PubMed Health⌕ Search

Biomedical subjects

B Vergès

Publications and source records attributed to B Vergès.

At least 19 recordsLinked to original sources
PubMed2002

High-density lipoprotein apolipoprotein A-I kinetics in obese insulin resistant patients. An in vivo stable isotope study.

AIMS/HYPOTHESIS: Mechanisms responsible for the decreased high-density lipoprotein (HDL) cholesterol level associated with insulin resistance in obese patients are not clearly understood. To determine the influence of insulin resistance at an early stage on HDL metabolism, we performed a stable isotope kinetic study of apolipoprotein (apo) A-I, in five obese insulin resistant women with normal fasting triglycerides and without impaired glucose tolerance, and in five age-matched control women. METHODS: Each subject received a 16 h constant infusion of L-[1-(13)C]leucine at 0.7 mg/kg/h following a primed bolus of 0.7 mg/kg. RESULTS: ApoA-I fractional catabolic rate (FCR) was significantly increased in insulin-resistant women compared to controls (0.316+/-0.056 vs 0.210+/-0.040 per day, P<0.01), indicating a significant 50% increase of apoA-I catabolism, leading to an important reduction of plasma apoA-I residence time (3.25+/-0.59 vs 4.92+/-1.11, P<0.01). ApoA-I production rate tended to be higher in insulin resistant women than in controls (364+/-77 vs 258+/-60 mg/l/day, P=0.13), but the difference was not statistically significant. ApoA-I FCR was correlated with triglycerides during the fed state (r=0.69; P=0.026) and HDL triglycerides-esterified cholesterol ratio (r=0.73; P=0.016), suggesting that alteration of apoA-I metabolism in insulin resistance may be partly related to HDL enrichment in triglycerides. CONCLUSIONS: Our kinetic study shows that patients, at an early stage of insulin resistance (without impaired glucose tolerance nor fasting hypertriglyceridaemia), already have a significant alteration of apoA-I metabolism (increased apoA-I catabolism), which is consistent with the increased risk of atherosclerosis in this population.

Adult↗
PubMed2002

The impact of prandial glucose regulation in practice.

Post-prandial hyperglycaemia, which occurs early in the development of impaired glucose tolerance and Type 2 diabetes mellitus (T2DM), has been receiving increased attention recently. Post-prandial hyperglycaemia is likely to promote or aggravate fasting hyperglycaemia and contributes entirely to HbA1c elevation, which is associated with microvascular and macrovascular complications in people with T2DM. Moreover, post-prandial hyperglycaemia is coupled with coagulation activation and may be associated with an increased risk of cardiovascular disease in people with or without diabetes. For these reasons, reduction of post-prandial hyperglycaemia is an important target in patients with impaired glucose tolerance or T2DM. Several treatments have therefore been developed to reduce post-prandial hyperglycaemia; of these, repaglinide, a prandial glucose regulator taken orally before each meal, is now available. Drugs that reduce post-prandial hyperglycaemia significantly also decrease HbA1c (up to 2% with repaglinide) and fasting glucose concentrations (up to 3.9 mmol/l with repaglinide), with consequent decreases in coagulation activation and, in some studies, post-prandial lipidaemia. In clinical trials in patients with T2DM, repaglinide significantly reduced 2-hr post-prandial glucose concentrations and significantly reduced the risk of hypoglycaemia, compared with sulphonylureas, especially when participants missed or postponed a meal. Treatment with the prandial glucose regulator repaglinide allows patients with T2DM to have a more flexible lifestyle, which is likely to improve their quality of life and compliance.

Blood Glucose↗
PubMed2001

[Blood lipid abnormalities during treatment with protease inhibitors].

