Glutathione in Human Disease

Henneman, Dorothy H.; Altschule, Mark D.; Goncz, Rose Marie

doi:10.1016/b978-1-4832-2900-3.50034-1

Cited by 9 publications

(10 citation statements)

References 46 publications

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“…Such factors include starvation, protein depletion, liver disease and HUMAN CHORION CELL CULTURES ketosis (6).…”

Section: Table I Blood Coilcentrations Of Glucose and Reduced Glutatmentioning

confidence: 99%

Blood Glutathione in Mild Diabetes Mellitus Before Treatment and During Sulfonylurea-Induced Hypoglycemia.

Seltzer

1957

Experimental Biology and Medicine

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and I-elerans .4 d nr inist ru t ici n Hospital, Dallas.To ascertain whether arylsulfonylurea compounds influence blood glutathione concentrations, determinations of reduced glutathione were made following oral administration of tolbutamide (Orinase) + or carbutamide (BZ-5 5 ) t to patients with normal carbohydrate metabolism and patients with mild diabetes niellitus. Glutathione values were much lower in the diabetic patients both before and after administration of the sulfonylureas. However. no change in glutathione levels was observed in either group during the acute hypoglycemic response to these compounds. nor in diabetic patients who received therapeutic doses of tolbutamide for several days. nlaterial and methods. The patients were all men. Each of 9 control patients had a normal oral glucose tolerance test. Twelve of the 15 diabetic patients were eating a t least 200 g of carbohydrate daily. while the others received 150 g daily. Insulin had never been given to 12 of the diabetics. and had been discontinued in the others a t least one week before the test. The ages of control patients ranged from 24 to 62 years, with a mean of 37 years. The diabetic patients were older, from 46 to 68 years of age with a mean of 59 years, since most of them were selected for probable susceptibility to sul fonylureas. Liver function tests were normal in all 24 individuals. Following an overnight fast 3 g of tolbutamide were given orally to all control patients and to 1 1 of those with diabetes. The other 4 diabetics received 3 g of carbutamide orally. Oxalated specimens of venous blood were obtained before administration of sulfonylurea and a t hourly intervals for 5 hours. Duplicate determinations on whole blood were done for glucose by the Somogyi-*This study was supported in part by research t Tolbutamide was kindly supplied by Upjohn Co., grant from U. S. Public Health Service. and carbutamide by Eli Lilly and Co.

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“…Such factors include starvation, protein depletion, liver disease and HUMAN CHORION CELL CULTURES ketosis (6).…”

Section: Table I Blood Coilcentrations Of Glucose and Reduced Glutatmentioning

confidence: 99%

Blood Glutathione in Mild Diabetes Mellitus Before Treatment and During Sulfonylurea-Induced Hypoglycemia.

Seltzer

1957

Experimental Biology and Medicine

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“…There is some evidence that glucose tolerance may be less following intravenous glucose than following oral glucose,19 22,85 and that the role of the liver and peripheral tissues may be quantitatively different in the two circumstances. 48,49,115 It has also been shown that the Staub-Traugott phenomenon does not occur if the two glucose doses are given intravenously. However, if glucose is given by mouth between the first and second intravenous glucose tolerance test, the second curve will be steeper than the first one.l9…”

Section: Methods and Interpretationmentioning

confidence: 99%

The Glucose Tolerance Test

Baird

Duncan

1959

Postgraduate Medical Journal

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“…Only a small number of patients, however, were investigated. Henneman et al (1954) also found in their six cases of active multiple sclerosis a rise in the plasma citrate level following glucose ingestion instead of the usual fall. A rise was also observed by Jeanes and Cumings (1958) at some point after glucose was ingested in nine out of 14 cases.…”

mentioning

confidence: 88%

“…A group of 38 patients in remission showed only a slight elevation of the fasting blood pyruvate and a normal response to glucose ingestion. Ervenich (1952,1953) and Sercl and Johnova ' (1956) also reported that the fasting pyruvate level was frequently raised in this disease, but Bauer (1956), Henneman, Altschule, Goncz, and Alexander (1954) and Jeanes and Cumings (1958) either found the fasting level normal, or raised in only a small proportion of cases. After glucose ingestion, however, Jeanes and Cumings (1958) found an abnormal rise in the blood pyruvate level in 15 of their 26 active and in two of their seven inactive cases.…”

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confidence: 90%