Biomedical subjects

Jean-Frederic Brun

Publications and source records attributed to Jean-Frederic Brun.

5 recordsLinked to original sources

PubMed2006

Evaluation of insulin sensitivity and glucose effectiveness during a standardized breakfast test: comparison with the minimal model analysis of an intravenous glucose tolerance test.

There is a need for reliable measurements of insulin sensitivity (SI) simpler than the euglycemic hyperinsulinemic clamp or the intravenous glucose tolerance test (IVGTT), which could be used when the simpler surrogates based on fasting insulin (Ib) and glucose (Gb) lose their validity. Several evaluations of SI derived from oral glucose tolerance test (OGTT) or its physiologic form, the standardized breakfast test (SBT), have been proposed. We aimed at determining which SBT-derived measurements of SI give the best prediction of the values obtained with the minimal model analysis of an IVGTT. Twenty-eight subjects (23 females and 5 males; age, 44.3+/-0.6 years) with a wide range of glucose tolerance randomly underwent a hyperglucidic SBT and an IVGTT with minimal model analysis. Correlations of 35 indices (converted if appropriated into similar units) with IVGTT-derived SI were calculated, and the accuracy of the empiric formulas obtained with the 11 best predictions were evaluated with Bland-Altman plots. Subjects covered all the spectrum of SI between 0.19 and 21.3 min-1/(microU.mL-1)x10(-4). Eight procedures yielded satisfactory predictions of minimal model SI: (1) SI (from Matsuda's composite index)=-1.24+65/(IbGbImGm)-0.5; (2) SI=1.89+2690/(IbGbImGm); (3) SI (from Bennett's index)=-2.93+5.16/(log Ibxlog Gb); (4) SI (from Sluiter's index)=0.2+2400/(IpGp); (5) SI=-8.54+38.4/(Belfiore's ISI index); (6) SI (from Cederholm's formula)=76/(Gm log Im); (7) SI=0.248+0.947/GbIm; (8) SI (from Mari's "oral glucose insulin sensitivity" index)=oral glucose insulin sensitivity/Ip; (9) Caumo's model. Glucose effectiveness Sg can also be accurately predicted by the following formula: Sg=2.921e-0.185(G60- Gb) (Ip=insulin peak; Gp=glucose peak; Ia=insulin area; Ga=glucose area; G60=glycemia at 60 minutes). The hyperglucidic SBT can provide accurate evaluations of SI and Sg, either by elaborated models or by simple empiric formulas.

Adolescent↗

PubMed2006

Hemorheologic effects of low intensity endurance training in sedentary patients suffering from the metabolic syndrome.

Hemorheologic effects of exercise training ("hemorheologic fitness") are very different according to the mode and the intensity of this training. We previously reported that low intensity endurance training in sedentary patients suffering from the metabolic syndrome sumultaneously improved blood rheology, body composition and lipid oxidation at exercise. We aimed at analyzing the link among these improvements in 24 patients submitted to a 2 months targeted training designed for increasing exercise lipid oxidation. Variations of whole blood viscosity at high shear rate (etab 1000 s(-1)) were explained here by two statistically independent determinants: hematocrit and red cell rigidity. etab decreased in 16 subjects, but increased in 8, due to a rise in hematocrit. Changes in RBC rigidity appeared to reflect weight loss and decrease in LDL cholesterol. Plasma viscosity was related to cholesterol and its training-induced changes are related to those of VO2 max ) but not to lipid oxidation. Red cell aggregability (Myrenne) reflected both the circulating lipids (Chol, HDL and LDL) and the ability to oxidize lipids at exercise. Factors associated to a post-training decrease in aggregability (M1) were weight loss and more precisely decrease in fat mass, improvement in lipid oxidation, rise in HDL-Chol, and decrease in fibrinogen. On the whole the major determinant of hemorheologic improvement was an increase in cardiorespiratory fitness (VO2 max ), correlated with a decrease in plasma viscosity, rather than an improvement in lipid metabolism, although RBC aggregability and deformability exhibited clear relationships with lipid metabolism. For which reason Hct increased in 30% of the patients during this kind of training remains unclear.

Aged↗

PubMed2005

Relationship between blood lactate concentration and substrate utilization during exercise in type 2 diabetic postmenopausal women.

