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Our study evaluated the performance of a selective screening strategy for hyperglycaemia in pregnancy (HIP) based on the presence of risk factors (RFs; body mass index ≥ 25 kg/m2, age ≥ 35 years, family history of diabetes, personal history of HIP or macrosomic infant) to diagnose HIP and to predict HIP-related events. Women with no known diabetes who had undergone complete universal screening (early, before 22 weeks of gestation and, if normal, in the second part of pregnancy) at our department (2012–2016) were selected, resulting in four groups of women according to the presence of HIP and/or RFs, with a predefined composite endpoint (preeclampsia or large-for-gestational-age infant or shoulder dystocia). Included were 4518 women: 23.5% had HIP and 71.1% had at least one RF. The distribution among our four groups was: HIP−/RF− (n = 1144); HIP−/RF+ (n = 2313); HIP+/RF− (n = 163); and HIP+/RF+ (n = 898). HIP was more frequent when RFs were present rather than absent (33.1% vs 15.4%, respectively; P < 0.001). Incidence of the composite endpoint differed significantly (P < 0.0001) across groups [HIP−/RF− 6.3%; HIP−/RF+ 13.2%; HIP+/RF− 8.6%; and HIP+/RF+ 17.1% (HIP effect: P < 0.05; RF effect: P < 0.001; interaction HIP * RF: P = 0.94)] and significantly increased with the number of RFs (no RF: 6.3%, 1 RF: 10.8%, 2 RFs: 14.7%, 3 RFs: 28.0%, 4–5 RFs: 25.0%; P < 0.0001). RFs are predictive of HIP, although 15.4% of women with HIP have no RFs. Also, irrespective of HIP status, RFs are predictive of HIP-related events, suggesting that overweight/obesity, the only modifiable RFs, could be targets of interventions to improve pregnancy prognosis. [ABSTRACT FROM AUTHOR]

Secondary prevention can easily be defined as referring to patients with a history of CV events although, in recently published cardiovascular outcome trials (CVOTs), inclusion criteria were slightly different, combining both patients with previous CVD events and those with established CVD. Thus, if guidelines highlight specific indications for patients in secondary prevention [3], then some patients considered as being in "primary" prevention but having a high CV risk profile, especially those with silent CAD, might also benefit from the treatment. CV risk assessment in asymptomatic patients with no history of CVD usually includes electrocardiography (ECG) and echocardiography, and often a stress test (ECG and/or myocardial scintigraphy and/or echography) as well, with subsequent coronary angiography in patients with clear evidence of silent myocardial ischaemia. Nevertheless, it should be emphasized that canagliflozin was recently found, in a subgroup of patients included in the Canagliflozin Cardiovascular Assessment Study (CANVAS), to reduce the overall risk of HF events in patients with T2D and high CVD risk whatever their EF status (preserved, reduced or unknown) [19]. [Extracted from the article]

1h-PG plasma glucose value 1h after 75-g oral glucose tolerance test 2h-PG plasma glucose value 2h after 75-g oral glucose tolerance test AGEs advanced glycation end-products BMI body mass index DIP diabetes in pregnancy eGDM early gestational diabetes mellitus FINDRISC Finnish Diabetes Risk Score FPG fasting plasma glucose GDM gestational diabetes mellitus SD standard deviation WG weeks of gestation DIP was defined as FPG>=7.0mmol/L and/or 2h-PG>=11.1mmol/L; eGDM was defined as FPG>=5.1mmol/L in early pregnancy, and regular GDM as FPG 5.1-6.9mmol/L and/or 1h-PG>=10.0mmol/L and/or 2h-PG 8.5-11.0mmol/L during OGTT performed after 22 WG. GDM: gestational diabetes mellitus; eGDM: early gestational diabetes mellitus; DIP: diabetes in pregnancy; SD: standard deviation. GDM: gestational diabetes mellitus; eGDM: early gestational diabetes mellitus; DIP: diabetes in pregnancy; BMI: body mass index; FINDRISC: Finnish Diabetes Risk Score; WG: weeks of gestation; NA: non-applicable. [Extracted from the article]

