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Biomedical subjects

J F Brun

Publications and source records attributed to J F Brun.

At least 55 records · Page 3Linked to original sources
PubMed1999

Insulin sensitivity measured with the minimal model is higher in moderately overweight women with predominantly lower body fat.

Lower-body obesity is associated with a lower incidence of diabetes and high values of HDL2 cholesterol and thus seems to have a metabolic profile opposite to upper-body obesity. We measured insulin sensitivity by the minimal model procedure in 20 lower-body overweight women (age 40.3+/-2.3 years, waist-to-hip ratio WHR 0.75+/-0.01, body mass index BMI 29.9+/-0.7 kg/m2), compared to 18 women with a similar degree of upper-body obesity (age 40.4+/-3years, WHR 0.91+/-0.02, BMI 29.4+/-0.7 kg/m2) and 28 control women matched for age and height. Insulin sensitivity and basal insulin effect were higher in lower-body obesity (11.2+/-0.2 min-1/[microU/ml]x 10(-4) and 0.8+/-0.2 min(-1) x 10(-2), respectively) compared to upper-body obesity (2.6+/-0.4, p < 0.001 and 0.3+/-0.05, p < 0.01) and controls (6.1+/-0.7, p < 0.02 and 0.5+/-0.07, p < 0.02). It is suggested that lower-body obesity could be associated with a reduced free fatty acids-induced inhibition of insulin action by the Randle mechanism. This study confirms that body fat distribution is a more relevant determinant than obesity itself in the pathogenesis of insulin resistance. Contrary to upper-body obesity, moderate lower-body overweight seems to be associated with high values on insulin sensitivity.

Adult↗
PubMed1999

Early hemorheologic aspects of overtraining in elite athletes.

A standardized questionnaire has been proposed by the French consensus group on overtraining of the Société Française de Médecine du Sport (SFMS) and allows the calculation of a 'score' that may help to quantify the early clinical symptoms of the overtraining syndrome in sportsmen submitted to a heavy training program. We investigated a possible relationship between this score and blood rheology in 36 male elite sportsmen (national level in football, volleyball and karate; age: 17-33 yr) who underwent a standardized check-up including biological measurements and an exercise-test. The overtraining score ranged between 0 and 21 items and was correlated with blood viscosity (r = 0.413, p < 0.02). This correlation was explained by a correlation of this score with plasma viscosity (r = 0.512, p < 0.01) and hematocrit (r = 0.387, p < 0.05). When subjects with a high score (>6) were compared to subjects with a lower score they appeared to have a higher blood viscosity at native (but not corrected) hematocrit (3.18 +/- 0.01 vs. 2.89 +/- 0.05 mPa.s, p < 0.02), explained by higher values in both plasma viscosity (1.39 +/- 0.02 vs. 1.31 +/- 0.02 mPa.s, p < 0.01) and hematocrit (42.8 +/- 0.45 vs. 41.1 +/- 0.44, p < 0.05). By contrast, there was no difference in RBC deformability and aggregation. Overtrained subjects have also lower levels of zinc (0.72 +/- 0.024 vs. 0.84 +/- 0.023 mg/l, p < 0.01), ferritin (55.1 +/- 7.3 vs. 92.3 +/- 9.4 ng/ml), and IGF-binding protein 3 (3.4 +/- 0.22 vs. 4.52 +/- 0.4 ng/ml). Neither zinc nor ferritin status were likely to explain the rheologic alterations since disturbances in zinc or iron are rather associated with abnormalities in erythrocyte deformability or aggregability. Therefore, the early signs of overtraining in elite sportsmen are associated with a hemorheologic pattern that suggests some degree of reversal of the 'autohemodilution' associated with fitness in athletes.

Adult↗
PubMed1999

Hemorheology of growth hormone-deficient adults.

