Multi-omics correlates of insulin resistance and circadian parameters mapped directly from human serum.

While it is generally known that metabolic disorders and circadian dysfunction are intertwined, how the two systems affect each other is not well understood, nor are the genetic factors that might exacerbate this pathological interaction. Blood chemistry is profoundly changed in metabolic disorders, and we have previously shown that serum factors change cellular clock properties. To investigate if circulating factors altered in metabolic disorders have circadian modifying effects, and whether these effects are of genetic origin, we measured circadian rhythms in U2OS cell in the presence of serum collected from diabetic, obese or control subjects. We observed that circadian period lengthening in U2OS cells was associated with serum chemistry that is characteristic of insulin resistance. Characterizing the genetic variants that altered circadian period length by genome-wide association analysis, we found that one of the top variants mapped to the E3 ubiquitin ligase MARCH1 involved in insulin sensitivity. Confirming our data, the serum circadian modifying variants were also enriched in type 2 diabetes and chronotype variants identified in the UK Biobank cohort. Finally, to identify serum factors that might be involved in period lengthening, we performed detailed metabolomics and found that the circadian modifying variants are particularly associated with branched chain amino acids, whose levels are known to correlate with diabetes and insulin resistance. Overall, our multi-omics data showed comprehensively that systemic factors serve as a path through which metabolic disorders influence circadian system, and these can be examined in human populations directly by simple cellular assays in common cultured cells.

[Diabetic gastroparesis and type 1 diabetes]. / Gastroparésie diabétique et diabète de type 1.

Gastroparesis is a rare and late microvascular complication, but a significant one of diabetes. Defined by a slowing of gastric emptying, this condition manifests with nonspecific gastrointestinal symptoms, including nausea, vomiting, abdominal pain, postprandial fullness, and early satiety. Faced with such a clinical presentation, it is often challenging to diagnose gastroparesis. In this article, we discuss the diagnostic procedures, as well as therapeutic approaches and management of the disease.

La gastroparésie est une complication microvasculaire rare et tardive, mais conséquente, du diabète. Définie par un ralentissement de la vidange gastrique, cette pathologie se présente sous la forme de symptômes gastro-intestinaux aspécifiques incluant des nausées, des vomissements, des douleurs abdominales, une sensation de réplétion postprandiale et une satiété précoce. Face à une présentation clinique de ce type, il est souvent difficile de poser le diagnostic de gastroparésie. Dans cet article, nous évoquons donc les examens complémentaires permettant de poser le diagnostic, ainsi que les propositions thérapeutiques et la prise en charge de la maladie.

[Diabetology: what's new in 2023]. / Diabétologie: ce qui a changé en 2023.

Diabetology is a continuously evolving discipline, many molecules are developed and treatment recommendations change often according to the latest published studies. It is therefore often difficult for the primary care physician to be up to date. After lifestyle measures that must always be preferred before any drug, metformin remains the pharmacological basis of treatment. Current recommendations favor the introduction of an SGLT2 inhibitor or a GLP-1 receptor agonist after metformin because these molecules have shown beneficial cardiovascular and renal effects. The purpose of this article is to guide the primary care physician to choose the most suitable pharmacological treatment for each patient, in the light of the 2023 novelties in the field of diabetes.

La diabétologie est une discipline en évolution continue, de nombreuses molécules sont développées et les recommandations de traitement changent fréquemment en fonction des dernières études publiées. Il est donc souvent difficile pour le médecin de premier recours d'être à jour. Après les mesures du style de vie qu'il faut toujours privilégier avant toute approche médicamenteuse, la metformine reste la base pharmacologique du traitement. Les recommandations actuelles préconisent d'instaurer un inhibiteur du SGLT2 ou un agoniste du récepteur du GLP-1 après la metformine car ces molécules ont montré des effets bénéfiques cardiovasculaires et rénaux. Le but de cet article est de fournir une aide au médecin de premier recours dans le choix du traitement pharmacologique le plus adapté à chaque patient, à la lumière des nouveautés 2023 dans le domaine du diabète.