In addition to screening for hyperglycaemia during pregnancy after 24 weeks of gestation (WG), the current guidelines also suggest screening in early pregnancy and referring women with early gestational diabetes mellitus (eGDM) or overt diabetes (OD) for immediate care. Our aim was to evaluate this strategy. This study evaluated, at our hospital (2012–2016), whether the incidence of a predefined composite outcome (preeclampsia, large-for-gestational-age infant, shoulder dystocia) and secondary outcomes was different when women were screened only after 22WG ('late screening only') or before 22WG and treated for eGDM or OD if present, with repeat screening after 22WG if absent ('early ± late screening'). Early ± late screening (n = 4605, 47.0%) increased between 2012 and 2016 (P < 0.0001) and was associated with more risk factors for GDM than late screening only. Glycaemic status differed in both groups (early ± late screening: eGDM 10.3%, GDM 12.1%, OD 0.9% vs. late screening only: GDM 16.8%, OD 1.2%; P < 0.001), with a higher rate of insulin therapy (8.9% vs. 6.0%; P < 0.001) and less gestational weight gain (11.1 ± 5.4 kg vs. 11.4 ± 5.5 kg; P = 0.013) in the early ± late screening group. Rates of those meeting the composite criterion were similar in both groups [11.6% vs. 12.0%, respectively; odds ratio (OR): 1.040, 95% confidence interval (CI): 0.920–1.176; P = 0.53] and remained comparable after adjusting for Propensity Scores (OR: 1.046, 95% CI: 0.924–1.185; P = 0.4790). Rates for secondary outcomes were also similar in both groups. While a strategy including early measurement of fasting plasma glucose during pregnancy increases the incidence and care of hyperglycaemia during pregnancy, it may not significantly improve pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Abstract Aim Because type 2 diabetes (T2D) is related to obesity, it is often associated with obstructive sleep apnoea syndrome (OSAS), although OSAS is also frequently diagnosed in patients with type 1 diabetes (T1D) and may promote gestational diabetes. Thus, this systematic review of the scientific evidence aimed to evaluate the epidemiological association between OSAS and all forms of diabetes, the current understanding of the pathophysiological mechanisms behind these associations, the expected benefits and limitations of OSAS treatment in patients with diabetes and, finally, to propose which patients require screening for OSAS. Methods A panel comprising French expert endocrinologists and pneumologists was convened. Two of these experts made a search of the relevant literature for each subpart of the present report; all panel experts then critically reviewed the entire report separately as well as collectively. Results There is little evidence to support the notion that OSAS treatment improves glycated haemoglobin, although it may improve nighttime blood glucose control and insulin sensitivity. However, there is robust evidence that OSAS treatment lowers 24-h blood pressure. Conclusion The high prevalence of OSAS in patients with T1D and T2D justifies screening for the syndrome, which should be based on clinical symptoms, as the benefits of OSAS treatment are mainly improvement of symptoms related to sleep apnoea. There are also several clinical situations wherein screening for OSAS seems justified in patients with diabetes even when they have no symptoms, particularly to optimalize control of blood pressure in cases of resistant hypertension and microvascular complications. [ABSTRACT FROM AUTHOR]

Aim This study assessed whether male fetal gender increases the risk of maternal gestational diabetes mellitus (GDM) and investigated the association with placental weight. Methods The study included 20,149 women without pregestational diabetes who delivered singletons at our hospital between January 2002 and December 2010. There was universal screening for GDM, and all placentas were weighed at delivery. Results GDM (affecting 14.2% of women) was not associated with fetal gender (male fetuses in women without and with GDM: 51.8% vs. 51.7%, respectively; P = 0.957), and remained likewise after logistic-regression analysis of risk factors for GDM (OR: 1.007, 95% CI: 0.930–1.091; P = 0.858). Placental weights were 600 ± 126 g, 596 ± 123 g, 584 ± 118 g and 587 ± 181 g in women with GDM/female, GDM/male, no GDM/female and no GDM/male fetuses, respectively (GDM effect: P = 0.017; gender effect: P = 0.41; GDM * gender effect: P = 0.16). Conclusion The present results suggest that fetal gender is not associated with GDM and, while placental weights were higher in cases of GDM, there were still no gender effects. [ABSTRACT FROM AUTHOR]

