Le cas clinique du mois. Troubles electrolytiques severes dans l'anorexie mentale.
in Revue Médicale de Liège (1995), 50(1), 16-7Detailed reference viewed: 54 (1 ULg)
Amylin/islet amyloid polypeptide: biochemistry, physiology, patho-physiology.
; Scheen, André ; Lefebvre, Pierre
in Diabète & Métabolisme (1995), 21(1), 3-25
Amylin is a 37 amino-acid peptide mainly produced by the islet beta-cell. Aggregation of amylin is partly responsible for amyloid formation. Amyloid deposits occur both extracellularly and intracellularly ... [more ▼]
Amylin is a 37 amino-acid peptide mainly produced by the islet beta-cell. Aggregation of amylin is partly responsible for amyloid formation. Amyloid deposits occur both extracellularly and intracellularly and may contribute to beta-cell degeneration. Amylin is packed in beta-cell granules and cosecreted with insulin in response to the same stimuli but, unlike other beta-cell products, it is produced from specific a gene on chromosome 12. Basal, plasma amylin concentrations are around 5 pM, and increase fourfold after meals or glucose. Higher levels are found in cases of insulin resistance, obesity, gestational diabetes and in some patients with NIDDM. Low or absent levels are found in insulin-dependent diabetic patients. There are similarities between amylin and non beta-cell peptides such as calcitonin gene related peptides (CGRP). They may bind to the same receptor, determine similar post-receptor phenomena and qualitatively similar actions but with different degree of potency. The actions of amylin are multiple and mostly exerted in the regulation of fuel metabolism. In muscle, amylin opposes glycogen synthesis, activates glycogenolysis and glycolysis (increasing lactate production). Consequently, amylin increases lactate output by muscle and increases the plasma lactate concentration. In fasting conditions, this lactate may serve as a gluconeogenic substrate for the liver, contributing to replenish depleted glycogen stores and to increase glucose production. In non-fasting conditions, lactate can be transformed by liver in triglycerides. It is not clear at present whether amylin actions on the liver are direct or mediated by changes in circulating metabolites. A probably indirect effect of amylin in muscle is to decrease insulin- (or glucose)-induced glucose uptake, which may contribute to insulin resistance. Other actions include inhibition of glucose-stimulated insulin secretion and, in general, actions mimicking CGRP effects. Some of these actions are seen at supraphysiological concentrations. The physiopathological consequences of amylin deficiency, or excess are under active by investigated. [less ▲]Detailed reference viewed: 40 (1 ULg)
Retinopathy, but not neuropathy, is influenced by the level of residual endogenous insulin secretion in type 2 diabetes.
Bozet, Marie-Claire ; Scheen, André ; Gerard, Pascale et al
in Diabète & Métabolisme (1995), 21(5), 353-9
The files of 132 patients with Type 2 diabetes were retrospectively studied to characterize the influence of metabolic control and residual insulin secretion on neuropathy and retinopathy, the two most ... [more ▼]
The files of 132 patients with Type 2 diabetes were retrospectively studied to characterize the influence of metabolic control and residual insulin secretion on neuropathy and retinopathy, the two most frequent degenerative diabetic complications. Patients were classified according to their metabolic control (mean HbA1C either < or > or = 8%; reference values: 3-6%) and residual endogenous insulin secretion (fasting plasma C-peptide levels either < or > or = 0.600 nmol/l). Neuropathy was more frequent in patients with poor metabolic control (32/64 = 50%) than in those adequately controlled (17/68 = 25%; p < 0.005). In both subgroups, the level of endogenous insulin secretion did not influence the prevalence of neuropathy. Retinopathy was less effected than neuropathy by the degree of metabolic control (37.5% in the subgroup with HbA1C > or = 8% v.s. 25% in the subgroup with HbA1C < 8%; p < 0.10), but was influenced by residual insulin secretion. Indeed, in patients with inadequate metabolic control, the prevalence of retinopathy was significantly increased in those with higher endogenous insulin secretion (51.4 versus 20.6%, p < 0.02) and thus probably higher insulin resistance. Furthermore, higher systolic arterial blood pressure was observed in the subgroups with a higher prevalence of retinopathy. Such conclusions were confirmed using multivariate analysis. Thus, in Type 2 diabetes, neuropathy is essentially affected by the degree of metabolic control, whereas retinopathy is also influenced by the level of residual endogenous insulin secretion and the presence of systolic hypertension. [less ▲]Detailed reference viewed: 9 (0 ULg)
Antihyperglycaemic agents. Drug interactions of clinical importance.
