Glucose turnover in presence of changing glucose concentrations: error analysis for glucose disappearance

1995 ◽  
Vol 269 (3) ◽  
pp. E557-E567 ◽  
Author(s):  
A. Caumo ◽  
M. Homan ◽  
H. Katz ◽  
C. Cobelli ◽  
R. Rizza
Keyword(s):  
Error Analysis ◽  
Glucose Uptake ◽  
Specific Activity ◽  
Insulin Dependent Diabetes Mellitus ◽  
Postprandial Glucose ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Glucose Turnover ◽  
Glucose Disappearance ◽  
Analytic Expressions

The present studies were undertaken to determine whether 1) the cold- and hot-GINF techniques used with Steele's model provide equivalent estimates of the rates of glucose appearance (R(a)) and disappearance (R(d)) in the presence of physiological changes in glucose and insulin concentrations, 2) the conditions for the best estimation of R(a) are the same as those for R(d), 3) the magnitude of error (if present) differs in diabetic and nondiabetic subjects, and 4) situations exist in which the knowledge of R(d) allows inferences to be made on whole body glucose uptake. To do so we performed experiments in non-insulin-dependent diabetes mellitus and nondiabetic subjects using simultaneous infusions of [6-3H]glucose and [6-14C]glucose; glucose and insulin were infused to mimic normal postprandial glucose and insulin profiles; the infused glucose contained [6-14C]glucose but not [6-3H]glucose. Compared with the hot-GINF method, the traditional cold-GINF method underestimated (P < 0.05) R(a) and R(d) by 10-15% and hepatic glucose release by 25-50% during the 1st h of the study, with the magnitude of error being the same in both diabetic and nondiabetic subjects. Error analysis demonstrated that errors in R(a) and R(d) have different analytic expressions containing common structural but different volume errors. Both R(a) and R(d) can be accurately measured in diabetic and nondiabetic subjects if glucose specific activity is kept constant and the volume of the accessible pool is used to calculate glucose disappearance. The relationship between R(d) and whole body glucose uptake was also derived. Although R(d) can be determined by relying on measurements in the accessible pool only, the assessment of whole body glucose uptake requires a model of the nonaccessible portion of the glucose system. However, knowledge of R(d) can provide useful insights into the behavior of whole body glucose uptake.

scholarly journals Dodecanedioic acid infusion induces a sparing effect on whole-body glucose uptake, mainly in non-insulin-dependent diabetes mellitus

1997 ◽  
Vol 78 (5) ◽  
pp. 723-735 ◽  
Author(s):  
G. Mingrone ◽  
A. De Gaetano ◽  
A. V. Greco ◽  
E. Capristo ◽  
G. Benedetti ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Uptake ◽  
Insulin Dependent Diabetes Mellitus ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent ◽  
Sparing Effect ◽  
Dodecanedioic Acid ◽  
Niddm Patients ◽  
Normal Controls

Even-numbered dicarboxylic acids (DA) have been proposed as an alternative fuel substrate in parenteral nutrition. In particular, dodecanedioic acid (C12) shows a rapid plasma clearance from tissues, a very low urinary excretion compared with other DA and a high oxidation rate. The aim of the present study was to investigate the effect of C12 infusion on insulin-stimulated glucose uptake in patients with non-insulin-dependent diabetes mellitus (NIDDM) compared with healthy volunteers. A primed-constant infusion of C12 (0·39 mmol/min) was administered over 240 min, and at 120 min a 2 h euglycaemic hyperinsulinaemic clamp was performed. Blood specimens were sampled every 30 min and fractioned urines were collected over 24 h. The levels of C12 were measured by HPLC. Indirect calorimetry was performed continuously during the entire session. Body composition was assessed in all subjects studied to obtain fat-free mass (FFM) values. Whole-body glucose uptake decreased significantly during C12 infusion in both groups, although this effect was much more evident (P < 0·01) in NIDDM patients (52·4 (sd 15·8) % decrease compared with saline) than in controls (25·9 (sd 12·1) % decrease). The M value (μmol/kgffm per min) was reduced by C12 to lower levels in NIDDM patients than in normal controls (12·6 (sd 3·9) ν. 25·9 (sd 4·5), P < 0·01). Urinary excretion of C12 over 24 h was significantly lower in NIDDM patients than in controls (4·26 (sd 0·30) mmol ν. 5·43 (sd 0·48), P < 0·01), corresponding to less than 3 % of the administered dose. The infusion of C12 decreased non-protein RQ significantly in both groups of patients. In conclusion, this study shows, for the first time, that C12 significantly reduces glucose uptake in both normal controls and NIDDM patients, although this sparing effect on glucose uptake is much more pronounced in diabetic patients. These data suggest that C12 decreases glucose uptake and oxidation, mainly through a mechanism of substrate competition. Thus, it might be a useful alternative substrate in enteral or parenteral nutrition, sparing glucose utilization and increasing glycogen stores, in those clinical conditions, like NIDDM, where reduced insulin-induced glucose uptake and oxidation are observed.