HYPERLIPIDEMIA: HIV-1 protease-inhibitors therapy is associated with increased levels of triglycerides, LDL-cholesterol and Lp(a). But the understanding of hyperlipidaemia occurring in patients treated with HIV-1 protease-inhibitors is not easy since HIV infection itself is associated with lipid abnormalities and since HIV-1 protease-inhibitors therapy is also responsible for the development of a lipodystrophy syndrome (insulin resistance) which may influence lipid metabolism. However, many data indicate that HIV-1 protease-inhibitors therapy itself modifies significantly lipid metabolism. UNDERLYING MECHANISMS: The mechanisms involved in HIV-1 protease-inhibitors induced hyperlipidaemia are still unclear. HIV-1 protease-inhibitors could bind to LRP (Low density lipoprotein receptor Related Protein), impairing hepatic chylomicron-remnants and VLDL uptake. They could interact with the retinoid X receptor (RXR), which functions as a heterodimer with PPAR (Peroxisome Proliferator Activator Receptor). HIV-1 protease-inhibitors could also modify lipoprotein metabolism through cytokines.

HIV Infections↗
PubMed2001

[Hypercalcemia in the elderly].

UNLABELLED: A COMMON FINDING: Hypercalcemia is not rare among elderly patients. Hyperparathyroidism and neoplasia are the most frequent causes of hypercalcemia in old patients. Symptoms due to hypercalcemia are usually non specific in old subjects, leading to consider easily this diagnosis and to measure plasma calcium level. DIAGNOSIS: Biological diagnosis of hypercalcemia is not always obvious in old patients because of frequently decreased plasma albumin levels leading to lower plasma total calcium level. Thus, it is always necessary to calculate plasma total calcium level corrected by albumin in order not to underestimate hypercalcemia in elderly subjects. PROGNOSIS: The short-term risk of hypercalcemia is acute hypercalcemia, which may be lifethreatening. The long-term risk of hypercalcemia is renal failure. TREATMENT: When hypercalcemia is due to primary hyperparthyroidism, the treatment of choice is surgery. However, for old patients with high surgical risk surgery with local anesthesia or ultrasonically guided percutaneous ethanol injection into parathyroid adenoma can be proposed.

Age Factors↗
PubMed2001

Hyperparathyroidism in multiple endocrine neoplasia type I: surgical trends and results of a 256-patient series from Groupe D'etude des Néoplasies Endocriniennes Multiples Study Group.

The French and Belgian GENEM study group's multiple endocrine neoplasia type I (MEN-I) database was used to evaluate trends in clinical presentation, surgical treatment of primary hyperparathyroidism (pHPT) (n = 245), and prognostic factors for hypercalcemia correction among 256 MEN-I cases. The patients were retrieved through the GENEM network from various Belgian and French institutions with the help of genetics laboratories. Among the 245 pHPT patients (96%), 42% were men. The mean age at the time of diagnosis was 39.5 +/- 13.3 years. Trends were studied for three periods: before 1986, from 1986 to 1990, and thereafter. After 1990 MEN-I patients were more often diagnosed with isolated pHPT (8%, 11%, 28%, for the three periods, respectively; p = 0.002); it was seen more often in screened patients (31%, 28%, 53%; p = 0.001), more often among those in already known MEN-I families (64%, 45%, 72%; p = 0.005), and among those with lower preoperative calcemia (2.93, 2.87, 2.79 mmol/L; p = 0.001). The age at pHPT diagnosis remained constant throughout the study. The percentage of cervical explorations dropped during the entire study (87%, 87%, 53%; p < 0.0001). After 1985 the percentage of subtotal parathyroidectomies increased (25%, 59%, 51%; p = 0.0004). Pathology disclosed more hyperplasias (59%, 85%, 74%; p = 0.008). Postoperative hypercalcemia decreased (47%, 15%, 19%; p < 0.0001); and postoperative hypocalcemia increased nonsignificantly (5%, 15%, 15%; p = 0.1). Subtotal parathyroidectomy [odds ratio (OR) 13], no MEN-I family background (OR 3), and the most recent study period (> 1985) (OR 3) were significant predictive factors of hypercalcemia correction according to the multivariate analysis. This is the first multicentric study on the management of MEN-I-related pHPT. Immediate postoperative hHPT cure increased, but only 80% of the operated patients were cured after 1990. Fifteen percent were hypocalcemic. Because MEN-I-related hHPT cure remains difficult to achieve, we advocate that subtotal parathyroidectomies be performed in specialized centers.