Scheen, André ; Lefebvre, Pierre
in Drug Safety : An International Journal of Medical Toxicology & Drug Experience (1995), 12(1), 32-45
Non-insulin-dependent (type 2) diabetes mellitus (NIDDM) affects middle-aged or elderly people who frequently have several other concomitant diseases, especially obesity, hypertension, dyslipidaemias ... [more ▼]
Non-insulin-dependent (type 2) diabetes mellitus (NIDDM) affects middle-aged or elderly people who frequently have several other concomitant diseases, especially obesity, hypertension, dyslipidaemias, coronary insufficiency, heart failure and arthropathies. Thus, polymedication is the rule in this population, and the risk of drug interactions is important, particularly in elderly patients. The present review is restricted to the interactions of other drugs with antihyperglycaemic compounds, and will not consider the mirror image, i.e. the interactions of antihyperglycaemic agents with other drugs. Oral antihyperglycaemic agents include sulphonylureas, biguanides--essentially metformin since the withdrawn of phenformin and buformin--and alpha-glucosidase inhibitors, acarbose being the only representative on the market. These drugs can be used alone or in combination to obtain better metabolic control, sometimes with insulin. Drug interactions with antihyperglycaemic agents can be divided into pharmacokinetic and pharmacodynamic interactions. Most pharmacokinetic studies concern sulphonylureas, whose action may be enhanced by numerous other drugs, thus increasing the risk of hypoglycaemia. Such an effect may result essentially from protein binding displacement, inhibition of hepatic metabolism and reduction of renal clearance. Reduction of the hypoglycaemic activity of sulphonylureas due to pharmacokinetic interactions with other drugs appears to be much less frequent. Drug interactions leading to an increase in plasma metformin concentrations, mainly by reducing the renal excretion or the hepatic metabolism of the biguanide, should be avoided to limit the risk of hyperlactaemia. Owing to its mode of action, pharmacokinetic interferences with acarbose are limited to the gastrointestinal tract, but have not been extensively studied yet. Pharmacodynamic interactions are quite numerous and may result in a potentiation of the hypoglycaemic action or, conversely, in a deterioration of blood glucose control. Such interactions may be observed whatever the type of antidiabetic treatment. They result from the intrinsic properties of the coprescribed drug on insulin secretion and action, or on a key step of carbohydrate metabolism. Finally, a combination of 2 to 3 antihyperglycaemic agents is common for treating patients with NIDDM to benefit from the synergistic effect of compounds acting on different sites of carbohydrate metabolism. Possible pharmacokinetic interactions between alpha-glucosidase inhibitors and classical antidiabetic oral agents should be better studied in the diabetic population. [less ▲]Detailed reference viewed: 33 (0 ULg)
Postgastroplasty recovery of ideal body weight normalizes glucose and insulin metabolism in obese women.