Aim This study retrospectively evaluated the complications associated with prepregnancy overweight (OW) or obesity (OB) and gestational weight gain (GWG) in women with or without universally screened and treated gestational diabetes mellitus (GDM). Methods A total of 15,551 non-Asian women without pregravid diabetes or hypertension who delivered singleton babies (2002–2010) were classified according to GDM (13.5%), pregestational body mass index (BMI; normal range: 18.5–24.9 kg/m 2 ), OW (26.2%), OB (13.9%; BMI ≥ 30 kg/m 2 ) and GWG (< 7 kg: 32%; 7–11.5 kg: 37%; 11.6–16 kg: 23%; > 16 kg: 8%). Main outcome measures were large/small for gestational age (LGA/SGA), caesarean section, preeclampsia, preterm delivery and shoulder dystocia. Results GDM was associated with more LGA babies [Odds Ratio (OR): 2.12, 95% confidence interval (CI): 1.85–2.43], caesarean section (OR: 1.49, 95% CI: 1.34–1.65) and preeclampsia (OR: 1.59, 95% CI: 1.21–2.09). OW/OB and GWG were associated with LGA infants whatever the GDM status, and with SGA babies only in women without GDM. LGA status was independently associated with GWG in women with GDM (11.6–16 kg: OR: 1.74, 95% CI: 1.49–2.03 and > 16 kg OR: 3.42, 95% CI: 2.83–4.13 vs 7–11.5 kg) and in women without GDM (OR: 2.14, 95% CI: 1.54–2.97 or OR: 2.65, 95% CI: 1.68–4.17, respectively), and with BMI only in women without GDM (OR: 1.12, 95% CI: 1.00–1.24, per 10 kg/m 2 ). SGA status was independently associated with OW (OR: 0.86, 95% CI: 0.77–0.98), OB (OR: 0.84, 95% CI: 0.72–0.98) and GWG < 7 kg (1.14, 95% CI: 1.01–1.29) only in women without GDM. Conclusion In our European cohort and considering the triumvirate of GDM, BMI and GWG, GDM was the main contributor to caesarean section and preeclampsia. OW/OB and GWG contributed to LGA and SGA infants mainly in women without GDM. [ABSTRACT FROM AUTHOR]

To explore (i) in what proportion and direction coronary artery calcium (CAC) score reclassifies coronary risk in asymptomatic diabetic patients at high a priori coronary risk, and (ii) whether screening for asymptomatic myocardial ischemia / coronary stenosis only in patients at very high coronary risk - whether a priori or combined with those reclassified at very high risk according to their CAC score - has good sensitivity to detect these conditions. We retrospectively selected 377 asymptomatic primary prevention diabetic patients at high or very high a priori coronary risk according to national guidelines. All had their CAC score measured and underwent stress myocardial scintigraphy to detect myocardial ischemia. Those identified with ischemia then had a coronary angiography to identify coronary stenoses. Of the selected patients, 242 and 135 patients had a high and very high a priori coronary risk, respectively. After taking into account their CAC score, the former were reclassified into three risk categories: moderate (n = 159, 66%), high (n = 38) and very high (45 patients) risk. Myocardial ischemia was identified in 35 patients and coronary stenoses in 14 of the latter. Had a stress scintigraphy been performed only in the 135 patients at very high risk a priori , 18 patients would have been detected with ischemia (sensitivity 51%), and 9 with coronary stenoses (sensitivity 64%). Had a scintigraphy also been performed on the 45 patients at very high risk after CAC-reclassification, an additional 7 and 5 patients with ischemia and coronary stenoses, respectively, would have been identified. Following national guidelines, 66% of our population of asymptomatic diabetic persons at high a priori coronary risk were reclassified into the moderate risk category, translating into less stringent goals for risk factor control. Eighteen percent were reclassified into the very high-risk category, leading to 100% detection sensitivity for patients with ischemia and coronary stenoses. [ABSTRACT FROM AUTHOR]

Prediabetes is a very prevalent condition associated with an increased risk of developing diabetes and/or other chronic complications, in particular cardiovascular disorders. Early detection is therefore mandatory since therapeutic interventions may limit the development of these complications. Diagnosis of prediabetes is currently based on glycemic criteria (fasting plasma glucose (PG), and/or glycemia at 120 min during a 75 g oral glucose tolerance test (OGTT) and/or glycated hemoglobin (HbA1c). Accumulating longitudinal evidence suggests that a 1-hour PG ≥155 mg/dl (8.6 mmol/l) during the OGTT is an earlier marker of prediabetes than fasting PG, 2-h post-load PG, or HbA1c. There is substantial evidence demonstrating that the 1-h post-load PG is a more sensitive predictor of type 2 diabetes, cardiovascular disease, microangiopathy and mortality compared with conventional glucose criteria. The aim of this review is to highlight the paramount importance of detecting prediabetes early in its pathophysiological course. Accordingly, as recommended by an international panel in a recent petition, 1-h post-load PG could replace current criteria for diagnosing early stages of "prediabetes" before prediabetes evolves as conventionally defined. [ABSTRACT FROM AUTHOR]

