Growth hormone level at admission and its evolution during refeeding are predictive of short-term outcome in restrictive anorexia nervosa

International audienceThe growth hormone (GH)– insulin-like growth factor-1 (IGF-1) axis is dramatically altered in patients with anorexia nervosa (AN). The aim of the present study was to investigate whether GH and IGF-1 could be predictors of outcome in patients with a restrictive form of AN. Blood levels of GH, IGF-1, adipocytokines, ghrelin, insulin, glucose, and sex and thyroid hormones were measured in eleven women inpa-tients with AN and in ten healthy women controls. Three stages were compared during refeeding: admission (T0), when BMI reached 16 kg/m 2 (T1) and at discharge when BMI reached 17·5 kg/m 2 (T2). Clinical status was assessed 6 months after discharge from hospital (T3), and remission was defined by the maintenance of a BMI $ 17·5 kg/

Unacylated Ghrelin is associated with the isolated low HDL-cholesterol obese phenotype independently of insulin resistance and CRP level

<p>Abstract</p> <p>Background</p> <p>Low plasma high-density lipoprotein-cholesterol (HDL-c) level is commonly present in obesity and represents an independent cardiovascular risk factor. However, obese patients are a very heterogeneous population and the factors and mechanisms that contribute to low HDL-c remain unclear. The aim of this study was to investigate the association between plasma HDL-c levels and plasma hormonal profiles (insulin, adiponectin, resistin, leptin and ghrelin) in subsets of class II and III obese patients.</p> <p>Methods</p> <p>Fasting plasma levels of glucose, total cholesterol, LDL-c, HDL-c, triglycerides, free fatty acids, apoproteins A-I, B-100, B-48, C-II, C-III, insulin, hs-CRP, adipocytokines (adiponectin, resistin, leptin), unacylated ghrelin, body composition (DXA) and resting energy expenditure were measured in three subsets of obese patients: 17 metabolically abnormal obese (MAO) with metabolic syndrome and the typical metabolic dyslipidaemia, 21 metabolically healthy obese (MHO) without metabolic syndrome and with a normal lipid profile, and 21 isolated low HDL-c obese patients (LHO) without metabolic syndrome, compared to 21 healthy lean control subjects.</p> <p>Results</p> <p>Insulin resistance (HOMA-IR) increased gradually from MHO to LHO and from LHO to MAO patients (<it>p </it>< 0.05 between MHO and MAO and between LHO and MAO). In multiple regression analysis, serum unacylated ghrelin levels were only positively and independently associated with HDL-c levels in the LHO group (<it>p </it>= 0.032).</p> <p>Conclusions</p> <p>These results suggest that, in class II and III obese patients with an isolated low HDL-c phenotype, unacylated ghrelin is positively associated with HDL-c level independently of insulin resistance and CRP levels, and may contribute to the highly prevalent low HDL-c level seen in obesity.</p

Triglycérides et risque cardiovasculaire

National audienceCardiovascular diseases are the leading cause of death in the world. Residual cardiovascular risk, which is defined as the risk of cardiovascular events that persists despite achievement of treatment goals for LDL-cholesterol (LDL-C), blood pressure and glycemia, is often associated with atherogenic dyslipidemia (AD). This AD, which is mainly characterized by fasting and postprandial hypertriglyceridemia (postprandial hyperlipidemia), low HDL-cholesterol (HDL-C) and an increase of small and dense LDL, is frequently found in subjects with an insulin resistance profile such as patients with type 2 diabetes, subjects who are overweight or obese, subjects with a metabolic syndrome. The pathophysiological mechanisms of this AD are widely explained by the blood accumulation of triglyceride-rich lipoproteins (TRL) from liver (VLDL) and intestine (chylomicrons). There are extensive epidemiological, genetic and biological data showing that the increase of TRL reflected by the blood triglyceride level and/or the measurement of remnant-cholesterol (remnant-C = total cholesterol - LDL-C - HDL-C) is a causal risk factor for atherosclerosis through direct and indirect mechanisms. Clinical trial data are less convincing, but relevant studies are currently underway. A better understanding of the atherogenic role of TRL elevation and the validation of therapeutic options are needed to reduce their plasma concentration and consequently AD and residual cardiovascular risk.Les maladies cardiovasculaires représentent la première cause de mortalité dans le monde. Le risque cardiovasculaire résiduel qui se définit par le risque d’événements cardiovasculaires qui persiste malgré des objectifs thérapeutiques atteints en ce qui concerne le LDLcholestérol (LDL-C), la pression artérielle et l’équilibre glycémique, est souvent associé à la dyslipidémie athérogène (DA). Cette DA qui est principalement caractérisée par une hypertriglycéridémie à jeun et en post-prandial (hyperlipidémie post-prandiale), une baisse du HDL-cholestérol (HDL-C), une augmentation de la quantité de LDL petites et denses, est fréquemment retrouvée chez les sujets ayant un profil d’insulinorésistance, comme les patients diabétiques de type 2, les sujets ayant un surpoids ou une obésité, ou ayant un syndrome métabolique. Les mécanismes physiopathologiques de cette DA sont largement expliqués par une accumulation sanguine des lipoprotéines riches en triglycérides (LRT) d’origine hépatique (VLDL) et intestinale (chylomicrons). De nombreuses données épidémiologiques, génétiques et biologiques, montrent que l’élévation des LRT reflétée par le dosage sanguin des triglycérides et/ou la mesure du remnant-cholestérol (remnant-C = cholestérol total – LDL-C – HDL-C) représente un facteur de risque causal d’athérosclérose par des mécanismes directs et indirects. Les données des essais cliniques sont moins convaincantes, mais des études pertinentes sont actuellement en cours. Une meilleure compréhension du rôle athérogène de l’élévation des LRT et la validation d’options thérapeutiques sont nécessaires dans le but de réduire leur concentration plasmatique et, par voie de conséquence, la DA et le risque cardiovasculaire résiduel