Letiexhe, Michel ; Scheen, André ; Gerard, Pascale et al
in Journal of Clinical Endocrinology and Metabolism (1995), 80(2), 364-9
To study the metabolic effects of normalizing body weight, a frequently sampled iv glucose tolerance test (0.3 g/kg) was performed before [body mass index (BMI), 37.7 +/- 0.5 kg/m2] and 14 +/- 2 months ... [more ▼]
To study the metabolic effects of normalizing body weight, a frequently sampled iv glucose tolerance test (0.3 g/kg) was performed before [body mass index (BMI), 37.7 +/- 0.5 kg/m2] and 14 +/- 2 months after successful gastroplasty (BMI, 23.7 +/- 0.6 kg/m2) in eight obese women and, for comparison, in eight age- and weight-matched nonobese control women (BMI, 23.6 +/- 0.7 kg/m2). All subjects had normal oral glucose tolerance. The insulin secretion rate (ISR) was derived by deconvolution of plasma C-peptide levels and the insulin MCR (MCRI) by dividing the 0-180 min area under the curve (AUC) of ISR by that of plasma insulin levels (IRI). The insulin sensitivity index (SI) and the glucose effectiveness index (SG) were calculated using Bergman's minimal model. Before gastroplasty, obese subjects showed higher AUC-IRI (P < 0.001) and AUC-ISR (P < 0.02), lower MCRI (P < 0.005) and SI (P < 0.002), but similar SG values, compared to nonobese controls. After gastroplasty, the AUC-IRI dramatically decreased, due to both a reduction of AUC-ISR (from 58,252 +/- 8,437 to 36,675 +/- 4,274 pmol; P < 0.05) and an increase in MCRI (from 658 +/- 117 to 1,299 +/- 127 mL/min.m-2; P < 0.02). SI significantly rose from 4.74 +/- 0.74 to 9.15 +/- 0.96 10(-5) min-1/pmol.L (P < 0.01), whereas SG remained unchanged. All of these parameters became similar to those in nonobese controls (respectively, 32,522 +/- 3,458, 1,180 +/- 101, and 8.48 +/- 1.25; all P = NS). In conclusion, after gastroplasty-induced normalization of body weight, postobese women recover normal insulin secretion, clearance, and action on glucose metabolism. [less ▲]Detailed reference viewed: 15 (1 ULg)
Modified glucagon test allowing simultaneous estimation of insulin secretion and insulin sensitivity: application to obesity, insulin-dependent diabetes mellitus, and noninsulin-dependent diabetes mellitus.
; Scheen, André ; Lefebvre, Pierre
in Journal of Clinical Endocrinology and Metabolism (1995), 80(2), 393-9
The aim of this study was to describe an adaptation of the glucagon test allowing the simultaneous characterization of insulin secretion and sensitivity. A glucagon test (1 mg/m2) was performed in healthy ... [more ▼]
The aim of this study was to describe an adaptation of the glucagon test allowing the simultaneous characterization of insulin secretion and sensitivity. A glucagon test (1 mg/m2) was performed in healthy subjects (n = 11), obese patients (n = 5), insulin-dependent diabetics (n = 9), nonobese noninsulin-dependent diabetics (n = 7), and overweight noninsulin-dependent diabetics (n = 8). Previously, they had been connected to the Biostator, modified for continuous blood collection. Endogenous insulin secretion induced by glucagon was derived from integrated C-peptide concentrations. An index of insulin sensitivity was obtained by dividing the rate of decrease in blood glucose by the total amount of insulin entering the circulation (secreted+infused by the Biostator). The indices of insulin sensitivity obtained in the above groups of subjects were, respectively, 0.064 +/- 0.006, 0.030 +/- 0.006, 0.037 +/- 0.007, 0.021 +/- 0.006, and 0.016 +/- 0.002 mmol/L.U.min (P < 0.001). The estimated insulin secretion values in the 20 min following glucagon injection were, respectively, 0.38 +/- 0.05, 0.65 +/- 0.08, 0.05 +/- 0.01, 0.26 +/- 0.15, and 0.30 +/- 0.07 U (P < 0.001). The insulin sensitivity index obtained from this test correlated with the glucose MCR obtained from a euglycemic glucose clamp (r = 0.816; P < 0.001; n = 12). C-Peptide levels after glucagon administration were also significantly correlated with the estimated endogenous insulin secretion (r = 0.808; P < 0.001; n = 30). This adaptation of the classical glucagon test is an efficient and simple method to simultaneously evaluate insulin secretion and insulin sensitivity. [less ▲]Detailed reference viewed: 40 (0 ULg)
Improving the action of insulin.