[Obstetrics and Gynecology. Management and screening for gestational diabetes : what's new in 2023]. / Gynécologie-obstétrique. Prise en charge et dépistage du diabète gestationnel : ce qui a changé en 2023.

Gestational diabetes (GDM) is becoming increasingly common as a result of the increase in overweight, obesity and maternal age among pregnant women. As a result, in order to provide early hygienic and dietary management, it is recommended that targeted screening be carried out in the first trimester of pregnancy, based on the identification of risk factors in women. In the absence of risk factors, screening for gestational diabetes should be carried out for all pregnant women between 24 and 28 weeks' gestation. During pregnancy, the safest pharmacological treatment remains insulin, and the term of delivery should take account of additional risk factors, insulin requirements, fœtal growth kinetics and the balance of GDM. In the longer term, gestational diabetes should be regarded as a metabolic and cardiovascular warning sign.

Dû à l'augmentation du surpoids, de l'obésité et de l'âge maternel chez les femmes enceintes, le diabète gestationnel (DG) est de plus en plus fréquent. De ce fait, afin d'offrir une prise en charge hygiénodiététique précoce, il est recommandé d'effectuer un dépistage ciblé au premier trimestre de la grossesse pour identifier les facteurs de risque. En leur absence, le dépistage du DG doit être réalisé chez toutes les femmes enceintes entre 24 et 28 SA. Au cours de la grossesse, le traitement pharmacologique le plus sécuritaire reste l'insuline et le terme d'accouchement doit tenir compte des facteurs de risque surajoutés, des besoins en insuline, de la cinétique de croissance fœtale et de l'équilibre du DG. À plus long terme, le DG doit être considéré comme une alerte métabolique et cardiovasculaire.

Role of Oxidative Stress and Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 in Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) has become a widely studied subject due to its increasing prevalence and links to diseases such as type 2 diabetes and obesity. It has severe complications, including nonalcoholic steatohepatitis, cirrhosis, hepatocellular carcinoma, and portal hypertension that can lead to liver transplantation in some cases. To better prevent and treat this pathology, it is important to understand its underlying physiology. Here, we identify two main factors that play a crucial role in the pathophysiology of NAFLD: oxidative stress and the key role of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1). We discuss the pathophysiology linking these factors to NAFLD pathophysiology.

[News in diabetology: what's new in 2022]. / Diabétologie : ce qui a changé en 2022.

Diabetology is a constantly evolving discipline, many molecules appear on the market and treatment recommendations change quite frequently according to the latest published studies. It is therefore often difficult for the primary care physician to be up to date. After lifestyle measures that must of course be preferred before any drug approach, metformin remains the pharmacological basis of treatment. Current recommendations favor the introduction of an SGLT2 inhibitor or a GLP-1 receptor agonist after metformin because these molecules have shown beneficial cardiovascular and renal effects. The purpose of this article is to help the primary care physician to choose the most suitable pharmacological treatment for each patient, in the light of the 2022 novelties in the field of diabetes.

La diabétologie est une discipline en constante évolution. De nombreuses molécules apparaissent sur le marché et les recommandations de traitement changent assez fréquemment en fonction des dernières études publiées. Il est donc souvent difficile pour le médecin de premier recours d'être à jour. Après les mesures sur le style de vie, qu'il faut bien sûr privilégier avant toute approche médicamenteuse, la metformine reste la base pharmacologique du traitement. Les recommandations actuelles préconisent d'instaurer un inhibiteur du SGLT2 (sodium-glucose transporteur de type 2) ou un agoniste du récepteur du GLP-1 (Glucagon-like Peptide-1) après la metformine car ces molécules ont montré des effets bénéfiques cardiovasculaires et rénaux. Le but de cet article est d'aider le médecin de premier recours à choisir le traitement pharmacologique le plus adapté à chaque patient, à la lumière des nouveautés 2022 dans le domaine du diabète.

[The diabetic foot : a complex and multidisciplinary management]. / Pied diabétique : une prise en charge complexe et multidisciplinaire.

