[Gestonoroncapronate and carbohydrate metabolism during radiotherapie of female patients suffering from cancer of the genitals (author's transl)].
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Carbohydrate Metabolism
Glucose tolerance test
Radiation Tolerance
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Increased in vivo resistance to insulin-mediated glucose disposal has been observed in obese subjects with normal glucose tolerance and in nonobese subjects with glucose intolerance. To determine whether the insulin resistance of glucoseintolerant obese subjects can be accounted for by obesity alone, insulin-mediated glucose disposal was measured in 14 glucoseintolerant and 21 nondiabetic Southwestern American Indians with similar degrees of obesity. A mixture of insulin, glucose, and somatostatin was infused which delivered the same quantity of glucose and achieved similar plasma insulin concentrations in all subjects. Despite similar steady state plasma insulin levels, the mean steady state plasma glucose concentration was higher in the glucose-intolerant subjects than in weight-matched subjects with normal glucose tolerance (226 ± 10 vs. 136 ± 13 mg/dl; P < 0.0001). This increased resistance to insulin action was found in the presence of similar insulin binding to mononuclear cells (measured in 8 glucose-intolerant subjects and 9 subjects with normal glucose tolerance). In obese Southwestern American Indians with glucose intolerance, abnormalities beyond the site of insulin binding to its receptor may explain the observed increase in in vivo insulin resistance.
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The effect of the combination type oral contraceptive and its estrogen (mestranol) and progesterone (ethynodiol diacetate) components on the intravenous glucose tolerance test (IVGTT), intravenous tolbutamide test (IVTT), serum insulin like activity (ILA) and morphology of beta cells of the pancreas was investigated in female rabbits. The combination produced impairment of glucose tolerance in all animals after 24 weeks treatment. Fifty percent of animals in the estrogen treated group and 33.3 percent of animals in the progesterone treated group developed impairment of glucose tolerance after 24 weeks. A reduction in the glucose response to IVTT was observed in all the animals following 24 weeks treatment with the combination, estrogen or progesterone. A significant decline in fasting serum ILA and post glucose ILA was observed in animals treated with the combination and estrogen. A small but consistent decline in the serum ILA was observed in animals treated with ethynodiol diacetate. A rise in serum FFA paralleled the abnormality of glucose tolerance. Morphological changes in the cytostructure of pancreatic islets in the form of degranulation and degeneration of cells were observed in the pancreas of animals treated with the combination, and to lesser extent in animals treated with estrogen and progesterone. These observations indicate that the disturbances in carbohydrate and lipid metabolism produced by oral contraceptives may be associated with damage to beta cells and low circulating insulin in rabbits.
Tolbutamide
Glucose tolerance test
Mestranol
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The effect of variations in glucose tolerance on insulin's ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Patients with IGT had ambient insulin levels that were higher than normal, associated with elevated postprandial glucose levels and a marked reduction in insulin-stimulated glucose uptake. On the other hand, plasma FFA levels were relatively normal in IGT, possibly because of the hyperinsulinemia. Patients with NIDDM were also hyperinsulinemic, with insulin levels throughout the day that were approximately twice normal. Hyperinsulinemia in patients with NIDDM was associated with a significant decline in insulin-stimulated glucose uptake as well as with significant increases in both ambient plasma glucose and FFA concentrations. Thus, and in contrast to patients with IGT, plasma FFA metabolism in NIDDM was grossly abnormal, despite the concomitant hyperinsulinemia. These data indicate that insulin resistance in obese individuals varies as a function of degree of glucose tolerance, and insulin resistance in patients with NIDDM involves defects in the regulation of both plasma glucose and FFA metabolism.