Lefebvre, Pierre ; Scheen, André
in Clinical & Investigative Medicine = Médecine Clinique et Experimentale (1995), 18(4), 340-7
Improving the action of insulin is a relatively new concept in diabetes management. Insulin sensitivity can be improved by reduction of excessive body weight, regular physical activity and, possibly, by ... [more ▼]
Improving the action of insulin is a relatively new concept in diabetes management. Insulin sensitivity can be improved by reduction of excessive body weight, regular physical activity and, possibly, by correcting a subclinical magnesium deficiency. Pharmacological means of improving insulin action include metformin, antiobesity serotoninergic agents and, possibly, benfluorex. New compounds aiming at improving the action of insulin are in development and include thiazolidinedione derivatives (known as "insulin sensitizers"), inhibitors of adipose tissue lipolysis (e.g. acipimox), and inhibitors of free fatty acid oxidation (e.g. etomoxir). Avoidance of drugs that reduce insulin sensitivity, such as beta blockers and thiazide diuretics, is recommended. Finally, cigarette smoking is associated with resistance to insulin but it remains to be demonstrated that cessation of cigarette smoking does in fact increase sensitivity to insulin. [less ▲]Detailed reference viewed: 7 (0 ULg)
Short administration of metformin improves insulin sensitivity in android obese subjects with impaired glucose tolerance.
Scheen, André ; Letiexhe, Michel ; Lefebvre, Pierre
in Diabetic Medicine : A Journal of the British Diabetic Association (1995), 12(11), 985-9
In a double-blind, randomized, cross-over study, the metabolic effects of a short treatment with metformin (2 x 850 mg day-1 for 2 days and 850 mg 1 h before evaluation) were compared to those of placebo ... [more ▼]
In a double-blind, randomized, cross-over study, the metabolic effects of a short treatment with metformin (2 x 850 mg day-1 for 2 days and 850 mg 1 h before evaluation) were compared to those of placebo in 15 obese subjects (BMI: 33.2 +/- 0.9 kg m-2), with abdominal distribution of adipose tissue and impaired glucose tolerance. An intravenous glucose tolerance test (0.3 g glucose kg-1) was performed after each period of treatment. Areas under the curve (AUC0-180 min) were calculated for plasma glucose, insulin, and C-peptide levels. Glucose tolerance was estimated by the coefficient of glucose assimilation (KG). Insulin sensitivity (SI) and glucose effectiveness (SG) indices were calculated using Bergman's minimal model. Insulin secretion rate (ISR) was determined by deconvolution of plasma C-peptide levels and insulin metabolic clearance rate (MCR) was estimated by dividing AUC 1SR by AUC insulin. Fasting plasma insulin levels were reduced after metformin (89.3 +/- 15.9 vs 112.4 +/- 24.3 pmol l-1; p = 0.04). AUC glucose, KG and SG were similar in both tests. However, AUC insulin was reduced (39.7 +/- 6.5 vs 51.8 +/- 10.4 nmol min l-1; p = 0.02), while SI (6.98 +/- 1.14 vs 4.61 +/- 0.42 10(-5) min-1 pmol-1 l; p = 0.03) and insulin MCR (715 +/- 116 vs 617 +/- 94 ml min-1 m-2; p = 0.03) were increased after metformin. The demonstration that metformin rapidly improves insulin sensitivity should encourage further research to evaluate the long-term effects of metformin in android obese subjects with impaired oral glucose tolerance. [less ▲]Detailed reference viewed: 17 (1 ULg)
Exogenous glucose oxidation during exercise in relation to the power output.