Diabetic foot syndrome is a common complication in people with diabetes and peripheral sensory impairment. This complex situation requires early clinical detection by various health care professionals, but also by patients and their relatives. The clinical course, the severity of the prognosis and the management will be determined by the speed of the diagnosis. In the case of confirmed disease, multidisciplinary management is necessary. The most important intervention, both for prevention and treatment, is the discharge of the affected foot.

Le syndrome du pied diabétique est une complication fréquente chez les personnes ayant un diabète et une atteinte de la sensibilité périphérique. Cette situation complexe nécessite une détection clinique précoce, par les divers professionnels de la santé mais aussi par les patients et leurs proches. L'évolution clinique, la gravité du pronostic et la prise en charge seront déterminées par la rapidité du diagnostic. En cas d'atteinte confirmée, une prise en charge multidisciplinaire est nécessaire. L'intervention la plus importante, tant pour la prévention que le traitement, est la décharge du pied atteint.

[Non-Alcoholic Fatty Liver Disease and Diabetes: the bad marriage]. / Stéatopathie non alcoolique (NAFLD) et diabète : le mauvais mariage.

NAFLD, whose prevalence keeps growing, is strongly linked with type 2 diabetes (T2D) through insulin resistance and oxidative stress. A multifactorial association with T1D has recently been found. NAFLD screening aims to identify non-alcoholic steatohepatitis (NASH) and fibrosis and to better refer to liver specialists. It is recommended for patients at higher risk, such as those with T2D. NAFLD treatment cornerstone is weight loss, obtained through lifestyle interventions, obesity pharmacotherapy, and bariatric surgery. When treating patients suffering from NAFLD and T2D, we should prioritize GLP-1 analogues and PPAR agonists, capable of regressing NASH, and SGLT2i, efficient on liver steatosis.

La stéatopathie non alcoolique (NAFLD), dont la prévalence est à la hausse, est une pathologie fortement liée au diabète de type 2 (DT2) par la résistance à l'insuline et le stress oxydatif. Une association multifactorielle avec le diabète de type 1 (DT1) a été récemment mise en évidence. Le dépistage de la NAFLD vise l'identification des formes plus sévères (NASH avec fibrose) et une orientation correcte vers les hépatologues. Il s'adresse à des sous-groupes à risque, dont les patients avec un DT2. La pierre angulaire du traitement de la NAFLD est la perte pondérale, les mesures hygiéno-diététiques, la pharmacologie de l'obésité ou la chirurgie bariatrique. Pour les patients avec NAFLD et DT2, il faut considérer en priorité les analogues du GLP-1 et les agonistes PPAR, capables de faire régresser la NASH, et les iSGLT2, efficaces sur la simple stéatose.

Moderate to Severe Soft Tissue Diabetic Foot Infections: A Randomized, Controlled, Pilot Trial of Post-debridement Antibiotic Treatment for 10 versus 20 days.

BACKGROUND: The optimal duration of antibiotic therapy for soft-tissue infections of the diabetic foot remains unknown. OBJECTIVE: We determine if antibiotic therapy after debridement for a short (10 days), compared with a long (20 days), duration for soft-tissue infections of the diabetic foot results in similar rates of clinical remission and adverse events (AE). SUMMARY OF BACKGROUND DATA: The optimal duration of systemic antibiotic therapy, after successful debridement, for soft tissue infections of diabetic patients is unknown. Because of the high recurrence risk, overuse is commonplace. METHODS: This was a randomized, controlled, non-inferiority pilot trial of cases of diabetic foot infection (excluding osteomyelitis) with the primary outcome of "clinical remission at 2-months follow-up". RESULTS: Among 66 enrolled episodes (17% females; median age 71 years), we randomized 35 to the 10-day arm and 31 to the 20-day arm. The median duration of the parenteral antibiotic therapy was 1 day, with the remainder given orally. In the intention-to-treat population, we achieved clinical remission in 27 (77%) patients in the 10-day arm compared to 22 (71%) in the 20-days arm ( P = 0.57). There were a similar proportion in each arm of AE (14/35 versus 11/31; P = 0.71), and remission in the per-protocol population (25/32 vs 18/27; P = 0.32). Overall, 8 soft tissue DFIs in the 10-day arm and 5 cases in the 20-day arm recurred as a new osteomyelitis [8/35 (23%) versus 5/31 (16%); P = 0.53]. Overall, the number of recurrences limited to the soft tissues was 4 (6%). By multivariate analysis, rates of remission (intention-to-treat population, hazard ratio 0.6, 95%CI 0.3-1.1; per-protocol population 0.8, 95%CI 0.4-1.5) and AE were not significantly different with a 10-day compared to 20-day course. CONCLUSIONS: In this randomized, controlled pilot trial, post-debridement antibiotic therapy for soft tissue DFI for 10 days gave similar (and non-inferior) rates of remission and AEs to 20 days. A larger confirmatory trial is under way. TRIAL REGISTRATION: ClinicalTrials NCT03615807.