Adult↗
PubMed2001

[Statins and diabetic hyperlipidemia].

Type 2 diabetic patients show frequent lipid abnormalities characterized by increased triglyceride and decreased HDL-cholesterol levels, but also by qualitative and metabolic abnormalities of all lipoproteins (VLDL, IDL, LDL et HDL). Treatment of diabetic hyperlipidemia is important in order to reduce the incidence of cardiovascular events, which is high in type 2 diabetes. Treatment with statins is recommended when hypercholesterolemia is associated with diabetes. But the efficacy of statins in the treatment of the typical diabetic hyperlipidemia (hypertriglycerideùmia, decreased HDL-cholesterol) remains to be demonstrated, since their effects on triglycerides and HDL-cholesterol is moderate. However, the new statins (cerivastatine, atorvastatine), which are more powerful to reduce hypertriglyceridemia could be useful for the treatment of diabetic hyperlipidemia. But, only on going clinical trials with statins in diabetic patients will be able to precise their possible efficacy on the prevention of cardiovascular disease.

Cholesterol, HDL↗
PubMed2001

[Insulin sensitiviy and lipids].

Insulin plays a central role in regulation of lipid metabolism, with different sites of action. In the adipose tissue, insulin inhibits lipolysis via an inhibition of the lipase, leading to reduce the flux of free fatty acids into the circulation. Insulin inhibits the VLDL production by the liver. Insulin is a potent activator of the lipoprotein lipase, promoting the catabolism of triglyceride-rich lipoproteins (Chylomicrons, VLDL). insulin promotes the clearance of LDL. Indeed, insulin stimulates apoB/E receptor (LDL-receptor) activity and enhances LDL degradation via the LDL-receptor pathway. Insulin also plays an important role in HDL metabolism since it activates LCAT activity, it reduces PLTP activity and modulates the hepatic triglyceride lipase activity. Because of the key role of insulin in lipid metabolism, we can easily understand that all diseases with impaired insulin action, such as insulin resistance or diabetes mellitus, will be characterized by important lipid abnormalities, which are important factors responsible for the increased cardiovascular risk in the patients.

Adipose Tissue↗
PubMed2001

Analysis of the postprandial lipid metabolism: use of a 3-point test.

OBJECTIVES: The oral fat load tests used to study postprandial lipemia are complex and costly and time consuming. A simplified fat load test could be more convenient and more appropriate in routine clinical practice because of the number of lipid determinations required. RESEARCH DESIGN AND METHODS: We evaluated the capacity of a postprandial test model that reduced the number of blood samples taken in thirty three normal weight controls and 17 normotriglyceridemic obese patients (study 1), 10 normolipidemic type 2 diabetic patients and 7 healthy controls (study 2), and 10 hyperlipidemic type 2 diabetic patients studied before and after hypolipidemic therapy (study 3). Blood samples were taken before and up to 8 hours after giving the oral fat load containing retinol. Triglyceride (TG) and retinyl palmitate (RP) concentrations in the plasma, chylomicrons (CM) and non-chylomicron (nCM) fractions were measured. Postprandial lipid responses using conventional area under the curves (AUCc using 5 to 7 lipid determinations) were compared to a 3-point test that uses only three sample points to predict the area under the curve (AUCp: triglycerides at T0, triglycerides at average peak-time (T4), and triglycerides at T8). RESULTS: The AUCc and AUCp for triglycerides and retinyl palmitate were highly correlated in each of the groups and whatever the lipid subfraction (r=0.664 - 0.995, p<0.0001). When incremental AUC (iAUC) were used, the coefficients of correlation for triglycerides remained highly significant between iAUCc and iAUCp (r=0.718 - 0.979, p<0.01 - 0.0001). The same trend of differences was found between cases and controls when AUCp was used instead of AUCc. The means of differences between AUCc and AUCp for triglyceride values were small (0.34 - 0.74 mmol/L.h), and the confidence intervals were acceptable considering the range of the AUCs values (5.60 to 79.8 mmol/L.h for plasma triglycerides). CONCLUSIONS: We found that data obtained with a simplified model of AUC using only 3 points to analyse postprandial lipemia are well correlated with those obtained by conventional AUC, and that the AUCp allows to the same conclusions as AUCc when healthy subjects were compared to patients with altered postprandial metabolism. Thus AUCp may be a good evaluation of the AUCc, and the simplified 3-point protocol may well be used and suitable for studies on large groups of subjects who are eligible for an oral fat load test.