Pirnay, Freddy ; Scheen, André ; et al
in International Journal of Sports Medicine (1995), 16(7), 456-60
In order to study the influence of the power output on the oxidation rate of exogenous glucose and on the contribution of the various substrates to the energy demand, we combined the use of artificially ... [more ▼]
In order to study the influence of the power output on the oxidation rate of exogenous glucose and on the contribution of the various substrates to the energy demand, we combined the use of artificially enriched 13C-glucose with classical indirect calorimetry during uphill treadmill exercise. Six young male healthy subjects underwent three exercise bouts, in a randomized order and at least two weeks apart, at a low (45% VO2max, 1822 +/- 194 ml O2/min for 4 hours), moderate (60% VO2max, 2582 +/- 226 ml O2/min for 3 hours), and high intensity (75% VO2max, 3036 +/- 287 ml O2/min for 2 hours). After 10 min of exercise, each subject ingested 100 g of artificially 13C-labelled glucose dissolved in 400 ml of water. Over the four hours of the exercise at 45% VO2max, the amount of exogenous glucose oxidized was 89.5 +/- 5.9 g from the 100 g ingested. In all exercise bouts, the oxidation of exogenous glucose already began during the first 30 min after ingestion and peaked at 120 min. The maximum oxidation rates averaged 0.64 +/- 0.07, 0.75 +/- 0.04, and 0.63 +/- 0.08 g/min, and the mean amounts of exogenous glucose oxidized over the first two hours averaged 51.7 +/- 8.0, 61.5 +/- 6.6 and 50.9 +/- 8.45 g, at 45, 60 and 75% VO2max respectively. The contribution of the oxidation of exogenous glucose to the total energy supply progressively decreased when the power output increased, from 19.6 to 12.2%. In the meantime, the contribution of total carbohydrates (exogenous+endogenous) progressively increased from 55.1 to 77.8% while the contribution of lipids decreased from 35.5 to 16.6%. In conclusion, exogenous glucose ingested during exercise is largely oxidized and strongly contributes to the energy supply. The oxidation rate first increases with the power output, but levels off or even decreases at high intensity exercise. [less ▲]Detailed reference viewed: 32 (0 ULg)
Le pied diabétique: etiopathogénie, prévention et traitement
Van Damme, Hendrik ; Paquet, Philippe ; et al
in Revue Médicale de Liège (1994), 49(1), 1-13
-Le pied diabétique est la conséquence des altérations dégénératives du système vasculonerveux observées dans un diabète de longue durée. La neuropathie diabétique est le facteur essentiel dans la plupart ... [more ▼]
-Le pied diabétique est la conséquence des altérations dégénératives du système vasculonerveux observées dans un diabète de longue durée. La neuropathie diabétique est le facteur essentiel dans la plupart des cas, responsable d'hypoalgésies, microtraumatismes et ulcérations, déformation du pied (amyotrophie), et d'une eutosympethectomie (peau sèche, fissurée). Une macroangiopathie (médiacalcinose, occlusions artérielles périphériques) n'est retrouvée que dans 30 % des cas. Une microangiopathie compromet la trophicité des tissus et ralentit leur cicatrisation. Enfin, tout diabétique présente une susceptibilité élevée aux infections. Cette multitude de facteurs en cause impose des mesures de prévention. Un équilibre du profil glycémique retardera les atteintes vasculo-nerveuses. L'hygiène du pied consistera en bains de pieds, soins d'ongles et d'hyperkératoses, chaussures adaptées. En cas de troubles trophiques, une décharge d'appui sers nécessaire. Une désinfection rigoureuse, associée à une antibiothérapie (après prélèvement, si possible) aidera à éviter l'évolution vers l'abcès profond. La moindre collection sera drainée, après excision large des tissus nécrotiques. Les nécroses sèches (talons, orteils) traduisent souvent une artériopethie, pour laquelle un geste de revascularisation (protondoolestie; pontage distal) pourra être pris en considération. Parfois, l'état septique du patient, ou l'étendue de la gangrène, imposera une amputation. L'approche du pied diabétique doit toujours être multidisciplinaire (diabétologue, dermatologue, orthésiste, orthopédiste, chirurgien vasculaire), et doit commencer par des mesures préventives. [less ▲]Detailed reference viewed: 132 (4 ULg)
Estimation de la sensibilité à l'insuline par le "minimal model" : comparaison de différents protocoles d'hyperglycémie provoquée intraveineuse.
SCHEEN, André ; LETIEXHE, Michel ; DUYSINX, Bernard et al
in Diabète & Métabolisme (1994), 20(suppl),Detailed reference viewed: 8 (0 ULg)
Le diabète de type 2 insulino-requérant: caractéristiques des patients et effets de l'insulinothérapie
DUYSINX, Bernard ; SCHEEN, André ; PAQUOT, Nicolas et al
in Diabète & Métabolisme (1994), 20(suppl),Detailed reference viewed: 37 (0 ULg)
Measurement of insulin sensitivity by the minimal model method using a simplified intravenous glucose tolerance test: validity and reproducibility.