La prescription des statines en pratique

International audienceStatins are the pivotal treatment for cardiovascular prevention, whether primary or secondary. In order to decide when to start statin therapy, which statin to choose and what dose to choose, the patient's cardiovascular risk must first be assessed. The main objective is to treat patients at high cardiovascular risk who will benefit from treatment and not to treat patients at low cardiovascular risk. The European SCORE tables are used to assess cardiovascular risk. In primary prevention, statins are started at a low dose and then the dosage can be increased to the LDL-cholesterol target. Statins have different pharmacokinetic properties, and some are preferentially indicated in cases of renal failure or concomitant treatments metabolised by hepatic cytochromes (antiretroviral, immunotherapies, cyclosporin etc.). In addition, statins associated muscle symptoms are frequent, leading to premature discontinuation of treatment, which is a loss of chance in cardiovascular prevention. It is important to properly manage muscle symptoms under statins therapy to maintain the treatment. (C) 2020 Societe francophone nutrition clinique et metabolisme (SFNCM). Published by Elsevier Masson SAS

Lipid-lowering treatments and cardiovascular prevention in diabetic subjects: news and perspectives

National audienceThe atherosclerotic cardiovascular disease is the leading cau of death in diabetes. The treatment of the dyslipidemias and especially the exce of LDL-cholesterol (LDL-C) which is a major cardiovascul, risk factor allows the primary and the secondary preventic of cardiovascular events in diabetes. A new French consensus and guidelines from the Frenc National Authority for Health (HAS) have set the framewo for the management of dyslipidemias. Statins represent the first-line treatment of the excess of LDL The statin-fenofibrate association can be used in high ar very high cardiovascular risk patients with LDL-C at targ but with a residual atherogenic dyslipidemia. PCSK9 (Proprotein Convertase Subtilisin Kexin type 9) inhibitc are a new therapeutic class highly effective in the reduction LDL-C whose launch on the market is still pending in Fran

Hyperlipidaemia in diabetes: are there particular considerations for next-generation therapies?

International audienceAbstract Dyslipidaemias are major cardiovascular risk factors, especially in people with diabetes. In this area, next-generation therapies targeting circulating lipoparticle metabolism (LDL, VLDL, chylomicrons, HDL) have recently been approved by the European and US medical agencies, including anti- proprotein convertase subtilisin/kexin 9 (PCSK9) antibodies; an siRNA targeting PCSK9; bempedoic acid, which targets ATP citrate lyase; an antisense oligonucleotide targeting apolipoprotein C-III; an anti-angiopoietin-like 3 antibody; and a purified omega-3 fatty acid, icosapent ethyl. Other therapies are in different phases of development. There are several important considerations concerning the link between these new lipid-lowering therapies and diabetes. First, since concerns were first raised in 2008 about an increased risk of new-onset diabetes mellitus (NODM) with intensive statin treatment, each new lipid-lowering therapy is being evaluated for its associated risk of NODM, particularly in individuals with prediabetes (impaired fasting glucose and/or impaired glucose tolerance). Second, people with diabetes represent a large proportion of those at high or very high cardiovascular risk in whom these lipid-lowering drugs are currently, or will be, prescribed. Thus, the efficacy of these drugs in subgroups with diabetes should also be closely considered, as well as any potential effects on glycaemic control. In this review, we describe the efficacy of next-generation therapies targeting lipoprotein metabolism in subgroups of people with diabetes and their effects on glycaemic control in individuals with diabetes and prediabetes and in normoglycaemic individuals. Graphical Abstrac

Is ionic choline and geranate (CAGE) liquid caging diet-derived fat, limiting its absorption?

