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Biomedical subjects

E Jequier

Publications and source records attributed to E Jequier.

61 records · Page 4Linked to original sources
PubMed1967

Tryptophan hydroxylation: measurement in pineal gland, brainstem, and carcinoid tumor.

Development of a rapid and sensitive radioassay has permitted study of the conversion of tryptophan to 5-hydroxytryptophan in mammalian tissues. Of normal tissues examined, beef and rat pineal gland contained the highest activity. This is the first direct demonstration of tryptophan hydroxylase in this hydroxyindole-rich tissue. Rat and rabbit brainstem and human carcinoid tumor also had quantities of enzyme that could be measured easily. The reaction requires a reduced pteridine and oxygen and is inhibired by Para-Chorophenylalanine.

Animals↗
PubMedDate not supplied

Measurement of energy expenditure in clinical nutritional assessment.

Indirect calorimetry with the ventilated-hood open circuit is a useful and accurate technique to measure energy expenditure in acutely ill patients. This approach should be useful to evaluate the energy and the nutrient needs of a patient under acute conditions. The measurement of energy expenditure is of obvious importance in assessing protein-calorie malnutrition. A better understanding of energy balance and nitrogen balance in critically ill patients is needed to determine the best caloric and nutrient intake to avoid tissue depletion. It is foreseen that this method will become more widely used when reliable equipment is made available.

Calorimetry, Indirect↗
PubMedDate not supplied

Glucose disposal in obese non-diabetic and diabetic type II patients. A study by indirect calorimetry and euglycemic insulin clamp.

Insulin resistance is a characteristic finding in obesity and in non insulin dependent (Type II) diabetes mellitus. However, the interaction between diabetes and obesity has been poorly characterized and the metabolic disturbances contributing to the defect in insulin-mediated glucose uptake have not been defined. To examine these questions euglycemic and hyperinsulinemic clamp studies (40 mU/m2/min) were performed in 10 control non-obese subjects, 10 non diabetic obese subjects, 8 normal weight Type II diabetics, and 12 obese Type II diabetics. During the insulin clamp study total body glucose uptake in the obese non diabetics (157 +/- 18 mg/m2.min, p less than 0.01), the normal weight diabetics (159 +/- 21, p less than 0.01) and the obese diabetics (125 +/- 11, p less than 0.001) was significantly reduced compared to the non-obese non diabetic control group (249 +/- 22 mg/m2.min). The impairment in total body glucose uptake was the result mainly of a defect in non-oxidative glucose disposal. Indeed non-oxidative glucose disposal was blunted by 50% in the obese groups (p less than 0.01), somewhat less significantly in the non-obese diabetic group (p less than 0.05) but more when obesity and diabetes mellitus were combined (p less than 0.001). Total glucose oxidation was significantly diminished (p less than 0.01) in both diabetic groups but not in the obese non diabetic group when compared to lean control. A significant inverse correlation between the fasting free fatty acids levels and total glucose uptake (r = -0.453, p less than 0.001) and total glucose oxidation (r = -0.446, p less than 0.001) during the clamp was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Oxidative and nonoxidative glucose metabolism following graded doses of oral glucose in man.

The oxidative and nonoxidative glucose metabolism represent the two major mechanisms of the utilization of a glucose load. Eight normal subjects were administered oral loads of 50, 100 and 150 g glucose and gas exchange measurements were performed for eight hours by means of computerized continuous indirect calorimetry. The glycemic peaks were almost identical with all three doses with a rise to between 141 and 147 mg/dl at 60 min. The fall back to basal level was reached later with the high than with the low glucose doses. The glucose oxidation rate rose to values between 223 and 253 mg/min after the three glucose doses, but while falling immediately after the peak at 120 min following the 50 g load, the glucose oxidation rate remained at its maximum rate until 210 min for the 100 g glucose load and plateaued up to 270 min for the 150 g glucose dose. The oxidation rates then fell gradually to reach basal levels at 270, 330 and 420 min according to the increasing size of the load. Altogether 55 +/- 3 g glucose were oxidized during the 8 hours following the 50 g glucose load, 75 +/- 3 g after the 100 g load and 80 +/- 5 g after the 150 g load. The nonoxidative glucose disposal, which corresponds essentially to glucose storage, varied according to the size of the glucose load, with uptakes of 20 +/- 1, 60 +/- 1 and 110 +/- 1 g glucose 180 min after the 50, 100 and 150 g glucose loads respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