The International Association of Diabetes and Pregnancy Study Group (IADPSG) has proposed that blood glucose levels for the diagnosis of gestational diabetes mellitus (GDM) be the values associated with a 1.75-fold increase in the risk of neonatal complications in the Hyperglycaemia and Adverse Pregnancy Outcomes (HAPO) study. However, this recommendation was not adopted by the US National Institutes of Health (NIH) panel as it would have been responsible for a huge increase in the prevalence of GDM with no clear evidence of a reduction of events at such blood glucose values. Considering this aspect, we now propose the use of a blood glucose threshold combination associated with an odds-ratio of 2.0 for neonatal disorders [fasting plasma glucose (FPG) ≥ 95 mg/dL, or a 1-h glucose value after a 75-g oral glucose tolerance test (OGTT) ≥ 191 mg/dL or a 2-h glucose value ≥ 162 mg/dL] for GDM diagnosis. This would lead to a lower prevalence of GDM and concentrate medical resources on those with the highest risk of complications. This would also allow the use of a similar FPG value for both the diagnosis and therapeutic target of GDM. The IADPSG also proposed screening for dysglycaemia during early pregnancy, using FPG measurement with a similar threshold after 24 weeks of gestation. We propose the same strategy considering an FPG value ≥ 95 mg/dL as abnormal, but only after confirmatory measurements. We also believe that an OGTT should not be used before 24 weeks of gestation as normal values during that time are as yet unknown. [ABSTRACT FROM AUTHOR]

Aim The study compared the duration of maintenance of treatment in patients with type 2 diabetes (T2D) using dual therapy with either metformin and sitagliptin (M-Sita) or metformin and a sulphonylurea (M-SU). Materials and methods This observational study included adult patients with T2D who had responded inadequately to metformin monotherapy and therefore had started de-novo treatment with Met-Sita or Met-SU within the previous eight weeks. Patient follow-up and changes to treatment were performed according to their general practitioner's usual clinical practice. The primary outcome was time to change in treatment for whatever cause. HbA 1c and symptomatic hypoglycaemia were also documented. Results The median treatment duration for patients in the M-Sita group (43.2 months) was significantly longer ( P < 0.0001) than in the M-SU group (20.2 months). This difference persisted after adjusting for baseline differences and confounders. A similar reduction in HbA 1c was noted in both arms (–0.6%), and the incidence of hypoglycaemia prior to treatment modification was lower with M-Sita (9.7%) than with M-SU (21.0%). Adverse events potentially related to treatment were reported in 2.8% ( n = 52) and 2.7% ( n = 20) of patients in the M-Sita and M-SU arms, respectively. Conclusion Under everyday conditions of primary diabetes care, dual therapy with M-Sita can be maintained for longer than M-SU. In addition, while efficacy, as measured by changes in HbA 1c , was similar between treatments, the incidence of hypoglycaemia was lower in patients taking M-Sita. [ABSTRACT FROM AUTHOR]

Objectives This study aimed to estimate, in a large group of Algerian adolescents, the prevalence of the metabolic syndrome (MetS), using four definitions (by Cook, De Ferranti, Viner and the IDF), and to test the validity of unique thresholds of waist circumference, waist/height ratio and BMI in screening for the MetS regardless of the definition used. Subjects and methods A total of 1100 adolescent students, aged 12–18 y, were randomly selected from schools and classrooms in the city of Constantine; all had anthropometric measurements taken and 989 had blood tests. Results Prevalences of the MetS were: 2.6% for boys and 0.6% for girls by the Cook definition; 4.0% for boys and 2.0% for girls by the De Ferranti definition; 0.7% for boys and 0% for girls by the Viner definition; and 1.3% for boys and 0.5% for girls by the 2007 IDF definition. Prevalences ranged from 3.7% to 13.0% in obese adolescents. Unique thresholds, independent of gender, age and height, of 80 cm for waist circumference, 0.50 for waist/height ratio and 25 kg/m 2 for BMI had sensitivities of 72–100%, 67–100% and 72–100%, respectively, and specificities of 74–78%, 74–86% and 74–78%, respectively, depending on the MetS definition used. Conclusion The MetS is present in Algerian adolescents and the prevalence is especially high in obese young people. Our thresholds for waist circumference, waist/height ratio and BMI for screening for the MetS should now be tested in other adolescent populations. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Although it is important to screen women who have had gestational diabetes mellitus (GDM) for abnormal post-partum glucose levels, such testing is rarely performed. The aim of this study was to use data from the first observational phase of the IMPACT study to determine rates of screening within 6 months of delivery in a multiethnic cohort, focusing in particular on the effects of social deprivation and the risk of future diabetes. Patients and methods: To investigate the frequency of post-partum screening, charts were analyzed, and all women attending four centres located in a deprived area who had had GDM between January 2009 and December 2010 were contacted by phone. The Evaluation of Precarity and Inequalities in Health Examination Centres (EPICES) deprivation index and Finnish Diabetes Risk Score (FINDRISK) questionnaire were also evaluated. Results: Data were evaluable for 589 of the 719 women contacted (mean age: 33.4±5.2years; mean body mass index: 27.6±5.4kg/m2), and 196 (33.3%) reported having been screened. On multivariate analysis, factors associated with a lack of screening were smoking [odds ratio (OR): 0.42 (0.20–0.90), P <0.05], low consumption of fruit and vegetables [OR: 0.58 (0.39–0.82), P <0.01] and heavier offspring birth weight (P <0.05), although there were no differences in FINDRISK and EPICES scores between screened and unscreened women. Conclusion: One-third of women who had had GDM reported having been screened for dysglycaemia at 6 months post-partum. However, it is expected that the interventional phase of the IMPACT study will increase screening rates, especially in women with the risk factors associated with lower screening rates during this observational phase. [Copyright &y& Elsevier]