Hyperinsulinemia
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To investigate the level of blood glucose, cholesterol (Cho), triglycerides (TG), insulin secretion and the efficacy of acarbose in preventing impaired glucose tolerance (IGT) in Otsuka Long-Events Tokushima Fatty (OLETF) rats.10 OLETF rats with IGT, 8 IGT OLETF rats with acarbose treatment, and 36 LETO rats with normal glucose level were observed for their blood glucose, Cho, TG, insulin secretion and histological changes in the pancreas and skeletal muscles.OLETF rats with IGT were mild obese, with fat infiltration in the islets and skeletal muscles. Their blood Cho and TG were higher than those of LETO rats (2.5 mmol/L +/- 0.3 mmol/L vs 2.1 mmol/L +/- 0.3 mmol/L, P < 0.01; 0.7 mmol/L +/- 0.2 mmol/L vs 0.4 +/- 0.2 mmol/L, P < 0.01), but their TG was lower than that of diabetic rats (1.8 +/- 1.0). The Cho, TG and post-challenge glucose levels were normal in the IGT rats with 4-week acarbose treatment, with their insulin secretion and glucose tolerance improved and fat infiltration decreased.Acarbose can prevent obesity and fat infiltration in islets and muscles, improve glucose and lipid metabolism, and insulin secretion in OLETF rats with IGT.
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Adults with GHD have normal overnight fasting glucose levels and normal overall glucose turnover. In the absence of GH, insulin secretion is reduced and may be associated with impaired glucose tolerance. The lack of GH is associated with normal insulin sensitivity but reduced hypoglycaemic responsiveness, probably due to a reduced supply of gluconeogenic substrates. When GHD is associated with obesity, however, hyperinsulinaemia and insulin resistance ensue and hypoglycaemic responsiveness is restored. In adults with GHD, treatment with recombinant human GH for 6 months increased fasting plasma glucose to within the normal range, with no change in overall glucose turnover and carbohydrate tolerance, in the presence of elevated basal insulin levels.
Chemical pathology
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The effects of impaired glucose tolerance and obesity, in isolation and in combination, on basal (postabsorptive) intermediary metabolism were examined in four groups of subjects (n = 10 for each) matched for age and gender: Group 1: Non-obese healthy controls with normal glucose tolerance (75 g); Group 2: Non-obese subjects with impaired glucose tolerance; Group 3: Morbidly obese subjects with normal glucose tolerance; Group 4: Morbidly obese subjects with impaired glucose tolerance. While there was no significant difference in fasting blood glucose concentrations between the four groups plasma immuno-reactive insulin concentrations were elevated (p < 0.01 or less) in the obese subjects relative to the non-obese subjects within each category of glucose tolerance. Basal immunoreactive insulin concentrations in non-obese subjects with impaired glucose tolerance were also elevated (p < 0.01) relative to the non-obese healthy controls. Concentrations of glycerol (p < 0.01), non-esterified fatty acids (p < 0.01), and total ketone bodies (p < 0.001) were significantly higher in the obese/normal glucose tolerance and obese/impaired glucose tolerance groups relative to their matched non-obese counterparts. Compared with the subjects with normal glucose tolerance, only lactate (p < 0.05) and pyruvate (p < 0.05) concentrations were elevated in the non-obese/impaired glucose tolerance and obese/impaired glucose tolerance groups, respectively. In conclusion, in addition to fasting hyperinsulinaemia the regulation of lipolysis and ketone body metabolism is abnormal in the basal state in morbid obesity. By contrast, despite normal fasting blood glucose concentrations, impaired glucose tolerance is associated with disturbances of other aspects of basal carbohydrate metabolism.