Growth hormone deficiency (GHD) in adults results in alterations of body composition and metabolism associated with a lowered insulin sensitivity and an increased cardiovascular risk. Since hemorheologic disturbances (putative factors of vascular risk) are found in the insulin-resistance syndrome, we investigated blood rheology in 9 adults GHDs (5 men, 4 women; age 37.9+/-4.7 years; body mass index 30.23+/-3.2 kg/m2) compared with 23 lean controls and 37 controls matched for sex, age and body mass index. While this sample of GHDs exhibits the typical metabolic picture of this syndrome (upper body overweight with a waist-to-hip ratio at 0.91+/-0.07; low HDL cholesterol at 1.07+/-0.09 mmol x l(-1); low insulin sensitivity with the minimal model technique at 3.3+/-1.29 min(-1)/(microU/ml) x 10(-4)) they have similar values of blood viscosity at either native or corrected hematocrit, similar hematocrit, similar red cell rigidity viscometric index, similar red cell aggregation parameters than overweight matched controls. There is only a nonsignificant tendency for plasma viscosity to be higher in GHDs: this tendency becomes significant when women are considered alone (GHDs: 1.44+/-0.04 mPa.s; controls: 1.31+/-0.04 mPa.s, p<0.05) while it is no longer found in men. This study suggests that GHDs exhibit the classical hemorheological disturbances of non-GHD individuals with the same degree of obesity. There is no evidence for a further impairment of blood rheology associated with the specific metabolic and endocrine pattern of GHDs that may be involved in their increased vascular risk.

Adult↗
PubMed1999

[Insulin resistance: from clinical diagnosis to molecular genetics. Implications in diabetes mellitus].

Insulin resistance is observed in several diseases such as non insulin dependent diabetes mellitus (NIDDM) or polycystic ovarian syndrome (PCOS). To understand genetic determinism of this abnormality we have developed a multidisciplinary approach including selection of phenotypes with insulin resistance confirmed in vivo by minimal model of Bergman and characterization of cellular defects in insulin action on circulating erythrocytes and monocytes. Exploration of variability in candidate genes by direct sequencing in some genetic syndromes of severe insulin resistance and acanthosis nigricans (mainly the Type A syndrome) revealed mutations of the insulin receptor gene associated with major defects in insulin binding or kinase activity. In other rare genetic syndromes or patients affected by NIDDM or PCOS defects appear to be located at post-receptor level, where IRS (insulin receptor substrate) genes are the most attractive candidates. Prevalence of some allelic variants suggested a potential role of IRS genes in insulin resistance, although their involvement in the pathogenesis of NIDDM remains controversial. Genotype-phenotype correlations in first degree relatives of an index case caring the Type A syndrome, suggested that association of allelic variants of IRS-1 and IRS-2 with insulin receptor mutations contribute, by synergistic effects, to phenotypic expression of defects in signal transduction. These mechanisms through genetic epistasis, involving several genes in insulin action, fit better with the polygenic nature of current forms of NIDDM and represent a good model in the study of pathogenesis of insulin resistance.

Acanthosis Nigricans↗
PubMed1999

Effects of zinc supplementation on blood rheology during exercise.

We previously reported a higher blood viscosity at corrected hematocrit (45%) (explained by a higher value of erythrocyte rigidity) in football players with low serum zinc (Zn) and thus presumably Zn deficiency; subjects with low serum zinc had also an impairment in performance. This interventional study was undertaken in order to assess the effects of zinc supplementation (compared to placebo) on blood rheology and performance either at rest or during exercise. Ten male healthy volunteers (age: 26+/-1.3 yr; weight 67.9+/-2.24 kg; height 177+/-3 cm) received at random order either zinc (20 mg/day) and placebo, according to a double blind cross-over procedure, during seven days. In each case on the eighth day they performed a 25 min submaximal exercise-test. At rest blood viscosity at corrected hematocrit 45% (gamma = 1000 s(-1)) was lower after Zn (3.56+/-0.14 vs. 4.13+/-0.16 mPa.s, p = 0.009), explained by a lower RBC rigidity index 'k' according to Quemada's equation (1.65+/-0.07 vs. 1.84+/-0.08, p = 0.03). Hematocrit and plasma viscosity were unchanged, but RBC aggregation was decreased (laser retrodiffusion-derived aggregation time 'Ta' 3.52+/-0.51 vs. 2.75+/-0.59, p = 0.02). The increase in blood viscosity during exercise is lower after Zn than placebo. Blood viscosity at corrected hematocrit 45% remains unchanged during exercise after Zn, yet it increases after placebo. RBC rigidity index 'k' remains lower during exercise after Zn. The rating of perceived exertion (Borg's scale) at the 20th minute of exercise is lower after zinc (5.6+/-0.4 vs. 6.6+/-0.4, p = 0.008). This study confirms that Zn improves erythrocyte deformability, decreases the exercise-induced acute increase in blood viscosity, and improves exercise tolerance. Since Zn deficiencies are not unfrequent in sportsmen, these findings may be potentially relevant to sports nutrition.