• In previous studies, women with pregnancies complicated by hyperglycaemia in pregnancy (HIP) and insulin resistance (IR), but not those without IR, had a greater risk of adverse pregnancy outcomes than those with normoglycaemic pregnancies. • Considering only women with HIP, we found that HOMA-IR index was positively associated with insulin therapy, gestational hypertension, preeclampsia, large-for-gestational-age infants and neonatal hypoglycaemia. • The association between a high HOMA-IR and insulin therapy, hypertensive disorders and large-for-gestational-age infants remained after adjustment for confounders, including body mass index. • On clinical practice, HIP stratification according to presence of IR might help decision makers adapt care to prevent adverse pregnancy outcomes. Aim. Recent studies have shown that women with hyperglycaemia in pregnancy and insulin resistance have a greater risk of adverse pregnancy outcomes than women with normoglycaemic pregnancies. This study aimed to determine adverse pregnancy outcomes of women with hyperglycaemia in pregnancy only as a function of insulin resistance. Methods. From a prospective cohort study, we included 1,423 women with hyperglycaemia in pregnancy whose insulin resistance was evaluated using homoeostatic model assessment for insulin resistance (HOMA-IR) when care was first provided for this condition. We compared the adverse pregnancy outcomes for different tertiles of HOMA-IR (intertertile range 1.9 and 3.3). Results. Increasing HOMA-IR tertiles were positively associated with the rate of insulin therapy (tertile 1, 2 and 3: 32.7, 47.0 and 58.7%, P < 0.0001), caesarean section (23.7, 26.0 and 32.2%, respectively, P < 0.01), gestational hypertension (1.3, 2.8 and 5.4% respectively, P < 0.01), preeclampsia (1.5, 2.8 and 4.5% respectively, P < 0.05), large-for-gestational-age infant (13.3, 10.4 and 17.6% respectively, P < 0.05), and neonatal hypoglycaemia (0.8, 1.5 and 3.2% respectively, P < 0.05). Women in the 3rd HOMA-IR tertile were more likely to have insulin therapy (odds ratio 2.09 (95% interval confidence 1.61–2.71)), hypertensive disorders (2.26 (1.42–3.36)), and large-for-gestational-age infant (1.42 (1.01–1.99)) than those in the 1st and 2nd tertiles combined in multivariable logistic regression analyses adjusted for gestational age at HOMA-IR measurement, glycaemic status, age, body mass index, family history of diabetes, parity and ethnicity. Conclusion. Despite suitable care and increased rates of insulin therapy during pregnancy, higher insulin resistance in women with hyperglycaemia in pregnancy was associated with a greater risk of adverse pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetes & Metabolism is the property of Masson Editeur and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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The puzzle of the multifaceted actions of sodium–glucose cotransporter type-2 inhibitors (SGLT2is) is still incomplete. For diabetologists (who are accustomed to dealing with the burden of cardiovascular autonomic neuropathy), the relationship between SGLT2is and the autonomic nervous system (ANS) represents one of the most intriguing aspects of the multiple effects of this family of drugs, especially given the poor availability of disease-modifying treatments for such complication. Therefore, the present review has considered both preclinical and clinical studies of this topic with autonomic perspectives by exploring the pathophysiological background of the interactions between the ANS and SGLT2, including sympathetic control of kidney function and the role of renal afferent nerves, and also by providing insights into the effects of SGLT2is on 24-h blood pressure (BP) and heart rate variability (HRV), with particular attention focused on the EMBODY trial. Indeed, despite the difficulties of exploring such a complex network comprising the kidney, heart and the ANS while targeting a single outcome—circadian BP and HRV—the available studies do offer evidence that SGLT2i actions are in part mediated by neural circuitry and the ANS. Thus, at this time, the worthwhile incidental result of these (and future) studies has been to highlight the role of autonomic innervation in the pathophysiology of kidney and heart disease. [ABSTRACT FROM AUTHOR]