Cardiovascular outcomes trials: a paradigm shift in the current management of type 2 diabetes.

Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in patients with type 2 diabetes (T2D). Historical concerns about cardiovascular (CV) risks associated with certain glucose-lowering medications gave rise to the introduction of cardiovascular outcomes trials (CVOTs). Initially implemented to help monitor the CV safety of glucose-lowering drugs in patients with T2D, who either had established CVD or were at high risk of CVD, data that emerged from some of these trials started to show benefits. Alongside the anticipated CV safety of many of these agents, evidence for certain sodium-glucose transporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have revealed potential cardioprotective effects in patients with T2D who are at high risk of CVD events. Reductions in 3-point major adverse CV events (3P-MACE) and CV death have been noted in some of these CVOTs, with additional benefits including reduced risks of hospitalisation for heart failure, progression of renal disease, and all-cause mortality. These new data are leading to a paradigm shift in the current management of T2D, with international guidelines now prioritising SGLT2 inhibitors and/or GLP-1 RAs in certain patient populations. However, clinicians are faced with a large volume of CVOT data when seeking to use this evidence base to bring opportunities to improve CV, heart failure and renal outcomes, and even reduce mortality, in their patients with T2D. The aim of this review is to provide an in-depth summary of CVOT data-crystallising the key findings, from safety to efficacy-and to offer a practical perspective for physicians. Finally, we discuss the next steps for the post-CVOT era, with ongoing studies that may further transform clinical practice and improve outcomes for people with T2D, heart failure or renal disease.

[News in diabetology 2021]. / Diabétologie.

Diabetes is a rapidly evolving discipline ; numerous new molecules are available and recommendations regarding treatment change. However, these rapid changes are sometimes difficult to follow for general practitioners. Metformin remains the cornerstone of type 2 diabetes treatment after lifestyle modifications, which should always be encouraged before medications. Currently, the best classes to add after metformin are SGLT2 inhibitors and GLP-1 receptor agonists, as these molecules showed some cardiovascular and renal beneficial effects in dedicated studies. The aim of this article is to guide the general practitioner in choosing the most suitable pharmacological treatment for each patient, in light of the novelties in the field of diabetes that appeared during the year 2021.

La diabétologie est une discipline qui évolue rapidement, de nombreuses molécules apparaissent sur le marché et les recommandations de traitement changent. Il est donc souvent difficile pour le médecin de premier recours d'être à jour. Après les mesures du style de vie qu'il faut bien sûr privilégier avant toute approche médicamenteuse, la metformine reste le pilier pharmacologique du traitement. Les recommandations actuelles préconisent d'instaurer un inhibiteur du SGLT2 ou un agoniste du récepteur du GLP-1 après la metformine car ces molécules ont montré des effets bénéfiques cardiovasculaires et rénaux dans des études. Le but de ce bref article est d'aider le médecin de premier recours à choisir le traitement pharmacologique le plus adapté à chaque patient·e, à la lumière des nouveautés 2021 dans le domaine du diabète.

[Pancreatogenic Diabetes]. / Diabète pancréatoprive.

