Assessment of glucose metabolism in humans with the simultaneous use of indirect calorimetry and tracer techniques

2008 ◽  
Vol 15 (1) ◽  
pp. 1-12 ◽  
Author(s):  
L. Tappy ◽  
N. Paquot ◽  
P. Tounian ◽  
P. Schneiter ◽  
E. Jéquier
Keyword(s):  
Glucose Metabolism ◽  
Indirect Calorimetry ◽  
Tracer Techniques ◽  
Simultaneous Use

Mechanisms of starvation diabetes: a study with double tracer and indirect calorimetry

1990 ◽  
Vol 259 (6) ◽  
pp. E770-E777 ◽  
Author(s):  
F. Fery ◽  
N. P. d'Attellis ◽  
E. O. Balasse
Keyword(s):  
Glucose Metabolism ◽  
Glucose Intolerance ◽  
Indirect Calorimetry ◽  
Normal Subjects ◽  
Systemic Circulation ◽  
Oral Glucose ◽  
Glucose Ingestion ◽  
Before And After ◽  
Total Glucose ◽  
Glucose Output

To analyze the mechanisms of fasting-induced glucose intolerance, glucose metabolism was studied before and after the ingestion of 75 g glucose in 24 normal subjects fasted for either 14 h (n = 12) or 4 days (n = 12). The techniques included intravenous infusion of [6-3H]glucose and oral administration of [1-14C]glucose combined with indirect calorimetry. Compared with the controls, the starved subjects exhibited the following differences in glucose metabolism during the 5 h after glucose ingestion. 1) Mean incremental levels were fourfold higher for glucose and 40% higher for insulin. 2) Absorption of oral glucose was delayed and prolonged, but total amount reaching systemic circulation in 5 h was identical in the two groups (approximately 63 g). 3) Suppression of hepatic glucose output was reduced (-12 +/- 1 vs. -22 +/- 2 g). 4) Consequently, the increment in peripheral appearance of total glucose (exogenous plus endogenous) was augmented (+ 52 +/- 2 vs. +41 +/- 2 g). 5) Mean glucose clearance increased significantly less (+28 +/- 7 vs. +96 +/- 10 ml/min). 6) Oxidation of oral glucose was reduced (9 +/- 2 vs. 36 +/- 3 g), and nonoxidative disposal (presumably storage) was enhanced (56 +/- 2 vs. 36 +/- 3 g) in the presence of an elevated fat oxidation (35 +/- 2 vs. 22 +/- 4 g). Thus the alterations in glucose homeostasis responsible for the starvation-induced glucose intolerance are located both at the splanchnic (hepatic) and peripheral levels.

Time-dependent effect of hyperglycemia and hyperinsulinemia on oxidative and non-oxidative glucose metabolism in patients with NIDDM

1992 ◽  
Vol 127 (2) ◽  
pp. 100-106 ◽  
Author(s):  
Anja I Franssila-Kallunki ◽  
Johan G Eriksson ◽  
Leif C Groop
Keyword(s):  
Glucose Metabolism ◽  
Indirect Calorimetry ◽  
Major Part ◽  
Time Dependent ◽  
Glucose Disposal ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Dependent Effect ◽  
Insulin Resistant ◽  
Time Dependent Effect ◽  
Niddm Patients

The present study was undertaken to compare the effect of hyperglycemia and euglycemia during identical hyperinsulinemic conditions on glucose metabolism in NIDDM subjects. Eight NIDDM subjects participated in a 4 h hyperglycemic (12.1±0.7 mmol/l), hyperinsulinemic (475±43 pmol/l) and in a 4 h euglycemic (5.5±0.5 mmol/l), hyperinsulinemic (468±36 pmol/l) insulin clamp in combination with indirect calorimetry and [3H]-3-glucose. Six non-diabetic subjects were studied during euglycemia (5.1±0.2 mmol/l) and hyperinsulinemia (474±35 pmol/l) and served as controls. In NIDDM patients the rate of insulin-stimulated glucose disposal was 57% greater during hyperglycemia compared with euglycemia throughout the 4 h clamp (p<0.01). The major part of the increase in glucose metabolism during hyperglycemia was due to an increase in the non-oxidative glucose metabolism (89%). Whereas glucose metabolism could not be normalized during the prolonged euglycemic hyperinsulinemic clamp in NIDDM patients (49.9±6.8 vs 57.5±5.4 μmol·(kgLBM)−1·min−1 in controls) the addition of hyperglycemia resulted in complete normalization of the glucose disposal rates (78.3±5.8 μmol·(kgLBM)−1·min−1). The effect of hyperglycemia was apparent already at 60 min of the clamp. The data thus suggest that glucose metabolism in NIDDM is insulin resistant, but that the defect in insulin-stimulated glucose uptake can be overcome by increasing the glucose concentration.

Alterations of Glucose Metabolism in Viral and Toxic Liver Injury

1964 ◽  
Vol 46 (4) ◽  
pp. 424-433 ◽  
Author(s):  
Kurt J. Isselbacher ◽  
Wallace A. Jones
Keyword(s):  
Glucose Metabolism ◽  
Liver Injury ◽  
Toxic Liver Injury

640 Glucose metabolism in patients with advanced heart failure

2006 ◽  
Vol 5 (1) ◽  
pp. 149-149
Author(s):  
P MONTEIRO ◽  
J JONES ◽  
F FRANCO ◽  
C BAROSA ◽  
S COSTA ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucose Metabolism ◽  
Advanced Heart Failure
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