Duysinx, Bernard ; Scheen, André ; Gerard, Pascale et al
in Diabète & Métabolisme (1994), 20(4), 425-32
This study aimed at testing whether 12 rather than 26 plasma glucose and insulin determinations can be used to calculate the indices of insulin sensitivity and of glucose effectiveness using Bergman's ... [more ▼]
This study aimed at testing whether 12 rather than 26 plasma glucose and insulin determinations can be used to calculate the indices of insulin sensitivity and of glucose effectiveness using Bergman's minimal model during a simple intravenous glucose tolerance test performed without tolbutamide injection. Two intravenous glucose tolerance tests (separated by 1 week) were performed in 7 lean normal subjects and a single test was performed in 9 severely obese non-diabetic subjects. Intra-subject reproducibility of insulin sensitivity was not significantly different when 26 or 12 time-points were analyzed (CV = 16.8 +/- 3.4 versus 18.9 +/- 3.8% respectively). Compared with the insulin sensitivity of the lean subjects, that of obese subjects was significantly (P < 0.001) and similarly reduced when using 12 (2.14 +/- 0.34 versus 7.97 +/- 1.29 10(-4)min-1/mU.1-1) rather than 26 determinations (2.13 +/- 0.42 versus 6.95 +/- 1.12 10(-4) min-1/mU.1-1) respectively. Glucose effectiveness was less reproducible than insulin sensitivity and was slightly diminished by the reduction of blood samples (relative error: -9.7 +/- 4.4%; P < 0.05). Finally, glucose effectiveness tended to be slightly lower in the morbidly obese subjects than in the lean controls with both modes of calculation. In conclusion, in non-diabetic subjects, the insulin sensitivity index can be accurately measured during a simple intravenous glucose tolerance test, without tolbutamide injection and with only 12 blood samples. The possibility of performing a simplified test should contribute to increase the use of the minimal model method for estimating insulin sensitivity in clinical practice. [less ▲]Detailed reference viewed: 31 (2 ULg)
Measurement of apolipoproteins B and A by radial immunodiffusion: methodological assessment and clinical applications.
; ; Scheen, André et al
in Annales de Biologie Clinique (1994), 52(9), 657-61
The clinical evaluation of apolipoproteins is of interest in order to characterize the risk profile for ischemic heart disease both in normolipidemic and hyperlipidemic subjects. In the non-specialized ... [more ▼]
The clinical evaluation of apolipoproteins is of interest in order to characterize the risk profile for ischemic heart disease both in normolipidemic and hyperlipidemic subjects. In the non-specialized and/or small practice clinical laboratory, the measurement of some apolipoproteins can be undertaken by simple methods of immunological analysis, among which radial immunodiffusion can be of interest due to its simplicity of use and because it does not require specific equipment. In this work several methodological questions concerning the measurement of plasma apolipoproteins B and A by radial immunodiffusion have been addressed; the results show that this method is particularly reliable for the apo B assay. Regression analysis between values obtained with radial immunodiffusion and radioimmunoassay was r = 0.972 for apo B and r = 0.782 for apo A. The recovery rate was above 90% for both apolipoproteins (93.8% for apo B and 99.5% for apo A). The inter and intraassay coefficients of variation were below 5%, and the detection limits were estimated as 9.6 mg/dl for apo A and 6.9 mg/dl for apo B. Neither the ingestion of a standard breakfast (500 Cal, 17 g fat, 120 mg cholesterol) 2 h prior to testing nor freezing the sample significantly affected the measurement of apolipoproteins B and A. Mean plasma concentrations of both apolipoproteins measured by radial immunodiffusion in normo and hyperlipidemic subjects are also presented. [less ▲]Detailed reference viewed: 14 (0 ULg)
Detection of early sympathetic cardiovascular neuropathy by squatting test in NIDDM.