Often underdiagnosed and sometimes falsely considered as a type 2 diabetes, type 3c diabetes (mostly known as pancreatogenic diabetes) is composed by a heterogenous group of illnesses characterized by diabetes mellitus associated with exocrine pancreatic insufficiency. The clinical, physiopathological and treatment features differ from type 2 diabetes, and they are important to keep in mind when diabetes is diagnosed, to avoid potential complications. The aim of this article is to review the principal etiologies of this often-unrecognized pathology.

Souvent sous-diagnostiqué et parfois considéré à tort comme un diabète de type 2, le diabète de type 3c, plus connu sous le nom de diabète pancréatoprive, est composé d'un groupe hétérogène de maladies caractérisées par un diabète sucré lié à une insuffisance pancréatique exocrine. La présentation clinique, la physiopathologie et la prise en charge de ces pathologies diffèrent sensiblement du diabète de type 2, et il convient de s'en rappeler au moment du diagnostic d'un diabète sucré afin d'éviter de potentielles complications. Le but de cet article est de faire le point sur les principales étiologies de cette pathologie peu connue.

[Diabetic neuropathy: an update]. / Neuropathie diabétique : mise au point.

Diabetic neuropathy is a heterogeneous entity, grouping multiple disorders, of which the most classic form is distal symmetric polyneuropathy (DSPN). Its diagnosis is based in most cases on a compatible history and clinical examination. Screening for DSPN, to allow the implementation of preventive measures against its complications, remains the cornerstone of management, in the absence of specific treatment. In this article, we propose a review of the different forms of diabetic neuropathy and their management.

La neuropathie diabétique est une entité hétérogène regroupant des atteintes multiples, dont la forme la plus classique est la polyneuropathie distale symétrique (PNDS). Son diagnostic repose dans la majorité des cas sur une anamnèse et un examen clinique compatibles. Le dépistage de la PNDS, pour permettre la mise en place de mesures préventives de ses complications, reste la pierre angulaire de la prise en charge en l'absence de traitement spécifique. Nous proposons dans cet article une revue des différentes formes de neuropathie diabétique et de leur prise en charge.

[Insulin allergy: how to manage it?] / Allergie à l'insuline : comment faire ?

Insulin allergy is a rare entity, complex to manage. Several types of hypersensitivity reaction are described, depending on the allergens (insulin itself vs additives). Type I, so-called immediate, IgE-mediated reactions are the most common. Their management requires a careful history and examination, as well as an allergological consult. If an IgE-mediated allergy is confirmed, insulin avoidance is recommended whenever possible. If insulin treatment is mandatory, another type of insulin may be offered. In case of failure, desensitization should be discussed, either via a dedicated protocol, or via insulin pump. In this article, we summarize the available data from the literature.

L'allergie à l'insuline est une entité rare, complexe à prendre en charge. Plusieurs types de réactions d'hypersensibilité sont décrits, selon les agents allergènes (insuline même vs additifs). Les réactions de type I, dites immédiates, IgE (immunoglobulines E) médiées sont les plus fréquentes. Leur prise en charge nécessite une anamnèse et un examen minutieux, ainsi qu'un avis allergologique. En cas de confirmation d'allergie IgE médiée, une éviction des insulines est dans la mesure du possible recommandée. Si la poursuite des traitements insuliniques est inévitable, un autre type d'insuline peut être proposé. En cas d'échec, une induction de tolérance devrait être discutée, soit via un protocole dédié, soit via la mise sous pompe à insuline. Nous résumons dans cet article les données de la littérature à disposition.

Three Weeks Versus Six Weeks of Antibiotic Therapy for Diabetic Foot Osteomyelitis: A Prospective, Randomized, Noninferiority Pilot Trial.