Basal (medicine)
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Journal Article Glucose Metabolism and Insulin Secretion in the Carcinoid Syndrome Get access JEROME M. FELDMAN, JEROME M. FELDMAN 1Duke University Medical Center, Durham Veterans Administration Hospital Durham, North Carolina 27710; Department of Medicine, Division of Endocrinology Durham, North Carolina 27710 Search for other works by this author on: Oxford Academic Google Scholar RAYMOND L. MARECEK, RAYMOND L. MARECEK 1Duke University Medical Center, Durham Veterans Administration Hospital Durham, North Carolina 27710; Department of Medicine, Division of Endocrinology Durham, North Carolina 27710 Search for other works by this author on: Oxford Academic Google Scholar KENNETH E. QUICKEL, JR., KENNETH E. QUICKEL, JR. 1Duke University Medical Center, Durham Veterans Administration Hospital Durham, North Carolina 27710; Department of Medicine, Division of Endocrinology Durham, North Carolina 27710 Search for other works by this author on: Oxford Academic Google Scholar HAROLD E. LEBOVITZ HAROLD E. LEBOVITZ 1Duke University Medical Center, Durham Veterans Administration Hospital Durham, North Carolina 27710; Department of Medicine, Division of Endocrinology Durham, North Carolina 27710 Search for other works by this author on: Oxford Academic Google Scholar The Journal of Clinical Endocrinology & Metabolism, Volume 35, Issue 2, 1 August 1972, Pages 307–311, https://doi.org/10.1210/jcem-35-2-307 Published: 01 August 1972 Article history Received: 01 March 1972 Published: 01 August 1972
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The control of glucose metabolism is a complex process, and dysregulation at any level can cause impaired glucose tolerance and insulin resistance. These two defects are well-known characteristics associated with obesity and onset of type 2 diabetes. Here we introduce the N-terminal dipeptidase, DPP2, as a novel regulator of the glucose metabolism. We generated mice with a neurogenin 3 (NGN3)-specific DPP2 knockdown (kd) to explore a possible role of DPP2 in maintaining metabolic homeostasis. These mice spontaneously developed hyperinsulinemia, glucose intolerance, and insulin resistance by 4 months of age. In addition, we observed an increase in food intake in DPP2 kd mice, which was associated with a significant increase in adipose tissue mass and enhanced liver steatosis but no difference in body weight. In accordance with these findings, the mutant mice had a higher rate of respiratory exchange than the control littermates. This phenotype was exacerbated with age and when challenged with a high-fat diet. We report, for the first time, that DPP2 enzyme activity is essential for preventing hyperinsulinemia and maintaining glucose homeostasis. Interestingly, the phenotype of NGN3-DPP2 kd mice is opposite that of DPP4 knockout mice with regard to glucose metabolism, namely the former have normal glucagon-like peptide 1 levels but present with glucose intolerance, whereas the latter have increased glucagon-like peptide 1, which is accompanied by augmented glucose tolerance.
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We have characterized the abnormalities of glucose metabolism associated with Friedreich's ataxia (FA) by studying plasma glucose, insulin, growth hormone (GH), and glucagon before and after an oral glucose tolerance test (OGTT), an IV glucose load, and an IV arginine load, in 21 patients and in controls. Twelve patients were normotolerant (NT) to glucose, five glucose-intolerant (IT), and four diabetic (DM). Insulin secretion of IT patients was increased and delayed during OGTT. Interestingly, the insulin release during arginine load was significantly decreased in NT and IT as well as in DM patients. The GH response to OGTT was altered in IT patients. Plasma glucagon after an arginine load was significantly higher in patients than in controls. The results indicate that FA is associated with insulin resistance, beta-cell deficiency, and type I diabetes. These alterations might be genetically linked or metabolically related to the primary defect in FA. Their interplay or independent effects are responsible for abnormalities of glucose metabolism in FA.
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Glucose tolerance test
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Carbohydrate metabolism was studied in fourteen patients with myotonia dystrophica (MD) using oral glucose, fructose and galactose tolerance tests. Insulin responses to tolbutamide, glucagon, arginine and leucine were determined and insulin resistance was measured with exogenous iv insulin. Glucose tolerance was impaired in twelve of the four teen subjects while hyperinsulinism was found in all patients studied. Insulin response to the various substances was excessive. The insulin tolerance test revealed insulin resistance in all patients and this generally correlated well with the degree of hyperinsulinism to provocative tests. Serum galactose levels after an oral load were much lower in MD compared to normal subjects and were associated with a correspondingly greater rise in glucose, indicating an increased conversion of galactose to glucose. A similar response to oral galactose was found in diabetics. The hyperinsulinism seen with the fructose and galactose tests corresponded well to the rise in glucose during the test. Urinary sorbitol excretion was normal. It is concluded that the impaired carbohydrate metabolism seen in MD is due to peripheral insulin resistance affecting various organs including the liver and it is suggested that the excessive beta-cell response is secondayr to the peripheral resistance.
Tolbutamide
Carbohydrate Metabolism
Glucose tolerance test
Hyperinsulinemia
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