Area Under Curve↗
PubMed2001

Increased plasma apoA-IV level is a marker of abnormal postprandial lipemia: a study in normoponderal and obese subjects.

Plasma apolipoprotein A-IV (apoA-IV) levels are found elevated in hypertriglyceridemic patients. However, the relationship between plasma apoA-IV level and postprandial lipemia is not well known and remains to be elucidated. Thus, our objective was to study the relationship between plasma apoA-IV and postprandial TG after an oral fat load test (OFLT). Plasma apoA-IV was measured at fast and during an OFLT in 16 normotriglyceridemic, normoglucose-tolerant android obese subjects (BMI = 34.6 +/- 2.9 kg/m(2)) and 30 normal weight controls (BMI = 22.2 +/- 2.3 kg/m(2)). In spite of not statistically different fasting plasma TG levels in controls and obese patients, the former group showed an altered TG response after OFLT, featuring increased nonchylomicron TG area under the curve (AUC) compared with controls (516 +/- 138 vs. 426 +/- 119 mmol/l x min, P < 0.05). As compared to controls, obese patients showed increased apoA-IV levels both at fast (138.5 +/- 22.4 vs. 124.0 +/- 22.8 mg/l, P < 0.05) and during the OFLT (apoA-IV AUC: 79,833 +/- 14,281 vs. 68,176 +/- 17,463 mg/l x min, P < 0.05). Among the whole population studied, as among the control and obese subgroups, fasting plasma apoA-IV correlated significantly with AUC of plasma TG (r = 0.60, P < 0.001), AUC of chymomicron TG (r = 0.45, P < 0.01), and AUC of nonchylomicron TG (r = 0.62, P < 0.001). In the multivariate analysis, fasting apoA-IV level constituted an independent and highly significant determinant of AUC of plasma TG, AUC of chymomicron TG, AUC of nonchylomicron TG, and incremental AUC of plasma TG. In conclusion, we show a strong link between fasting apoA-IV and postprandial TG metabolism. Plasma fasting apoA-IV is shown to be a good marker of TG response after an OFLT, providing additional information on post-load TG response in conjunction with other known factors such as fasting TGs.

Adult↗
PubMed2000

Significant improvement of apolipoprotein B-containing lipoprotein metabolism by insulin treatment in patients with non-insulin-dependent diabetes mellitus.

AIMS/HYPOTHESIS: Patients with Type II (non-insulin-dependent) diabetes mellitus have multiple abnormalities in apolipoprotein B (apoB)-containing lipoprotein metabolism. These abnormalities are likely to play an important part in the development of premature atherogenesis in these patients. This stable isotope kinetic experiment was designed to study the effect of insulin therapy on apoB metabolism in poorly controlled Type II diabetic patients. METHODS: Using L-[1-13C] leucine, we studied apoB metabolism in five control subjects without insulin resistance and in six poorly controlled Type II diabetic patients before and 2 months after the introduction of insulin therapy. RESULTS: Insulin treatment induced a decrease of very low density lipoprotein apoB plasma concentration [121 +/- 42 vs 158 +/- 91 mg.l-1, p < 0.05 (control subjects: 48 +/- 20)], related to an increased catabolism of very low density lipoprotein towards intermediate density lipoprotein or low density lipoprotein [0.20 +/- 0.08 vs 0.14 +/- 0.07 pool.h-1, p < 0.05 (control subjects: 0.36 +/- 0.10)]. On the other hand, insulin treatment induced an acceleration of intermediate density lipoprotein apoB turn-over without changing its plasma concentration [77 +/- 37 vs 61 +/- 18 mg.l-1, (control subjects: 17 +/- 3)], by increasing both its production rate [22.6 +/- 9.2 vs 18.2 +/- 9.6 mg.l-1.h-1, p < 0.05 (control subjects: 18.4 +/- 3.2)] and its catabolic rate towards low density lipoprotein [0.34 +/- 0.22 vs 0.22 +/- 0.16 pool.h-1, p < 0.05 (control subjects: 1.02 +/- 0.13)]. Likewise, insulin treatment increased low density lipoprotein apoB production rate [20.2 +/- 7.4 vs 16.9 +/- 7.7 mg.l-1.h-1, p < 0.05 (control subjects: 16.9 +/- 2.3)] and restored a normal low density lipoprotein apoB fractional catabolic rate [0.022 +/- 0.004 vs 0.018 +/- 0.004 pool.h-1, p < 0.05 (control subjects: 0.025 +/- 0.004)], resulting in a constant low density lipoprotein apoB plasma concentration [965 +/- 485 vs 984 +/- 558 mg.l-1 (control subjects: 699 +/- 106)]. CONCLUSION/INTERPRETATION: Insulin treatment in Type II diabetes induces profound metabolic modifications of lipoprotein, resulting in significant decrease of the intravascular residence time of very low density lipoprotein, intermediate density lipoprotein and low density lipoprotein particles. This is likely to make these particles less harmful.

