9 research outputs found

    Facteurs maternels prédictifs du traitement par insuline dans le diabète gestationnel (résultats d une étude rétrospective de 167 patientes ayant un diabète gestationnel diagnostiqué selon les dernières recommandations françaises de décembre 2010)

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    L objectif de ce travail a été de déterminer s il existe d éventuels facteurs maternels prédictifs d insulinothérapie dans le traitement du diabète gestationnel, en examinant les différences notables entre deux groupes de traitement (diététique versus diététique et insuline) chez 167 patientes atteintes de diabète gestationnel, diagnostiqué selon les nouveaux critères des recommandations françaises de décembre 2010. Cette étude rétrospective a été menée au Centre Hospitalier Universitaire de Dijon entre janvier 2011 et juin 2012. Aucune étude à priori, n a été publiée à ce sujet depuis la parution des dernières recommandations. 121 patientes (75,2%) ont été traitées par mesures hygiéno-diététiques seules, et 40 patientes (24,4%) ont eu de l insuline. Le terme au diagnostic de diabète gestationnel et la prise de poids gestationnelle étaient abaissés dans le groupe de traitement par insuline comparé au groupe de traitement par diététique seule. En analyse multivariée, seule la valeur de la glycémie à jeun du dépistage du deuxième trimestre était un facteur maternel indépendant d insulinothérapie. Cette étude montre qu un diagnostic plus précoce de diabète gestationnel est partiellement prédictif d une insulinothérapie, à l instar d études antérieures. D autre part, les femmes de notre cohorte traitées par insuline ont pris moins de poids que les femmes traitées par diététique seule, sans retentissement sur la morbidité foetale. Enfin, seule la glycémie à jeun de l HGPO était indépendamment prédictive d insulinothérapie. Ce point soulève la question déjà discutée par d autres auteurs du maintien d un test de dépistage en trois temps au deuxième trimestre de grossesse.DIJON-BU Médecine Pharmacie (212312103) / SudocSudocFranceF

    Increased body fat mass reduces the association between fructosamine and glycated hemoglobin in obese type 2 diabetes patients

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    International audienceObesity is increasing in patients with type 2 diabetes (T2D). A possible reduced association between fructosamine and HbA1c in obese individuals has been previously discussed, but this has never been specifically evaluated in T2D and the potential influence of body fat mass and fat distribution has never been studied. We studied 112 T2D patients with assessment of fat mass, liver fat and fat distribution. Patients with BMI above the median (34.9 kg/m(2) ), versus BMI below the median, had a correlation coefficient between fructosamine and HbA1c significantly reduced (r=0.358 vs. r=0.765). In the whole population, fructosamine was correlated negatively with BMI and fat mass. In multivariate analysis, fructosamine was associated with HbA1c (positively) and fat mass (negatively) but not with BMI, liver fat or fat distribution. The association between fructosamine and HbA1c is significantly reduced in the most obese T2D patients and this is mostly driven by increased fat mass

    Liraglutide Reduces Postprandial Hyperlipidemia by Increasing ApoB48 (Apolipoprotein B48) Catabolism and by Reducing ApoB48 Production in Patients With Type 2 Diabetes Mellitus

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    International audienceObjectiveTreatment with liraglutide, a GLP-1 (glucagon-like peptide-1) agonist, has been shown to reduce postprandial lipidemia, an important feature of diabetic dyslipidemia. However, the underlying mechanisms for this effect remain unknown. This prompted us to study the effect of liraglutide on the metabolism of ApoB48 (apolipoprotein B48).Approach and ResultsWe performed an in vivo kinetic study with stable isotopes (D8-valine) in the fed state in 10 patients with type 2 diabetes mellitus before treatment and 6 months after the initiation of treatment with liraglutide (1.2 mg/d). We also evaluated, in mice, the effect of a 1-week liraglutide treatment on postload triglycerides and analysed in vitro on jejunum, the direct effect of liraglutide on the expression of genes involved in the biosynthesis of chylomicron. In diabetic patients, liraglutide treatment induced a dramatic reduction of ApoB48 pool (65±38 versus 162±87 mg; P=0.005) because of a significant decrease in ApoB48 production rate (3.02±1.33 versus 6.14±4.27 mg kg-1 d-1; P=0.009) and a significant increase in ApoB48 fractional catabolic rate (5.12±1.35 versus 3.69±0.75 pool d-1; P=0.005). One-week treatment with liraglutide significantly reduced postload plasma triglycerides in mice and liraglutide, in vitro, reduced the expression of ApoB48, DGAT1 (diacylglycerol O-acyltransferase 1), and MTP (microsomal transfer protein) genes.ConclusionsWe show that treatment with liraglutide induces a significant reduction of the ApoB48 pool because of both a reduction of ApoB48 production and an increase in ApoB48 catabolism. In vitro, liraglutide reduces the expression of genes involved in chylomicron synthesis. These effects might benefit cardiovascular health.Clinical Trial RegistrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT02721888

    Rosuvastatin 20 mg restores normal HDL-apoA-I kinetics in type 2 diabetes

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    Catabolism of HDL particles is accelerated in type 2 diabetes, leading to a reduction in plasma residence time, which may be detrimental. Rosuvastatin is the most powerful statin to reduce LDL-cholesterol, but its effects on HDL metabolism in type 2 diabetes remain unknown. We performed a randomized double-blind cross-over trial of 6-week treatment period with placebo or rosuvastatin 20 mg in eight patients with type 2 diabetes. An in vivo kinetic study of HDL-apolipoprotein A-I (apoA-I) with 13C leucine was performed at the end of each treatment period. Moreover, a similar kinetic study was carried out in eight nondiabetic normolipidemic controls. Rosuvastatin significantly reduced plasma LDL-cholesterol (−51%), triglycerides (TGs) (−38%), and HDL-TG (−23%). HDL-apoA-I fractional catabolic rate (FCR) was decreased by rosuvastatin (0.25 ± 0.06 vs. 0.32 ± 0.07 pool/day, P = 0.011), leading to an increase in plasma HDL-apoA-I residence time (4.21 ± 1.02 vs. 3.30 ± 0.73 day, P = 0.011). Treatment with rosuvastatin was associated with a concomitant reduction of HDL-apoA-I production rate. The decrease in HDL-apoA-I FCR, induced by rosuvastatin, was correlated with the reduction of plasma TGs and HDL-TG. HDL apoA-I FCR and production rate values in diabetic patients on rosuvastatin were not different from those found in controls. Rosuvastatin is responsible for a 22% reduction of HDL-apoA-I FCR and restores to normal the increased HDL turnover observed in type 2 diabetes. These kinetic modifications may have beneficial effects by increasing HDL plasma residence time
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