Adult↗
PubMed1998

Increased blood viscosity in iron-depleted elite athletes.

Since iron deficiency is associated with abnormal erythrocyte rheology, we investigated relationships between plasma ferritin and blood rheology in 36 male elite sportsmen (age: 22.38+/-0.9 years). On the whole, ferritin was negatively correlated with blood viscosity (r = -0.36, p < 0.05). When 23 subjects with low ferritin levels suggesting mild iron deficiency were compared with 13 matched sportsmen with normal ferritin levels, iron-deficient sportsmen were shown to have a higher blood viscosity at 1000 s(-l) (3.17+/-0.09 vs. 2.85+/-0.06 mPas, p < 0.05), explained by a higher plasma viscosity (1.38+/-0.02 vs. 1.31+/-0.02 mPa s, p < 0.05), while hematocrit and RBC rigidity index Tk were similar in the two groups. RBC aggregability index M (4.59+/-0.58 vs. 2.95+/-0.43 mPas, p < 0.05) and M1 (8.46+/-0.58 vs. 6.07+/-0.55, p < 0.01) were higher in iron-deficient subjects. Serum zinc was lower in iron-deficient sportsmen (0.73+/-0.02 vs. 0.83+/-0.02 mg/l, p < 0.01), but the score of early signs of overtraining was higher in this group (10.84+/-1.61 vs. 4.08+/-1.11, p < 0.01). These data suggest that mild iron deficiency as commonly seen in athletes, before anemia occurs, is associated with an increase in plasma viscosity and RBC aggregation, together with an increased subjective feeling of exercise overload.

Adult↗
PubMed1998

Negative correlation between plasma fibrinogen and insulin sensitivity measured with the minimal model technique.

We aimed at investigating relationship between plasma fibrinogen and insulin sensitivity, which are two major determinants of metabolic Syndrome X (insulin resistance syndrome). We designed a prospective study of 27 non-diabetic, non-hypertensive subjects, presenting a wide range of body mass index BMI (10 men, 17 women; mean age+/-SEM: 35.9+/-2.2 years; BMI ranging from 21.1-45.2 kg/m2). Insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with iterative sampling. Fibrinogen levels were determined by the method of Clauss. The insulin sensitivity index SI (i.e., the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranged from 0.0009 to 16 x 10(-4) min(-1)/(microU/ml), with a mean value of 4.76+/-0.73 x 10(-4). Mean values of plasma fibrinogen were 3.33+/-0.13 g/l, ranging from 2.21 to 5.07 g/l. There were highly significant negative correlations between SI and the level of plasma fibrinogen (r = -0.61, p = 0.0007) and between the basal effect of insulin BIE and plasma fibrinogen (r = -0.521, p = 0.005). Basal insulin was positively correlated to fibrinogen (r = 0.386, p = 0.046). When we analysed the data using partial correlation analysis, the negative relation between SI and fibrinogen was maintained independently from BMI (r = -0.45, p < 0.05). These data establish a strong negative association between insulin sensitivity and fibrinogen, involved in the increased cardiovascular risk of metabolic Syndrome X.

Adult↗
PubMed1998

The triphasic effects of exercise on blood rheology: which relevance to physiology and pathophysiology?