Apolipoproteins B↗
PubMed2000

[Treatment of parathyroid adenomas with ethanol injection under ultrasonographic guidance].

STUDY OBJECTIVE: The objective of this retrospective study was to report the results of ethanol injection in parathyroid adenomas. PATIENTS AND METHOD: Since 1988, 31 patients with inoperable primary hyperthyroidism have been treated by ultrasound-guided percutaneous ethanol injection into the adenoma. The main surgical contraindications were heart failure (n = 12) and age over 85 years (n = 11). Plasma calcium and PTH were measured 48 hours after ethanol injection and during subsequent follow-up. RESULTS: Patients had one to three ethanol injections. With a mean 5-year follow-up, total success with normal plasma calcium and PTH levels was achieved in 20 patients (64.5%), 4 of whom underwent another ethanol injection after 1 to 3 years. Partial success with correction of plasma calcium only was achieved in 9 patients (29%) resulting in an obvious clinical benefit. Failure was observed in 2 patients (6.5%) with nodular goiter, probably due to incorrect localization of the adenoma. Treatment was always well tolerated and no major side effect was observed. CONCLUSION: Ultrasound-guided percutaneous ethanol injection of parathyroid adenoma is effective in most cases of hyperparathyroidism and very useful in patients with a high surgical risk. The need for precise ultrasound localization of the adenoma is the main limitation of this treatment.

Adenoma↗
PubMed2000

Inefficiency of insulin therapy to correct apolipoprotein A-I metabolic abnormalities in non-insulin-dependent diabetes mellitus.

Non-insulin-dependent diabetes mellitus (NIDDM) is associated with low high density lipoprotein (HDL) cholesterol and apoA-I, related to an increased apoA-I fractional catabolic rate. This stable isotope kinetic experiment, using L-[1-(13)C] leucine, was designed to study the effect of insulin therapy on HDL apoA-I and A-II metabolism in poorly controlled NIDDM patients. A kinetic study was performed in five control subjects and in six NIDDM patients before and two months after the introduction of insulin therapy. ApoA-I and A-II were modelled using a monoexponential function. Insulin treatment was able to correct neither the low HDL apoA-I concentration observed in NIDDM patients (1.14+/-0.19 vs. 1.16+/-0. 12 g l(-1) (controls: 1.33+/-0.14)), nor the HDL apoA-I hypercatabolism (0.39+/-0.11 vs. 0.34+/-0.05 pool d(-1), (controls: 0.23+/-0.01, P< 0.01)). HDL apoA-I production rate was increased in NIDDM patients compared to control subjects and was not modified by insulin (0.45+/-0.12 vs. 0.39+/-0.08 g d(-1) l(-1), (controls: 0. 31+/-0.04, P< 0.05)). HDL apoA-II kinetic parameters were initially not significantly different between NIDDM patients and control subjects, and were not modified by insulin. The decreased insulin sensitivity, assessed by the insulin suppressive test, was not modified by insulin therapy in NIDDM patients. HDL apoA-I fractional catabolic rate was significantly correlated to HDL triglyceride/cholesteryl ester and triglyceride/protein ratios, which were significantly higher in NIDDM patients than in controls and were not modified by insulin therapy. The persistence of insulin resistance and of high neutral lipid exchanges between triglyceride rich lipoproteins and HDL in insulin-treated NIDDM patients probably explain the inefficiency of insulin therapy to correct HDL apoA-I metabolic abnormalities.