BACKGROUND: In patients with diabetic foot osteomyelitis (DFO) who underwent surgical debridement, we investigated whether a short (3 weeks) duration compared with a long (6 weeks) duration of systemic antibiotic treatment is associated with noninferior results for clinical remission and adverse events (AEs). METHODS: In this prospective, randomized, noninferiority pilot trial, we randomized (allocation 1:1) patients with DFO after surgical debridement to either a 3-week or a 6-week course of antibiotic therapy. The minimal duration of follow-up after the end of therapy was 2 months. We compared outcomes using Cox regression and noninferiority analyses (25% margin, power 80%). RESULTS: Among 93 enrolled patients (18% females; median age 65 years), 44 were randomized to the 3-week arm and 49 to the 6-week arm. The median number of surgical debridements was 1 (range, 0-2 interventions). In the intention-to-treat (ITT) population, remission occurred in 37 (84%) of the patients in the 3-week arm compared with 36 (73%) in the 6-week arm (P = .21). The number of AEs was similar in the 2 study arms (17/44 vs 16/49; P = .51), as were the remission incidences in the per-protocol (PP) population (33/39 vs 32/43; P = .26). In multivariate analysis, treatment with the shorter antibiotic course was not significantly associated with remission (ITT population: hazard ratio [HR], 1.1 [95% confidence interval {CI}, .6-1.7]; PP population: HR, 0.8 [95% CI: .5-1.4]). CONCLUSIONS: In this randomized controlled pilot trial, a postdebridement systemic antibiotic therapy course for DFO of 3 weeks gave similar (and statistically noninferior) incidences of remission and AE to a course of 6 weeks. CLINICAL TRIALS REGISTRATION: NCT03615807; BASEC 2016-01008 (Switzerland).

Is routine measurement of the serum C-reactive protein level helpful during antibiotic therapy for diabetic foot infection?

Clinicians frequently monitor serum C-reactive protein (CRP) levels during therapy for diabetic foot infections (DFIs), but evidence supporting this is unclear. Using a database from prospective controlled DFI trials, with fixed duration of antibiotic therapy, we correlated the CRP levels at study enrolment and at end of therapy (EOT). Among 159 DFI episodes, 93 involved the bone and 66 the soft tissues. Overall, treatment cured 122 infections (77%), while 37 episodes (23%) recurred after a median of 53 days. The median CRP in the groups with cure versus failure differed minimally at enrolment (median 67 vs. 81 mg/L) or EOT (7 vs. 10 mg/L). Similarly, there was negligible difference in the percentage of CRP levels that normalized at EOT (39% vs. 35%). In our prospective cohorts, a blunt iterative monitoring of CRP during DFI treatment, without correlation with clinical findings, failed to predict treatment failures.

Hypothyroidism-Associated Dyslipidemia: Potential Molecular Mechanisms Leading to NAFLD.

Thyroid hormones control lipid metabolism by exhibiting specific effects on the liver and adipose tissue in a coordinated manner. Different diseases of the thyroid gland can result in hypothyroidism. Hypothyroidism is frequently associated with dyslipidemia. Hypothyroidism-associated dyslipidemia subsequently results in intrahepatic accumulation of fat, leading to nonalcoholic fatty liver disease (NAFLD), which leads to the development of hepatic insulin resistance. The prevalence of NAFLD in the western world is increasing, and evidence of its association with hypothyroidism is accumulating. Since hypothyroidism has been identified as a modifiable risk factor of NAFLD and recent data provides evidence that selective thyroid hormone receptor ß (THR-ß) agonists are effective in the treatment of dyslipidemia and NAFLD, interest in potential therapeutic options for NAFLD targeting these receptors is growing. In this review, we summarize current knowledge regarding clinical and molecular data exploring the association of hypothyroidism, dyslipidemia and NAFLD.

[SGLT2 inhibitors : only beneficial ?] / Inhibiteurs du SGLT2 : que des bénéfices ?

SGLT2 inhibitors are more and more prescribed in the treatment of type 2 diabetes. Their cardioprotective and nephroprotective effects make them particularly attractive. However, it is important to be aware of their potential side effects. This article aims to summarize the actual evidence regarding the most studied ones. Euglycemic ketoacidosis, genital infections and hypovolemia have been well described. Evidence is less robust regarding the increased risk of amputations, fractures, urinary tract infection or acute kidney disease. This article also aims to summarize some key messages to discuss with patients, in order to prevent the occurrence of euglycemic ketoacidosis and hypovolemia.