scholarly journals Leg and arm lactate and substrate kinetics during exercise

2003 ◽  
Vol 284 (1) ◽  
pp. E193-E205 ◽  
Author(s):  
G. van Hall ◽  
M. Jensen-Urstad ◽  
H. Rosdahl ◽  
H.-C. Holmberg ◽  
B. Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Mass ◽  
Lactate Concentration ◽  
Whole Body ◽  
Glucose Turnover ◽  
Lactate Oxidation ◽  
Arterial Lactate ◽  
Lactate Uptake ◽  
High Lactate

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.

Glucose production, recycling, and gluconeogenesis in normals and diabetics: a mass isotopomer [U-13C]glucose study

1996 ◽  
Vol 270 (4) ◽  
pp. E709-E717 ◽  
Author(s):  
J. A. Tayek ◽  
J. Katz
Keyword(s):  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Tricarboxylic Acid Cycle ◽  
Glucose Production ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Glucose Turnover ◽  
Insulin Dependent ◽  
Gas Chromatography Mass Spectroscopy ◽  
Mass Isotopomer

Eight normal controls and nine non-insulin-dependent diabetes mellitus diabetics were, after an overnight fast, infused for 3 h with [6-3H]- and with [U-13C]glucose with six 13C carbons at rates from 0.03 to 0.15 mg.kg-1.min-1. Plasma glucose and lactate were assayed by gas chromatography-mass spectroscopy. Several parameters of glucose metabolism were calculated from the mass isotopomer distribution. Glucose production (GP) determined with [6-3H]- and [U-13C]glucose agreed closely. GP was 1.9 +/- 0.16 (range 1.3-2.5) mg.kg-1.min-1 in controls and 2.8 +/- 0.29 (1.7-4.5) mg.kg-1.min-1 in diabetics (P < 0.05). The correlation in diabetes between plasma glucose and GP (r = 0.911, P < 0.01) was close. Recycling of carbon (8 vs 7%) dilution by unlabeled carbon (2- vs 2.3-fold), and dilution via the tricarboxylic acid cycle (1.5-fold) were similar in controls and diabetics. Gluconeogenesis was 0.90 +/- 0.08 (0.5-1.3) mg.kg-1.min-1 in controls and 1.30 +/- 0.13 (0.8-1.9) mg.kg-1.min-1 in diabetics (P < 0.05). Gluconeogenesis contributions to GP were 46.6 +/- 4.0% (26-61%) in the controls and 48.8 +/- 5.7% (32-83%) in diabetics. We show that, using [U-13C]glucose infusion of 2-5% of glucose turnover (0.03-0.10 mg.kg-1.min-1), a large number of parameters of glucose metabolism may be determined in humans.

Effects of dietary protein restriction on regional amino acid metabolism in insulin-dependent diabetes mellitus

1996 ◽  
Vol 270 (1) ◽  
pp. E148-E157 ◽  
Author(s):  
I. G. Brodsky ◽  
J. T. Devlin
Keyword(s):  
Diabetes Mellitus ◽  
Dietary Protein ◽  
Protein Intake ◽  
Insulin Dependent Diabetes Mellitus ◽  
Protein Restriction ◽  
Insulin Dependent Diabetes ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Dietary Protein Restriction ◽  
Insulin Dependent

We studied subjects with insulin-dependent diabetes mellitus (IDDM) and controls by administering primed continuous infusions of L-[1-13C,15N)]leucine and L-[2,3-13C2]alanine to measure whole body and forearm metabolism of these amino acids during ample protein intake and again after 4 wk of moderately restricted protein intake. Decreased rates of whole body protein degradation, leucine transamination, leucine oxidation, and increased forearm alanine release produced by dietary protein restriction occurred equivalently in IDDM subjects under short-term tightly managed glycemia and in controls. Dietary protein restriction did not affect whole body alanine appearance or forearm leucine appearance, disposal, or balance in IDDM subjects or controls. IDDM subjects differed from controls only in that normal forearm leucine balance was maintained at higher rates of leucine appearance and disposal. We conclude that IDDM subjects adapt normally to dietary protein restriction. Undernutrition during moderate protein deprivation in these patients likely occurs during episodes of poor glycemic control.

