Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study conducted on 228 diabetic patients has shown a significant positive association between serum gamma-glutamyl transpeptidase (GGT) and triglyceride levels. Both fall with treatment, the most marked reduction occurring in patients on insulin. We suggest that the association between serum GGT and triglyceride levels and also the higher incidence of raised GGT and triglyceride levels in new diabetics may reflect hepatic microsomal enzyme induction of the rate-limiting enzymes of triglyceride synthesis. Serum GGT does not seem to correlate with hepatomegaly in diabetes mellitus.
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PMID:The association between serum triglycerides and gamma glutamyl transpeptidase activity in diabetes mellitus. 0 20

A field-trial on Etofibrat was performed on 4405 patients suffering from primary and secondary hyperlipoproteinemia. The results were proved statistically. After a 3 to 4 weeks treatment the concentration of cholesterol as well as tryglicerides in the serum decreased significantly. After 6 to 8 weeks treatment the lipid-lowering effect was even stronger. Nearly 90% of the patients investigated gave a positive response to the treatment. Part of the population had undergone a treatment with other lipid-lowering agents before-most likely without sufficient success-in these cases a further lipid-lowering effect due to Etofibrat could be shown. Under-dosage in premedication cannot be excluded. The stratification of the patients in different groups of diagnosis showed a nearly similarity of both blood lipids independent of the diagnosis. This could also be confirmed for the group of patients suffering from diabetes. To prove the lipid-lowering efficacy of Etofibrat a population was withdrawn from treatment. Cholesterol as well as tryglicerides increased significantly during the interval without treatment. During a long-term study both lipid fractions could be kept down without increasing of the daily Etofibrat dose. The tolerance of Etofibrat was stated to be good up to very good. Objectively the measured enzymes SGOT, SGPT and gamma-GT showed a decrease of the means. Subjectively the occurrence of an often intermediate heat sensation and/or rubedo was of relevance. The low daily dose compared with other lipid-lowering agents gives indication for a better pharmacocinetic behaviour of the drug;
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PMID:[Field study on the decrease of lipids using etofibrate]. 0 62

Oxyhemoglobin dissociation curves (ODC) from zero to full saturation were developed from tests performed on whole blood from various groups of diabetic and nondiabetic healthy subjects. P50 at in-vivo pH was slightly but significantly lower than normal in ambulatory nonacidotic, uncomplicated juvenile diabetics (26.0 vs. 27.3 mm. Hg, P less than 0.001), despite increased red cell 2,3-diphosphoglycerate (2,3-DPG) concentrations in diabetic erythrocytes (15.0 vs. 13.7 mumole/gm. Hb, P less than 0.001). This combination of changes is in keeping with the presence of increased proportions of hemoglobin AIc in insulin-treated diabetics. The position of the ODC was positively correlated with the 2,3-DPG concentration (P less than 0.01), which varied in response to fluctuations in plasma concentration of inorganic phosphate (Pi) (P less than 0.001). Optimal metabolic control may lead to a normalization of the ODC in association with increased concentrations of red cell 2,3-DPG and P. When the diabetes was uncontrolled, the ODC was usually unchanged during the acidotic phase because the lowered pH balanced the effect of diminished 2,3-DPG concentration on the ODC. After correction of acidosis, the disproportion between erythrocyte 2,3-DPG and pH became quite prominent, accompanied by a corresponding fall in P50 (21.0 vs. 26.1 mm. Hg, P less than 0.001). Following ketoacidosis, with a persistently lowered Pi, it may take up to one week for 2,3-DPG to return to an approximately normal level, and the P50 will be impaired for the same period. A diphosphonate (EHDP) known to enhance tubular phosphate reabsorption in man was given to nonacidotic insulin-treated diabetic and healthy volunteers for 28 days. It caused a significant increase in mean Pi and P50 in both healthy and diabetic subjects (r = 0.58, P less than 0.01). When a dietary supplement of dibasic calcium phosphate was given to diabetic subjects for 28 days, a significant increase in P50 also occurred (25.2 vs. 27.2 mm. Hg, P less than 0.001). It is recommended that the diabetes diet be supplemented by dibasic calcium phosphate to prevent the inhibitory effect of a low concentration of Pi on red cell oxygen delivery.
Diabetes 1976
PMID:Oxygen transport impairment in diabetes. 0 22

The present findings of increased microvascular protein passage are compatible with the hypothesis that the organic, histologically demonstrated diabetic microangiopathy is a long-term effect of periods of increased extravasation of plasma proteins, with subsequent protein deposition in the microvascular wall, i.e., the concept of plasmatic vasculosis. Arterial hypertension, frequently present in diabetes, enhances the development of arteriolar hyalinosis. Effective treatment of diabetes and hypertension arrests development of the microvascular lesions.
Diabetes 1976
PMID:Increased microvascular permeability to plasma proteins in short- and long-term juvenile diabetics. 0 23