International audienc

Prognostic models for short-term annual risk of severe complications and mortality in patients living with type 2 diabetes using a national medical claim database

International audienceAbstract Objective Prognostic models in patients living with diabetes allow physicians to estimate individual risk based on medical records and biological results. Clinical risk factors are not always all available to evaluate these models so that they may be complemented with models from claims databases. The objective of this study was to develop, validate and compare models predicting the annual risk of severe complications and mortality in patients living with type 2 diabetes (T2D) from a national claims data. Research design and methods Adult patients with T2D were identified in a national medical claims database through their history of treatments or hospitalizations. Prognostic models were developed using logistic regression (LR), random forest (RF) and neural network (NN) to predict annual risk of outcome: severe cardiovascular (CV) complications, other severe T2D-related complications, and all-cause mortality. Risk factors included demographics, comorbidities, the adjusted Diabetes Severity and Comorbidity Index (aDSCI) and diabetes medications. Model performance was assessed using discrimination (C-statistics), balanced accuracy, sensibility and specificity. Results A total of 22,708 patients with T2D were identified, with mean age of 68 years and average duration of T2D of 9.7 years. Age, aDSCI, disease duration, diabetes medications and chronic cardiovascular disease were the most important predictors for all outcomes. Discrimination with C-statistic ranged from 0.715 to 0.786 for severe CV complications, from 0.670 to 0.847 for other severe complications and from 0.814 to 0.860 for all-cause mortality, with RF having consistently the highest discrimination. Conclusion The proposed models reliably predict severe complications and mortality in patients with T2D, without requiring medical records or biological measures. These predictions could be used by payers to alert primary care providers and high-risk patients living with T2D

EPSAT-Niger : campagne 1990

La saison des pluies 1990 a été déficitaire presque partout au Sahel et la zone étudiée (environ 10 000 km2), autour de Niamey, n'est pas une exception. Sur le plan expérimental, le réseau de pluviographes a été fiable, tandis que la chaîne radar a été fragile. A l'aval des acquisitions ont été développées des banques de données sol (BADINAGE) et radar (BADORA). (Résumé d'auteur

Growth hormone (GH) and triglyceride-rich lipoprotein (TRL) metabolism : effect of one month of dicontinued growth hormone treatment in growth hormone hormone deficient patients

International audienceAim: Growth hormone (GH) deficiency is associated with increased cardiovascular mortality. Insulin resistant states and lipid profile alterations with hypertriglyceridemia, decreased HDL cholesterol, increased small and dense LDL and postprandial hyperlipidemia are commonly observed in GH deficient patients but GH specific function in triglyceride-rich lipoprotein (TRL) metabolism regulation remains unclear. Methods: Lipids and apolipoproteins (apo) profiles were investigated in fasting and postprandial states in plasma and TRL fractions during a test meal before (M0) and after one month of discontinued GH treatment (M1) in GH deficient patients (n=10). Results: After one month of discontinued GH treatment, GH levels remained unchanged but IGF-1 decreased significantly (-12,12±2,36nmol/L). We observed a significant weight loss (-1,31±0,45kg) together with body composition significant changes : lean mass decrease and fat mass increase (-1,17±0,41kg and +0,36±0,16kg respectively), and insulin resistance parameters modifications with a significant HOMA-index reduction (-0,45±0,19) associated with both significant decreased fasting insulin and C-peptide (-2,04±0,78Mui/L and -0,15±0,05nmol/L respectively) but fasting plasma glucose remained unchanged. Fasting plasma triglycerides and apoC-III levels decreased significantly (-0,41±0,16mmol/L and -23,07±6,93mg/L respectively), main other fasting lipid parameters assessed in the plasma fraction (total, LDL and HDL cholesterol, but also apoA1, apoB, apoB48 and apoC-II) were unchanged. Triglycerides but also apoC-II and apoC-III levels assessed in TRL fraction decreased significantly both in fasting and postprandial states after GH discontinuation. Conclusions: Lipid profiles alterations both in fasting and postprandial states were observed in GH deficient patients after GH treatment discontinuation suggesting a specific role of GH in TRL metabolism specifically altered in this pathology