; ; et al
in Diabetes Care (1994), 17(2), 149-51
OBJECTIVE--To determine the role of the squatting test in the detection of early sympathetic neuropathy in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS--Three ... [more ▼]
OBJECTIVE--To determine the role of the squatting test in the detection of early sympathetic neuropathy in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS--Three groups of nonsmoking, nonobese subjects were studied: 10 healthy subjects, 10 NIDDM patients without autonomic neuropathy (AN), and 10 NIDDM patients with AN defined by the presence of a pathological deep-breathing value. All subjects were given three postural tests: lying-to-standing, sitting-to-standing, and squatting test. Heart rate (HR) and finger arterial pressure were recorded with a noninvasive technique. RESULTS--Blood pressure (BP) fall (expressed as decremental area) was not significantly different among the groups at standing up after sitting or lying. By contrast, a significantly greater BP drop occurred in NIDDM patients with AN (1,123 +/- 245 mm2) compared with NIDDM patients without AN (460 +/- 232 mm2) or normal subjects (429 +/- 138 mm2, P < 0.001). The HR increase after all the orthostatic maneuvers was smaller in diabetic patients with AN (P < 0.01) compared with that recorded in other groups. Significant correlations were observed between BP fall after squatting and either the expiration:inspiration ratio at deep breathing (r = -0.77, P < 0.001) or the duration of diabetes (r = 0.76, P < 0.001). CONCLUSIONS--The intrinsic orthostatic load of the squatting test, which is greater than conventional postural maneuvers, makes the squatting test an easy and useful test to detect early orthostatic dysregulation in NIDDM. [less ▲]Detailed reference viewed: 22 (0 ULg)
Changes in glucose turnover parameters and improvement of glucose oxidation after 4-week magnesium administration in elderly noninsulin-dependent (type II) diabetic patients.
; Scheen, André ; et al
in Journal of Clinical Endocrinology and Metabolism (1994), 78(6), 1510-4
The aim of the present study was to investigate the effects of magnesium supplementation on glucose uptake and substrate oxidation in noninsulin-dependent (type II) diabetic patients. Nine elderly non ... [more ▼]
The aim of the present study was to investigate the effects of magnesium supplementation on glucose uptake and substrate oxidation in noninsulin-dependent (type II) diabetic patients. Nine elderly non-obese noninsulin-dependent (type II) diabetic patients, treated by diet only, participated in the study, which was designed as randomized, double blind, and cross-over. Each patient was followed up for a prestudy period of 3 weeks before inviting him/her to receive placebo or magnesium supplementation (15.8 mmol/day) for 4 weeks. At the end of each treatment period, a euglycemic hyperinsulinemic glucose clamp with simultaneous D-[3-3H]glucose infusion and indirect calorimetry was performed. Magnesium supplementation resulted in significantly increased plasma and erythrocyte magnesium levels, whereas body weight and fasting plasma glucose did not change. In the last 60 min of the glucose clamp, insulin-mediated glucose disappearance, total body glucose disposal (24.5 +/- 0.4 vs. 28.2 +/- 0.7 mumol/kg.min; P < 0.005), and glucose oxidation (13.0 +/- 0.4 vs. 16.3 +/- 0.8 mumol/kg.min; P < 0.01) were increased after chronic magnesium supplementation. Endogenous glucose production, nonoxidative glucose disposal, lipid and protein oxidation, and insulin MCR were not affected. In conclusion, a 4-week magnesium supplementation improves insulin sensitivity and glucose oxidation in the course of a euglycemic-hyperinsulinemic glucose clamp in noninsulin-dependent diabetic patients. Long term studies are needed to determine whether magnesium supplementation is useful in the management of type II diabetes. [less ▲]Detailed reference viewed: 18 (0 ULg)
Reduction of the acute bioavailability of metformin by the alpha-glucosidase inhibitor acarbose in normal man.