Adult↗
PubMed2000

Relationship between altered postprandial lipemia and insulin resistance in normolipidemic and normoglucose tolerant obese patients.

OBJECTIVE: Although there are changes in the postprandial lipid responses of obese patients, these are closely associated with high fasting triglycerides (TG). This study of 17 normotriglyceridemic, normoglucose-tolerant android obese subjects (body mass index, BMI = 34.3 +/- 3.1 kg/m2) and 33 normal-weight controls (BMI = 21.8 +/- 1.6 kg/m2) was done to examine their postprandial responses to an oral fat loading test containing retinol (890 calories, 85% fat) and to evaluate the possible association between clinical and biological features of obesity and/or insulin resistance and postprandial lipemia. SUBJECTS AND MEASUREMENTS: Blood samples were taken before giving the fat load and at 2,3,4,5,6 and 8 h after it. Insulin sensitivity was assessed using HOMA, and TG and retinyl palmitate (RP) in the plasma, chylomicrons and non-chylomicron fractions were measured each time. RESULTS: The areas under the curves (AUC) of chylomicron TG for the obese and controls were not different, indicating adequate lipolytic activity. By contrast, the AUC for non-chylomicron TG was significantly greater in the obese than in the controls (512 +/- 135 vs 429 +/- 141 mmol/lmin, P < 0.01). In addition, the AUC for RP in this same fraction was significantly lower in the obese than in the controls (103 +/- 55 vs 157 +/- 88 mg/l min, P < 0.05), suggesting that the TG from endogenous lipoproteins accounted for most of the increase in TG in the non chylomicron fraction. Parameters related to obesity showed no relationship with these postprandial abnormalities, whereas HOMA, which discriminated between the groups, partly explained (r2= 23%, P < 0.01) the significant increase in non-chylomicron TG. CONCLUSIONS: Android obese patients with a fasting TG in the normal range and not different from the fasting TG of lean controls had an abnormal postprandial lipemia response, indicated by a significantly greater TG in the non-chylomicron subfraction than in controls. These alterations may be partly due to postprandial changes in endogenous lipoproteins as a consequence of insulin resistance.

Adult↗
PubMed2000

Metabolic abnormalities of apolipoprotein B-containing lipoproteins in non-insulin-dependent diabetes: a stable isotope kinetic study.

BACKGROUND: Kinetic abnormalities of apolipoprotein B (apoB)-containing lipoproteins in noninsulin-dependent diabetes mellitus (NIDDM) remain poorly understood. To get further insight into these abnormalities we performed a stable isotope kinetic experiment comparing the metabolism of apoB-containing lipoproteins in moderately severe NIDDM patients and healthy control subjects. METHODS: The study was performed in the fed state. Subjects underwent a primed infusion of 0.7 mg kg(-1) of L-[1-(13)C]leucine followed by a 16-h constant infusion of 0.7 mg kg(-1) h(-1). [13C]Leucine enrichment in apoB was measured by gas chromatography/combustion/isotope ratio mass spectrometry. RESULTS: In NIDDM patients, we observed a 3.49- and 4.52-fold increase of very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) apoB plasma concentrations, respectively (P<0.01). VLDL apoB production was increased by 41% (P<0.05) and fractional catabolic rate towards IDL and low-density lipoprotein (LDL) was decreased by 61% (P<0.05). The increased IDL apoB plasma concentration was also related to a major catabolic defect (-78%; P<0.01). For most patients, plasma LDL apoB concentration was comparable to that of controls. Nevertheless, LDL apoB metabolism was impaired in NIDDM subjects, with both a decreased LDL catabolic rate (-28%; P<0.05) and a trend towards a diminished synthesis. CONCLUSION: NIDDM is associated with multiple apoB metabolism abnormalities that are potentially atherogenic. In addition to the increased number of circulating VLDL and IDL particles, the increased residence time observed on all apoB-containing lipoproteins may promote the development of atherosclerotic lesions, by potentiating their oxidizability.