The oxygen dissociation curve shifted less to the right in venous blood draining from muscle in eight insulin-deficient diabetics working at a constant submaximal workload than in seven normal controls (28.7 mm. Hg vs. 30.8 mm Hg; P less than 0.05). This diminution of the in-vivo Bohr effect at the muscle tissue level during exercise in diabetics was due to a significantly smaller decrease of venous blood pH (down to 7.33 vs. 7.27 in normals; P less than 0.05), probably a consequence of an latered muscle metabolism in insulin deficiency. Although no glucose was taken up, even during exercise, and less lactate was produced by insulin-deficient muscle (P less than 0.05), the differences in venous blood pH appeared to be brought about mainly by a different CO2 production of the exercising muscle in the two groups. The response of Krebs cycle activity to exercise in insulin-deficient muscle might have been inadequate, as suggested by the increased 3-hydroxybutyrate/acetoacetate ratio in the venous blood observed in the normal controls but not in the diabetics. Furthermore, proportionally less of the arterial ketone body concentration was utilized by the working muscle in the insulin-deficient diabetics. Changes in erythrocyte 2,3-diphosphoglycerate did not contribute to the differences in the in-vivo Bohr effect.
Diabetes 1976
PMID:Muscle metabolism during rest and exercise: influence on the oxygen transport system of blood in normal and diabetic subjects. 0 24

Studies of the thermal stability of rat liver glucose-6-phosphatase (EC 3.1.3.9) were carried out to further elevate the proposal that the enzymic activity is the result of the coupling of a glucose-6-P-specific translocase and a nonspecific phosphohydrolase-phosphotransferase. Inactivation was observed when micorsomes were incubated at mild temperatures between pH 6.2 and 5.6. The rate of inactivation increased either with increasing hydrogen ion concentration or temperature. However, no inactivation was seen below 15 degrees in media as low as pH 5 or at neutral pH up to 37 degrees. The thermal stability of the enzyme may be controlled by the physical state of the membrane lipids and the degree of protonation of specific residues in the enzyme protein. Microsomes were exposed to inactivating conditions, and kinetic analyses were made of the glucose-6-P phosphohydrolase activities before and after supplementation to 0.4% sodium taurocholate. The results support the postulate and the kinetic characteristics of a given preparation of intact microsomes are determined by the relative capacities of the transport and catalytic components. Before detergent treatment, inactivation (i.e. a decrease in Vmax) was accompanied by a decrease in Km and a reduction in the fraction of latent activity, whereas only Vmax was depressed in disrupted preparations. The possibility that the inactivating treatments caused concurrent disruption of the microsomal membrane was ruled out. It is concluded that exposures to mild heat in acidic media selectively inactivate the catalytic component of the glucose-6-phosphatase system while preserving an intact permeability barrier and a functional glucose-6-P transport system. Analyses of kinetic data obtained in the present and earlier studies revealed several fundamental mathematical relationships among the kinetic constants describing the glucose-6-P phosphohydrolase activities of intact (i.e. the "system") and disrupted microsomes (i.e. the catalytic component). The quantitative relationships appear to provide a means to calculate a velocity constant (VT) and a half-saturation constant (KT) for glucose-6-P influx. The well documented, differential responses of the rat liver glucose-6-phosphatase system induced by starvation, experimental diabetes, or cortisol administration were analyzed in terms of these relationships. The possible influences of cisternal inorganic phosphate on the apparent kinetic constants of the intact system are discussed.
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PMID:Quantitative aspects of relationship between glucose 6-phosphate transport and hydrolysis for liver microsomal glucose-6-phosphatase system. Selective thermal inactivation of catalytic component in situ at acid pH. 1 Mar 5

Male and female virgin rats and breeder rats with naturally-occurring diabetes, hypertension and arteriosclerosis, were made severely diabetic with a single, subcutaneous injection of alloxan (10 mg/100 g b.w.), after an 18 h fast. During five months of unrelenting diabetes, some animals became obese while others became emaciated. Only the emaciated animals survived but they were blind, their adrenal glands were hemorrhagic, hypertrophied and thrombosed, thymi involuted, kidneys swollen, hearts reduced in size while testes and ovaries were atrophic. Serum CPK, SGOT and SGPT were elevated concomitant with extensive cardiovascular damage, hepatic steatosis and generalized catabolism. Circulating triglycerides and free fatty acids were markedly elevated with total cholesterol only slightly increased. BUN and serum calcium levels were also greatly elevated. Sub-normal Cmpd. B levels indicated impaired adrenal steroidogenesis. Virgin rats developed arteriosclerosis and male and female breeder rats showed exacerbation of their pre-existing aortic sclerosis as well as P.A.N. lesions in their small-sized arteries. It is believed that severe diabetes causes exacerbation of the endogenous hormonal milieu resulting from abnormal hypothalamic-pituitary-adrenal function induced by repeated breeding, which conditions the connective tissue components of the arterial wall of rats toward accelerated degenerative changes.
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PMID:Polyarteritis nodosa induced in arteriosclerotic, male and female breeder rats by chronic alloxan diabetes. 1 32