Energy expenditure in humans: effects of dietary fat and carbohydrate

1990 ◽  
Vol 258 (2) ◽  
pp. E347-E351 ◽  
Author(s):  
W. G. Abbott ◽  
B. V. Howard ◽  
G. Ruotolo ◽  
E. Ravussin
Keyword(s):  
Energy Expenditure ◽  
Dietary Fat ◽  
Weight Maintenance ◽  
Caloric Intake ◽  
Insulin Dependent Diabetes Mellitus ◽  
Whole Body ◽  
Dependent Diabetes Mellitus ◽  
Pima Indians ◽  
High Fat ◽  
High Carbohydrate

A high-dietary fat intake may be an important environmental factor leading to obesity in some people. The mechanism could be either a decrease in energy expenditure and/or an increase in caloric intake. To determine the relative importance of these mechanisms we measured 24-h energy expenditure in a whole body calorimeter in 14 nondiabetic subjects and in six subjects with non-insulin-dependent diabetes mellitus, eating isocaloric, weight-maintenance, high-fat, and high-carbohydrate diets. All subjects were Pima Indians. In nondiabetics, the mean total 24-h energy expenditure was similar (2,436 +/- 103 vs. 2,359 +/- 82 kcal/day) on high-fat and high-carbohydrate diets, respectively. The means for sleeping and resting metabolic rates, thermic effect of food, and spontaneous physical activity were unchanged. Similar results were obtained in the diabetic subjects. In summary, using a whole body calorimeter, we found no evidence of a decrease in 24-h energy expenditure on a high-fat diet compared with a high-carbohydrate diet.

Manipulation of dietary carbohydrate and muscle glycogen affects glucose uptake during exercise when fat oxidation is impaired by β-adrenergic blockade

2004 ◽  
Vol 287 (6) ◽  
pp. E1195-E1201 ◽  
Author(s):  
Theodore W. Zderic ◽  
Simon Schenk ◽  
Christopher J. Davidson ◽  
Lauri O. Byerley ◽  
Edward F. Coyle
Keyword(s):  
Glucose Uptake ◽  
Plasma Glucose ◽  
Muscle Glycogen ◽  
Fat Oxidation ◽  
Whole Body ◽  
Moderate Intensity ◽  
Glucose Turnover ◽  
Adrenergic Blockade ◽  
High Fat ◽  
Carbohydrate Diet

We have recently reported that, during moderate intensity exercise, low muscle glycogen concentration and utilization caused by a high-fat diet is associated with a marked increase in fat oxidation with no effect on plasma glucose uptake (Rd glucose). It is our hypothesis that this increase in fat oxidation compensates for low muscle glycogen, thus preventing an increase in Rd glucose. Therefore, the purpose of this study was to determine whether low muscle glycogen availability increases Rd glucose under conditions of impaired fat oxidation. Six cyclists exercised at 50% peak O2 consumption (V̇o2 peak) for 1 h after 2 days on either a high-fat (HF, 60% fat, 24% carbohydrate) or control (CON, 22% fat, 65% carbohydrate) diet to manipulate muscle glycogen to low and normal levels, respectively. Two hours before the start of exercise, subjects ingested 80 mg of propanolol (βB), a nonselective β-adrenergic receptor blocker, to impair fat oxidation during exercise. HF significantly decreased calculated muscle glycogen oxidation ( P < 0.05), and this decrease was partly compensated for by an increase in fat oxidation ( P < 0.05), accompanied by an increase in whole body lipolysis ( P < 0.05), despite the presence of βB. Although HF increased fat oxidation, plasma glucose appearance rate, Rd glucose, and glucose clearance rate were also significantly increased by 13, 15, and 26%, respectively (all P < 0.05). In conclusion, when lipolysis and fat oxidation are impaired, in this case by βB, fat oxidation cannot completely compensate for a reduction in muscle glycogen utilization, and consequently plasma glucose turnover increases. These findings suggest that there is a hierarchy of substrate compensation for reduced muscle glycogen availability after a high-fat, low-carbohydrate diet, with fat being the primary and plasma glucose the secondary compensatory substrate. This apparent hierarchy likely serves to protect against hypoglycemia when endogenous glucose availability is low.

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