Increased blood lactate concentration and alterations of substrate utilization have been shown to be partly involved in development of insulin resistance in obese and type 2 diabetic patients. As blood represents the first great distribution space and participates to lactate exchange in whole body, we investigated lactate transport in red blood cells at rest and the potential relationships between elevated blood lactate and substrate utilization in 7 obese controls and 7 obese type 2 diabetic postmenopausal women during an incremental exercise test. Blood samples were collected at rest, 30%, 50%, and 60% of maximal power and at 8 and 20 minutes of recovery time. Baseline lactatemia and its increase during exercise were higher in the diabetic group (P < .05). We found a negative correlation between basal and 30% maximal power lactatemia and 2 indexes of substrate utilization (crossover point: r = -0.79, r = -0.82 and maximal lipid oxidation point: r = -0.83, r = -0.80; P < .05) in diabetic group only. Furthermore, there were positive correlations between the affinity constant, maximal velocity transport, and basal lactate level in diabetic subjects (r = 0.91 and r = 0.73, respectively; P < .05). These results show that the elevation of blood lactate is associated with a greater carbohydrate oxidation in type 2 diabetes, but the mechanisms underlying the alteration of substrate utilization need to be clarified. Furthermore, increased lactate levels cannot be explained by alterations of lactate transport in red blood cells, but it could affect monocarboxylate transporter 1 properties.

Diabetes Mellitus, Type 2↗

PubMed2004

Hemorheological aspects of the metabolic syndrome: markers of insulin resistance, obesity or hyperinsulinemia?

The metabolic syndrome is a major health problem in western countries, due to the deleterious metabolic consequences of sedentarity and rich diet in the large part of the population who exhibits the so-called "thrifty phenotype". This syndrome, which is at high risk for diabetes and atherothrombosis is associated with hemorheologic abnormalities. Initially, insulin resistance was considered as the core of the syndrome. However, it becomes clear that the syndrome is a cluster in which the combined effects of obesity, insulin resistance, and hyperinsulinemia can be inconstantly associated. Thus, we investigated in 157 nondiabetic subjects (53 males and 104 females, age 35.6+/-1.1 yr, mean BMI 29.2+/-0.6 kg/m2) the respective importance of each of these factors. Subjects were divided in 6 groups according to BMI (cut-off point 25 kg/m2) and insulin sensitivity (SI) measured with the minimal model (lowest quartile SI<1.1 min(-1)/(microU/ml) x 10(-4), highest quartile SI>9.5, middle zone between 1.1 and 9.5). Results show that whole blood viscosity at high shear rate is higher in obese subjects (p<0.01). Plasma viscosity is also higher in obese subjects 1.41+/-0.02 vs 1.34+/-0.012 (p<0.01), and, in addition, in lean subjects, is lower when SI is in the upper quartile. RBC rigidity index "Tk" is higher in obese subjects. A worsening effect of insulin resistance (SI<1.1) on Tk is found only in obese subjects. The aggregability index "M1" is increased when SI<1.1 in both obese and nonobese subjects. No clear effect of either SI or obesity on hematocrit is observed. On the whole, obesity and insulin resistance both impair blood rheology by acting on red cell rigidity and plasma viscosity. Whole blood viscosity at high shear rate reflects rather obesity than insulin resistance. Myrenne "M1" aggregation is rather a marker of hyperinsulinemia. Thus, the hemorheologic picture of the metabolic syndrome is far to be only a reflect of insulin resistance alone.

Adult↗

PubMed2004

Reciprocal relationships between blood lactate and hemorheology in athletes: another hemorheologic paradox?

Blood lactate increases during exercise. Although this increase was classically interpreted as a "Pasteur-like effect" resulting from anaerobiosis, it is now clear that it mostly results from a shift in the balance of oxidation of substrates in the muscle, with carbohydrate becoming the predominant fuel. However, we have repeatedly observed that the rise in blood lactate during exercise is correlated to blood viscosity and red cell aggregation. More recently we investigated this issue with the modelling of postexercise lactate kinetics, that allows a fair evaluation of lactate production by muscles (gamma1) and lactate disappearance (gamma2). Postexercise red cell aggregation (Myrenne M1) appears to be correlated to gamma2. Thus microcirculatory adaptations influenced by red cell aggregation may influence lactate disposal, adding its effect to that of the balance between carbohydrates and fat. On the other hand, the rise in blood lactate seems to induce some alterations in erythrocyte rheology at exercise. Correlations between its concentrations during exercise and erythrocyte rigidity support the concept that lactate, at least when it rises above the 4 mmol.l(-1) threshold impairs red cell deformability. Moreover, it seems that endurance training influences erythrocyte response to lactate. While lactate did not in vitro affect erythrocyte aggregation, it impaired (as expected) erythrocyte deformability in sedentary subjects but it (unexpectedly) improved it in trained subjects. This difference may be due to training-induced adaptations in erythrocyte metabolism, including transmembrane transfer via monocarboxylate transporters which show marked alterations in this context. This specific training-induced pattern of response to lactate may provide an alternative explanation to the exercise-induced arterial hypoxemia that occurs in such athletes.

Blood Viscosity↗