A patient in whom Cushing syndrome had been diagnosed at the age of 23 was found 14 years later to have subclinical diabetes mellitus, subcutaneous calcified fat tissue necroses, and hypergastrinemia suggesting Zollinger-Ellison syndrome. Histopathologic investigation revealed pancreatic adenomatosis of the glucagon producing A2-cells with accompanying B-cell hyperplasia, and hyperplasia of the adrenal cortex. The origin of the increased serum gastrin concentration in this patient is not yet known. The significance of A2-cell proliferation in Zollinger-Ellison syndrome and and in multiple endocrine adenomatosis is discussed.
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PMID:[Glucagon producing adenomatosis of Islands of Langerhans with polyendocrine symptoms]. 1 53

Examination of glucose kinetics, pancreatic alpha and beta cell function, plasma lipids, urinary acidification and calcium excretion has been undertaken in a patient with hereditary fructose intolerance. This case was unusual as it was associated with insulin-requiring diabetes, type IV hyperlipemia, hypercalciuria and renal calculi. He also demonstrated the previously described fructose-induced defect of urine acidification. Glucagon and C-peptide assays showed that the pancreatic alpha cells were stimulated by fructose and that the beta cells did not respond to fructose. It is not known whether the latter was due to his diabetes or to the lack of a beta cell response to this sugar. Primed 14C-glucose infusions were used for the first time to study nonsteady state glucose kinetics in man. They showed that, 24 hours after the last insulin injection and under basal conditions, the glucose concentrations increased because glucose production exceeded glucose utilization. However, after the administration of sorbitol the plasma glucose concentration decreased because glucose production decreased. After the administration of sorbitol there was no change in the metabolic clearance of glucose. This reflects the lack of a peripheral insulin effect and is consistent with the lack of any measurable C-peptide. Glucose utilization also decreased, but this decrease was less than the decrease in glucose production. Because the metabolic clearance of glucose remained unchanged, it was concluded that the change in glucose utilization was solely due to the decrease in glucose concentration. The absence of C-peptide in the plasma indicated that changes in glucose turnover were not related to any changes in endogenous plasma insulin. Furthermore, the plasma glucagon concentration increased and, hence, changes in this hormone could not account for the decrease in glucose production. Therefore, it was concluded that the sorbitol-induced decline in glucose production was due to a direct effect on hepatic metabolism.
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PMID:Studies of glucose turnover and renal function in an unusual case of hereditary fructose intolerance. 1 54

Postoperative coronary bypass flow was evaluated in two groups of randomly selected patients with grafts to the left anterior descending artery (LAD). Saphenous vein bypass grafts were placed in 27 patients and internal mammary artery grafts in 25 patients. Postoperative flow studies were performed in both groups with roentgendensitometric methods based on the transit time of radiopaque media along the graft plus the mean graft diameter. There was no significant difference between the two groups of patients for age, duration of symptoms, or the frequency of hypertension, diabetes mellitus, prior myocardial infarction, or cardiomegaly. Intraoperative bypass flows were 75+/-27 and 77+/-24 ml. per minute for the saphenous vein group (SVG) and internal mammary artery group (IMAG), respectively. There was no significant difference in the heart rate or mean aortic pressure at the time of the roentgendensitometric flow study. The mean graft diameters were 3.0+/-0.5 and 1.9+/-0.3 mm. for the SVG and IMAG, respectively (p less than 0.001). The ratios of graft diameter to LAD diameter were 1.9+/-0.3 and 1.2+/-0.2 for the SVG and IMAG, respectively (p less than 0.001). The roentgendensitometric postoperative flows were 68+/-27 ml. per minute in the SVG and 46+/-16 ml. per minute in the IMAG (p less than 0.01). The present study indicates that flow in significantly higher in saphenous vein than in internal mammary artery bypasses and that the difference in flow may in part be explained on the basis of the graft diameter.
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PMID:Comparative study of the postoperative flow in the saphenous vein and internal mammary artery bypass grafts. 1 96


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