor glycemic curve pattern was typical: a rapid and exaggerated increase of glycemia followed by an abrupt drop. Absolute insulinemic response to oral glucose was normal, but inappropriate to glycemic stimulus. Arginine infusion provoked a slightly above normal increase in blood glucose and a normal increase in blood glucagon. In three of the patients studied postoperatively, reduced glycemic response to glucose was observed, whereas there were no evident variations in blood insulin and glucagon response. These data suggest that in pheochromocytoma impaired glucose tolerance is partly due to the reduced insulin response to oral glucose load.
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PMID:Endocrine pancreatic function in pheochromocytoma. 207 24

Secondary diabetes mellitus was the main abnormal finding in a young lean woman with benign extra-adrenal para-aortic norepinephrine and dopamine secreting pheochromocytoma. Glucose and insulin response to oral glucose and C-peptide secretion after glucagon i.v. were evaluated before and after alpha-blockade with phenoxybenzamine. Alpha-blocking treatment restored the inhibited basal and stimulated C-secretion but did not normalize glucose tolerance. After tumor removal metabolic abnormalities were normalized, confirming the role of endogenous catecholamine excess in the pathogenesis of our patient's glucose intolerance.
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PMID:Diabetes mellitus as presenting feature in extra-adrenal pheochromocytoma: report of a case. 207 89

The effect of rioprostil, a methylprostaglandin E1 analog on circulating pancreatic hormones was evaluated in 13 healthy male subjects. Rioprostil administration, 300 micrograms twice daily resulted in a significant decrease of fasting insulin, C-peptide, glucagon, and pancreatic polypeptide. No change in fasting plasma glucose or somatostatin levels was observed. An oral glucose tolerance test induced similar increments in plasma glucose concentration before and during treatment, but a delayed rise of insulin and C-peptide levels occurred during the administration of the drug. On rioprostil, the glucose load no longer inhibited peripheral glucagon or somatostatin. Treatment with rioprostil remained without effect on mixed meal-induced changes in plasma glucose levels and concomitant increases in insulin, pancreatic polypeptide, and somatostatin levels. It is concluded that in healthy individuals rioprostil influences the basal and glucose-induced levels of glucagon, insulin, and somatostatin. In healthy men this effect did not, however, result in glucose intolerance.
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PMID:Effect of rioprostil, a methylprostaglandin E1 analog, on basal and stimulated plasma pancreatic hormone levels in man. 210 96


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