Adult↗
PubMed2000

[Specific factors of diabetes in the rehabilitation of coronary patients].

This prospective controlled trial included two groups of subjects with coronary artery disease: one of 33 patients with non-insulin-dependent diabetes mellitus (6 females and 27 males, mean age 57 +/- 9 years, left ventricular ejection fraction of 56 +/- 14%) and the control group of 33 subjects without diabetes (3 females and 33 males, mean age of 57 +/- 11 years, LVEF of 58 +/- 11%). Before training heart rate was faster for patients with diabetes at rest (72 +/- 11 vs 66 +/- 81 bpm, p = 0.03) and at the end of the stress test (127 +/- 15 versus 118 +/- 18 bpm, p = 0.03). After rehabilitation, resting heart rate and peak heart rate were similar. However cardiovascular capacities improvement was better in subjects without diabetes mellitus, especially concerning peak VO2 (28.98 +/- 8.88 versus 22.78 +/- 6.28 mL/min/kg, p < 0.01) and mechanical power (138 +/- 48 versus 118 +/- 23 watts, p < 0.01). Two groups were retrospectively distinguished among diabetic patients: one group of 17 patients showing a VO2 improvement superior to 5% and a second group non improved (VO2 < 5%). For the second group the two selective factors were higher fasting glycemia (1.83 +/- 0.75 versus 1.31 +/- 0.38 g/L, p = 0.01) and higher hemoglobin A1C (8.05 +/- 2.04 vs 6.62 +/- 1.03%, p = 0.02). Heart rate variability was not significantly different for these two groups: changes in autonomic nervous system cannot explain resistance of diabetic subjects to training. On the other hand, principal aim must be the equilibrium of glycemia in the management of diabetes.

Aged↗
PubMed1999

Delayed changes in postprandial lipid in young normolipidemic men after a nocturnal vitamin A oral fat load test.

The oral fat load tests (OFLT) used to study postprandial lipemia are generally conducted during the day. A nocturnal fat load test could be convenient and physiologically more appropriate. We have therefore compared the lipemic responses of 9 normolipidemic young men to OFLT given at 2200 h (nocturnal) and at 0700 h (diurnal). Triglyceride and retinyl palmitate concentrations were measured for 10 h. Peak plasma concentrations or areas under curves (AUC) for triglyceride after the diurnal and nocturnal tests were not significantly different [2.17 +/- 0.78 (diurnal) vs. 2.04 +/- 0.87 mmol/L (nocturnal) and 13.12 +/- 4.45 (diurnal) vs. 13.74 +/- 5.79 mmol/(L. h) (nocturnal)]. Peak plasma concentrations and AUC retinyl palmitate for the two tests were not different [1.71 +/- 0.69 (diurnal) vs. 1.42 +/- 0.66 mg/L (nocturnal) and 7.17 +/- 3.98 (diurnal) vs. 6.63 +/- 4.23 mg/(L. h) (nocturnal)]. The diurnal triglyceride peak occurred significantly earlier (4.3 +/- 1.2 h) than the nocturnal peak (5.8 +/- 1.7 h, P < 0.05). We have developed a model using only three sample time points to predict AUC [triglyceride at 0 h, triglyceride at average peak-time (4 h for diurnal and 6 h for nocturnal tests), and triglyceride at 10 h], thus reducing the number of blood samples. The predicted AUC was well correlated with the total AUC after nocturnal OFLT (r = 0.98, P < 0.0001). The nocturnal test appeared to be well tolerated by the subjects. The three-point simplified protocol may well be suitable for studies on large groups of subjects.

Adult↗