Scheen, André ; ; et al
in European Journal of Clinical Investigation (1994), 24 Suppl 3
In a double-blind cross-over study, we investigated a possible influence of the alpha-glucosidase inhibitor acarbose on the bioavailability of the biguanide compound metformin. Each of the six healthy ... [more ▼]
In a double-blind cross-over study, we investigated a possible influence of the alpha-glucosidase inhibitor acarbose on the bioavailability of the biguanide compound metformin. Each of the six healthy young male volunteers was randomly allocated during two consecutive 7 day periods to either acarbose (days 1-3: 3 x 50 mg day-1; days 4-7: 3 x 100 mg day-1) or placebo. At day 7 and 14 of the study, the overnight-fasted subjects ingested 1000 mg metformin with the first bite of a standardized breakfast (500 kcal; 60 g carbohydrates) and together with either placebo or 100 mg acarbose. Acarbose significantly (P < 0.05) reduced the meal-induced increase in blood glucose and plasma insulin levels. Acarbose induced a significant (P < 0.05) reduction in early (90, 120, 180 min) serum levels, peak concentrations (Cmax: 1.22 +/- 0.14 vs. 1.87 +/- 0.60 mg l-1) and area under the curve of metformin (AUC 0-540 min: 423 +/- 55 vs. 652 +/- 55 mg min l-1), but did not diminish its 24 h urinary excretion. In conclusion, acarbose significantly reduces the acute bioavailability of metformin in normal subjects. [less ▲]Detailed reference viewed: 32 (0 ULg)
The use of acarbose in the prevention and treatment of hypoglycaemia.
Lefebvre, Pierre ; Scheen, André
in European Journal of Clinical Investigation (1994), 24 Suppl 3
This paper reviews the use of acarbose in the prevention and treatment of hypoglycaemia. In diet- or sulfonylurea-treated patients, acarbose may reduce the incidence of late postprandial hypoglycaemia. In ... [more ▼]
This paper reviews the use of acarbose in the prevention and treatment of hypoglycaemia. In diet- or sulfonylurea-treated patients, acarbose may reduce the incidence of late postprandial hypoglycaemia. In insulin-treated patients, acarbose treatment usually requires reduction of the insulin dose; one study has shown that 100 mg acarbose at night significantly reduces the incidence of mid-evening and nocturnal hypoglycaemia. Several studies have suggested acarbose to be a useful adjunct to the management of reactive hypoglycaemia in the non-diabetic patients. Long-term prospective studies are still needed to document this last indication of acarbose or other alpha-glycosidase inhibitors. [less ▲]Detailed reference viewed: 63 (0 ULg)
Abnormal temporal patterns of glucose tolerance in obesity: relationship to sleep-related growth hormone secretion and circadian cortisol rhythmicity.
; ; et al
in Journal of Clinical Endocrinology and Metabolism (1994), 79(6), 1797-805
To define the chronobiology of glucose tolerance and insulin secretion in obesity, nine obese men and nine lean men were studied during constant glucose infusion for 53 h, including 8 h of nocturnal sleep ... [more ▼]
To define the chronobiology of glucose tolerance and insulin secretion in obesity, nine obese men and nine lean men were studied during constant glucose infusion for 53 h, including 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime sleep. Blood samples were collected at 20-min intervals to assay glucose, insulin, C-peptide, cortisol, and GH. Sleep was polygraphically monitored. Abnormal temporal profiles of glucose regulation were observed during wakefulness and sleep in obese subjects. During daytime hours, the normal profile of glucose tolerance was reversed, as an improvement, rather than a deterioration, was observed from morning to late evening. This reversal of the daytime pattern appeared to be caused by a dual defect in glucose regulation during the previous night. Indeed, during early sleep, GH secretion was markedly reduced, and the nocturnal rises of glucose and insulin secretion were dampened. During late sleep, obese subjects failed to suppress insulin secretion and plasma glucose, resulting in high morning levels. Comparisons of metabolic and hormonal patterns during nocturnal and daytime sleep suggest that the failure to suppress insulin secretion in late sleep may reflect a relative insensitivity of the beta-cell to acute inhibitory effects of cortisol in addition to insulin resistance. [less ▲]Detailed reference viewed: 25 (4 ULg)