The life-extending effects of regular exercise are related to a decrease in both coronary and peripheral vascular morbidity, associated with some improvements in cardiovascular risk factors. A possible link between the beneficial metabolic and hemodynamic effects of exercise could be blood rheology, which is markedly affected by exercise. We propose here a description of the hemorheological effects of exercise as a triphasic phenomenon. Short-term effects of exercise are an increase in blood viscosity resulting from both fluid shifts and alterations of erythrocyte rheologic properties (rigidity and aggregability). Increased blood lactate, stress, and acute phase play a role in this process. Middle-term effects of regular exercise are a reversal of these acute effects with an increase in blood fluidity, explained by plasma volume expansion (autohemodilution) that lowers both plasma viscosity and hematocrit. Long-term effects further improve blood fluidity, parallel with the classical training-induced hormonal and metabolic alterations. While body composition, blood lipid pattern, and fibrinogen improve (thus decreasing plasma viscosity), erythrocyte metabolic and rheologic properties are modified, with a reduction in aggregability and rigidity. On the whole, these improvements reflect a reversal of the so-called "insulin-resistance syndrome" induced by a sedentary lifestyle. Since impaired blood rheology has been demonstrated to be at risk for vascular diseases, the hemorheologic effects of exercise can be hypothesized to be a mechanism (or at least a marker) of risk reversal. This latter point requires further investigation. The physiological meaning of the triphasic pattern of exercise-induced alterations of blood rheology is uncompletely understood, but increased blood fluidity may improve several steps of oxygen transfer to muscle, as clearly demonstrated in hypoxic conditions. Increasing evidence emerges from the literature, that blood fluidity is a physiological determinant of fitness.

Exercise↗
PubMed1998

Fibrinogen is negatively correlated with aerobic working capacity in football players.

While it is well established that blood viscosity is decreased in sportsmen and related to fitness, the involvement of fibrinogen in this relationship is less well defined. Relationships among fitness, rheology and fibrinogen were investigated in 32 football players (age 17-33 years: 19 professionals and 13 leisure players). A submaximal 25 min exercise-test was performed and allowed the calculation of aerobic working capacity. Aerobic working capacity (W170 and VO2 max) was negatively correlated to fibrinogen (r = -0.531, p < 0.01 and r = -0.623, p < 0.01), while on the whole sample the correlation to viscosity and erythrocyte aggregation was not significant. When subjects were divided into two subgroups according to their plasma fibrinogen concentration, the aerobic working capacity (either expressed as W170 or VO2 max) is higher when plasma fibrinogen level is lower than 2.7 g/l. Thus, there is a highly significant negative correlation between fibrinogen and fitness in these sportsmen, independent of blood rheology. These data suggest that rheology and fibrinogen are to some extent separate determinants of an individual's fitness.

Adolescent↗
PubMed1998

Relationships among body composition, hemorheology and exercise performance in rugbymen.

We investigated relationships among body composition, blood rheology, and exercise performance in 14 rugbymen (19-31 yr, weight 65.8-109.2 kg, height 1.7-1.96 m, body mass index 21.7-33.1 kg/m2) who underwent a standardized submaximal exercise session on cycloergometer corresponding to 225 kJ over 30 min. The rheologic response to exercise was measured with the MT90 viscometer and the Myrenne aggregometer. Dehydration, evaluated by precision weighing, resulted in a loss of 360 to 973 g water, i.e., 1.69 to 4.32 g/kJ. This loss of water is not correlated to plasma volume contraction as assessed by the equation of Greenleaf. Hemorheologic changes are observed, but they are correlated neither to water loss, nor to plasma volume contraction. A 36% increase in blood viscosity (p < 0.01) is mainly explained by a red blood cell rigidification (p < 0.02), although hematocrit and plasma viscosity also increase (p < 0.01). Isometric adductor strength (specific ergometer) is correlated to erythrocyte flexibility (r = 0.680, p < 0.01). Red cell aggregability (Myrenne aggregometer) is correlated to fat mass measured by bioelectrical impedance (r = 0.634, p < 0.02). Aerobic working capacity index W170 is negatively correlated to the increase in plasma viscosity during exercise (r = -0.546, p < 0.05), suggesting that this event is less important in stronger individuals. This study shows that fat mass, even within a physiological range, is a determinant of erythrocyte aggregability, suggesting that training-induced alterations in body composition play a role in the specific hemorheologic profile of athletes. In addition, both erythrocyte flexibility and the magnitude of fluid shifts during exercise appear to be related to fitness in these sportsmen.