To evaluate whether the initial care of women with fasting plasma glucose (FPG) levels at 5.1–6.9 mmol/L before 22 weeks of gestation (WG), termed 'early fasting hyperglycaemia', is associated with fewer adverse outcomes than no initial care. A total of 523 women with early fasting hyperglycaemia were retrospectively selected in our department (2012–2016) and separated into two groups: (i) those who received immediate care (n = 255); and (ii) those who did not (n = 268), but had an oral glucose tolerance test (OGTT) at or after 22 WG, with subsequent standard care if hyperglycaemia (by WHO criteria) was present. The number of cases of large-for-gestational age (LGA) infants, shoulder dystocia and preeclampsia with initial care of early fasting hyperglycaemia were compared after propensity score modelling and accounting for covariates. Of the 268 women with no initial care, 134 had hyperglycaemia after 22 WG and then received care. Women who received initial care vs those who did not were more likely to be insulin-treated during pregnancy (58.0% vs 20.9%, respectively; P < 0.00001), gained less gestational weight (8.6 ± 5.4 kg vs 10.8 ± 6.1 kg, respectively; P < 0.00001), had a lower rate of preeclampsia [1.2% vs 2.6%, respectively; adjusted odds ratio (aOR): 0.247 (0.082–0.759), P = 0.01], and similar rates of LGA infants (12.2% vs 11.9%, respectively) and shoulder dystocia (1.6% vs 1.5%, respectively). When initial FPG levels were ≥5.5 mmol/L (prespecified group, n = 137), there was a lower rate of LGA infants [6.7% vs 16.1%, respectively; aOR: 0.332 (0.122–0.898); P = 0.03]. Treating women with early fasting hyperglycaemia, especially when FPG is ≥5.5 mmol/L, may improve pregnancy outcomes, although this now needs to be confirmed by randomized clinical trials. [ABSTRACT FROM AUTHOR]

Introduction En Septembre 2012, l'association Dianéfra 93 a mis en place en Seine-Saint-Denis un programme de prévention (PP) du diabète de type 2. Le but est ici d'analyser les modalités de recrutement et le taux d'adhésion au P P. Patients et Méthodes Les critères d'éligibilité au PP étaient un score FIN-DRISK ≥ 15 chez un obèse (critère 1), ou ≥ 12 avec une charge orale en glucose anormale ou un antécédent de diabète gestationnel (critère 2). À l'inclusion, étaient réalisées une charge en glucose et si possible une mesure d'HbA 1c . Le PP proposait pour 80 personnes 45 activités individuelles et collectives (diététique et activité physique) sur une période de 2 ans. Résultats Parmi les 80 personnes inscrites, 57,5 % ont été recrutées lors de campagnes de dépistage du diabète et 42,5 % par des professionnels de santé sensibilisés à la démarche ; 52 (65 %) remplissaient le critère 1 et 28 le critère 2. Les modalités de recrutement par les campagnes ont été analysées sur l'année 2015 : FINDRISK déterminé chez 332 personnes ; 83 étaient éligibles (25 %) ; 8 se sont inscrites au PP ; la glycémie capillaire pratiquée lors des campagnes était anormale dans environ 5 % des cas. Le taux d'HbA 1c a été déterminé chez 50 des 80 personnes inscrites, et 31 avaient un résultat ≥ 5,7 %, seuil du pré-diabète, dont 16 avaient une hyperglycémie à jeun et/ou une intolérance au glucose. Deux seulement des 19 personnes avec HbA 1c < 5,7 % avaient une hyperglycémie à jeun. À ce jour, les 20 personnes inscrites depuis 2 ans dans le PP ont participé en moyenne à 50 % des activités proposées. Conclusions Cette étude pilote montre que lors des campagnes de dépistage le taux de sujets répondant aux critères justifiant la participation au PP est important mais que peu de sujets éligibles s'y inscrivent finalement. Parmi les sujets inclus, 62 % ont une HbA 1c élevée, anomalie glycémique la plus fréquente. Une fois dans le programme, l'adhésion aux activités proposées est correcte quoique nécessitant des mesures de renforcement de la motivation. [ABSTRACT FROM AUTHOR]