Les iSGLT2 (inhibiteurs du sodium-glucose de type 2) sont prescrits de plus en plus précocement chez nos patients diabétiques de type 2. Leur cardio et néphroprotection ne font plus de doute, les rendant particulièrement attractifs. Cependant, ces traitements ne sont pas dénués de risque. Cet article propose une mise au point sur l'évidence actuelle concernant les effets indésirables les plus étudiés. L'augmentation du risque d'acidocétose euglycémique, d'infections génitales ou encore d'hypovolémie a été bien démontrée. La littérature est plus hétérogène concernant l'augmentation du risque d'amputations, de fractures, d'infections du tractus urinaire ou encore d'insuffisance rénale aiguë. Cet article reprend également les messages clés à transmettre aux patients afin de prévenir la survenue d'une acidocétose euglycémique ou d'un état hypovolémique.

[News in Diabetology 2020]. / Diabétologie.

Diabetes is a rapidly evolving discipline, numerous new molecules and recommendations are available. However, these rapid changes are sometimes difficult to follow for general practitioners. Metformin remains the cornerstone of type 2 diabetes treatment after lifestyle modifications, which should always be encouraged before medications. Currently, the best classes to add after metformin seem to be SGLT2 inhibitors and GLP-1 receptor agonists, as these molecules showed some cardiovascular and renal beneficial effects in dedicated studies. Nevertheless, the current pharmacological plethora is paradoxically associated with clinical inertia as general practitioners may be in trouble finding the right medication. This article will highlight novelties in the field of diabetes during the year 2020.

La diabétologie est une discipline qui évolue rapidement, de nombreuses molécules apparaissent sur le marché, de même que de nouvelles recommandations, qu'il est souvent difficile de suivre pour le médecin de premier recours. Les dernières recommandations, après les mesures du style de vie qu'il faut bien sûr privilégier avant toute approche médicamenteuse, sont d'initier un inhibiteur du cotransporteur sodium-glucose de type 2 ou un agoniste du récepteur du Glucagon-Like Peptide-1 après la metformine, cette dernière restant le pilier pharmacologique du traitement du diabète de type 2. Au vu de la jungle thérapeutique actuelle dans le traitement du diabète de type 2, le but de ce bref article est d'aider le médecin de premier recours à s'y retrouver en faisant le point sur les nouveautés 2020 dans le domaine du diabète.

[MODY type diabetes: an often-misunderstood entity]. / Diabète de type MODY : une entité souvent méconnue.

MODY diabetes, for Maturity Onset Diabetes of the Young, is a form of monogenic diabetes characterized by a typical onset before the age of 25 years, the lack of autoimmunity against the b cells of the pancreas, a preserved ß cells function and an autosomal dominant mode of inheritance. This type of diabetes constitutes 2 to 5% of all cases of diabetes but remains often undiagnosed. Nearly 15 MODY subtypes have been identified to date. The 3 most common subtypes are caused by mutations in the genes encoding glucokinase, HNF1a and HNF4a, and account for approximately 80% of all MODY cases. Carrying out a genetic test can thus make it possible to make the diagnosis of MODY diabetes and to set up an appropriate treatment. In this article we will discuss these 3 main MODY sub-type, although there are other forms, which may be characterized by associated specific organ damage.

Le diabète Maturity Onset Diabetes of the Young (MODY) est une forme de diabète monogénique se caractérisant par une apparition typique avant l'âge de 25 ans, l'absence d'autoimmunité contre les cellules ß du pancréas, une fonction préservée des cellules ß et un mode de transmission autosomique dominant. Ce type de diabète constitue 2 à 5 % de tous les cas de diabètes, mais reste souvent non diagnostiqué. Près de 15 sous-types sont, à ce jour, identifiés. Les 3 les plus fréquents sont causés par des mutations des gènes codant pour la glucokinase, HNF1α et HNF4α, qui représentent environ 80 % des cas de MODY. La réalisation d'un test génétique peut ainsi permettre de poser le diagnostic de MODY et mettre en place un traitement approprié. Dans cet article nous discutons de ces 3 sous-types principaux de MODY, bien qu'il existe d'autres formes plus rares pouvant se caractériser par des atteintes d'organes spécifiques associées.