Adipose Tissue↗
PubMed1997

Identification of two novel insulin receptor mutations, Asp59Gly and Leu62Pro, in type A syndrome of extreme insulin resistance.

To elucidate genetic determinants of insulin resistance, we investigated insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) genes, in vitro IR function and in vivo insulin sensitivity in a family with Type A syndrome. Two missense IR mutations (Asp59Gly and Leu62Pro) found in the proband, resulted in reduction by 90% of insulin binding to erythrocytes, decreased receptor autophosphorylation and a dramatic reduction of insulin sensitivity. The proband and mother were heterozygote for Gly972Arg IRS-1 variant. Asp59Gly mutation, also carried by proband's brother with no consequence on insulin sensitivity, was inherited from the mother who is diabetic and insulin resistant and Leu62Pro was from the father. We conclude that severity of insulin resistance in the proband may be explained by the genetic condition of compound heterozygote for IR mutations while severe insulin resistance in the mother raises the possibility that other genetic factors, like IRS-1 polymorphisms, may contribute to the phenotypic expression of IR mutations.

Amino Acid Sequence↗
PubMed1997

Metabolic and hormonal responses during repeated bouts of brief and intense exercise: effects of pre-exercise glucose ingestion.

We investigated metabolic and hormonal responses during repeated bouts of brief and intense exercise (a force-velocity test; Fv test) and examined the effect of glucose ingestion on these responses and on exercise performance. The test was performed twice by seven subjects [27 (2) years] according to a double-blind randomized crossover protocol. During the experimental trial (GLU), the subjects ingested 500 ml of glucose polymer solution containing 25 g glucose 15 min before starting the exercise. During the control trial (CON), the subjects received an equal volume of sweet placebo (aspartame). Exercise performance was assessed by calculating peak anaerobic power (W(an,peak)). Venous plasma lactate concentration increased significantly during the Fv test (P < 0.001), but no difference was found between CON and GLU. Blood glucose first decreased significantly from the beginning of exercise up to the 6-kg load (P < 0.001) and then increased significantly at W(an,peak) and for up to 10 min during the recovery period (P < 0.001) in both CON and GLU. Insulin concentrations decreased significantly in both groups, but were higher at W(an,peak) in GLU compared with CON (P < 0.05). Glucagon and epinephrine did not change significantly in either group, but epinephrine was significantly lower in GLU after glucose ingestion (P < 0.05) and at W(an,peak) (P < 0.05). W(an,peak) was not significantly different between CON and GLU. In conclusion, blood glucose and insulin concentrations decreased during repeated bouts of brief and intense exercise, while blood lactate concentration increased markedly without any significant change in glucagon and epinephrine concentrations. Glucose ingestion altered metabolic and hormonal responses during the Fv test, but the performance as measured by W(an,peak) was not changed.

Adult↗
PubMed1997

[Interrelation of visceral fat and muscle mass in non insulin-dependent diabetes (type II): practical implications].

Insulin resistance, which is found in 85-95% of non-insulin-dependent diabetes mellitus (NIDDM) patients, results from three factors: genetic background (which has been widely investigated), nutritional status (mostly obesity and fat distribution) and exercise. Upper body obesity, which can be found in 85% of these subjects, can increase muscular insulin resistance through several mechanisms, the best known being a free fatty acid-induced decrease in intracellular free CoA/acylCoA that inhibits the stimulatory effect of insulin on glycolysis, glucose transport across cell membrane, and glycogen storage. However, muscle insulin resistance in NIDDM exists before adiposity and is likely to induce it. Actually, muscles of subjects at risk for NIDDM exhibit a very early defect in both glycogen storage ability and free fatty acid oxidation capacity that can impair fuel utilization and increase fat storage. Regular exercise induces muscular metabolic changes which can compensate for those diabetogenic defects and thus prove useful in the management of NIDDM. Moreover, exercise has been shown to prevent subjects at risk for NIDDM from developing overt diabetes.

Abdomen↗