Aims Cardiac autonomic dysfunction (CAD) is characterized by sympatho-vagal imbalance (reduced vagal activity and relative sympathetic overdrive). This condition might shorten diastole duration (DD) and thus impair coronary perfusion. Arterial stiffness is also considered to impair coronary perfusion. The aim was to investigate the influences of CAD and arterial stiffness on subendocardial myocardial viability (SVI) and in particular the relation between the severity of CAD, DD and SVI in patients with type 2 diabetes (T2D). Methods In 42 T2Ds (55.2 ± 12.6 yrs, BMI 33.4 ± 7.3 kg/m 2 , HbA1c 8.04 ± 1.58%) free of cardiovascular history, we measured noninvasively heart rate (HR) and blood pressure (Finapres ® ) continuously during 5 minutes in supine position. We calculated then DD and arterial stiffness (augmentation index AIx and pulse wave velocity with a recently validated method: a Mac Apple dedicated software that reconstructs the central aortic pressure curve from the peripheral one (measured on finger) by a transfer function). Pulse wave velocity (PWV) was calculated from the equivalent index SI-DVP derived from the pulse pressure profile. The percentage of DD [DD% = (DD/duration of heart period) × 100] and SVI (area under aortic pressure curve during diastole/area during systole) were calculated as well. CAD was assessed using standard tests (deep-breathing, lying-to-standing, Valsalva), which mostly depend on vagal control. Results CAD was absent in 7 patients (Autonomic score 0: AS0), early (AS1: 1 abnormal test) in 14 patients, definite (AS2: 2 abnormal tests) in 15 patients and severe (AS3: 3 abnormal tests) in 6 patients. Mean HR in AS0 was 70.1 ± 11.6 bpm, in AS1: 74.9 ± 8.1, in AS2: 77.8 ± 11.2, in AS3: 95.0 ± 16.0 with a statistical significance ( P < 0.05) between AS0 vs. AS3, AS1 vs. AS3, AS2 vs. AS3. DD% correlated negatively with HR ( r = −0.747, P < 0.0001) and was lower in patients with higher AS. DD% differed significantly in AS3 and AS2 compared to AS0 (AS3: 52.8 ± 3.6%, AS2: 56.7 ± 4.1% and AS1: 59.7 ± 3.9% vs. AS0: 61.7 ± 3.3%; P = 0.0008, P = 0.011 and P = 0.25, respectively). Furthermore, the patients with AS2 or AS3 considered together showed lower DD% compared with the patients with AS0 or AS1 even after adjusting DD% with regression analysis at a conventional HR of 75 bpm (CAD+: 57.8 ± 3.3% vs. CAD−: 59.9 ± 2.6%; P = 0.030). SVI showed the same trend as DD%, with lower values in the patients with higher AS and reached the statistical significance in AS3 compared to AS0 (AS0: 1.23 ± 0.2; AS1: 1.16 ± 0.1, P = 0.41 vs. AS0; AS2: 1.02 ± 0.2, P = 0.056 vs. AS0; AS3: 0.88 ± 0.1, P = 0.006 vs. AS0). A strong positive linear correlation was found between SVI and DD% ( r = 0.921, P < 0.0001); conversely SVI showed a moderate negative linear correlation with aortic AIx adjusted at HR 75 bpm ( r = −0.489, P < 0.001). No correlations were found with pulse wave velocity. Conclusions In T2Ds CAD, expressed as reduced vagal activity, leads to HR acceleration and thus to diastole shortening, but it seems that CAD may shorten DD per se, independently of the effect on heart rate. Since DD influences strongly SVI, CAD plays a primary role in addition to arterial stiffness in the impairment of subendocardial myocardial viability and may thus worsen cardiovascular prognosis. [ABSTRACT FROM AUTHOR]

Introduction and aim Findrisk score has been validated for prediction of diabetes risk in many populations. The aim of this study was to examine the value of this score for the detection of dysglycemia (impaired fasting glucose and/or glucose intolerance or diabetes) in a high-risk population in Constantine (Algeria). Patients and method We had recruited 397 patients (281 women) with risk factors of diabetes, mean age 50.2 ± 11.7 years. All had fasting glycemia (FG) and oral post charge glycemia (PCG). Findrisk score was calculated. Carotid femoral pulse wave velocity (PWV) was measured by Complior ® device. Results FG and PCG were abnormal in 159 and 157 patients, respectively. Dysglycemia was found in 204 patients (51.4%), with diabetes in 17.6% and prediabetes in 33.8% of them. Findrisk score strongly correlated to FG ( r = 0.129, P = 0.01) and PCG ( r = 0.193, P = 10 −5 ) but also to systolic ( r = 0.33) and diastolic blood pressure ( r = 0.20), and to PWV ( r = 0.29). Discriminating threshold of this score for predicting dysglycemia was 13. It was significantly associated with prediabetes ( P = 0.001) and dysglycemia ( P = 10 −5 ), this association was found in women but not in men. Sensibility and specificity of this score for detecting dysglycemia were 76% and 37%, respectively. Their positive and negative predictive values were 54.7% and 60.7%, respectively. Conclusion FG and PCG detected dysglycemia in similar proportions. Identification of dysglycemia through Findrisk score was validated only in women. The correlation between Findrisk score and PWV suggests that a high score testified also of a high cardiovascular risk in these patients without glycemic abnormality or known cardiovascular history. [ABSTRACT FROM AUTHOR]

Background Microcirculation is altered in diabetic patients. In healthy subjects sequential compression/decompression by a pulsating suit may induce noninvasively endothelial activation by a pure mechanical effect, which is intended to increase the physiological shear stress. The objective was to evaluate the effects of sequential compression/decompression on the cutaneous forearm microcirculation in patients with type 2 diabetes. Materials and methods Sixteen patients with type 2 diabetes (6 men and 10 women, age 53.3 ± 11.4 yrs, 6 hypertensives, all on oral hypoglycaemic agents, no smoker, no cardiovascular disease, no renal failure, no retinopathy, HbA1c 7.1 ± 0.8%) were enrolled in a controlled cross-over study and were randomised into two groups: a verum (at V1) and a phantom (at V2, 13 ± 2 days after V1) compression at 65 mmHg/decompression session using Stendo ® pulsating suit was performed in group 1 and vice-versa in group 2. Each session spent 20 minutes. The pulsating suit generates heart rate synchronized compression/decompression applied to the lower part of the body (legs and abdomen). Cutaneous forearm microcirculation blood flow was measured continuously by laser Doppler flowmetry (LDF, Periflux System 5000 ® ) before, during and until 30 minutes after the end of the sessions. Results The 20-minutes area under curves (AUC) calculated during Stendo sessions were 1976 (SD: 3938) and −2043 (SD: 8302), respectively in verum and phantom sessions. The mean 40-minutes and 50-minutes AUCs (during Stendo plus 20 and 30 minutes after sessions stopped) were respectively 6936 and 7403 in verum, −7537 and −10,805 in phantom. The differences for AUC_40 min and AUC_50 min were higher between verum and phantom sessions ( P < 0.01 in all). Conclusion In T2D patients, sequential compression of the lower part of the body synchronized with each diastole period at a physiological pressure (65 mmHg) induces a significant increase of the cutaneous forearm microcirculation flow, away from the pulsatile stimuli. Pulsating suit session appears to produce a “shear stress like” effect. [ABSTRACT FROM AUTHOR]

Introduction Glycemic variability may play a role in diabetic microangiopathic complications. We recently showed that glycemic variability is more marked in nondiabetic obese patients with slightly elevated HbA1c levels. We aimed to examine the relations between glycemic variability and microcirculatory cutaneous blood flow (CBF) in patients with impaired glucose intolerance (IGT) or type 2 diabetes (T2D). Patients and methods We included 34 patients, 19 with IGT (HbA1c 5.1 ± 0.61%) and 15 with T2D on oral hypoglycemic treatments (HbA1c 7.1 ± 0.7%), with normal blood pressure and free of cardiovascular history. CBF (mean and standard deviation, SDCBF) was measured by laser doppler (Periflux ® ) on the forearm during 3 minutes, one hour after a standard breakfast including 75 g of carbohydrates. During the post-prandial period mean glucose was calculated and glycemic variability (standard deviation SDglucose, CONGA and J-index) evaluated during 3 hours after breakfast using CGMS. Lipids (HDL-cholesterol, LDL-cholesterol and triglycerides) were assayed. Results Compared with IGT patients, T2Ds had higher mean glucose, CONGA and J-indexes, and lower mean CBF and SDCBF ( P < 0.03 to < 0.0001). In the total population, mean CBF correlated negatively with SDglucose and J-index ( r = −0.41, P < 0.01; r = −0.34, P < 0.05, even after adjustment for age and BMI), but not with mean glucose. Mean CBF also correlated negatively with HbA1c ( r = −0.40, P < 0.01). In multivariate analysis, mean CBF remained significantly correlated with SDglucose and J-index independently from HbA1c only in IGTs. Glucose parameters from CGMS correlated with LDL-C and triglycerides and negatively correlated with HDL-C ( P < 0.002 to P < 0.0001). SDCBF correlated negatively with lipids but did not correlate with glucose parameters. Conclusion Microcirculatory CBF is lower in T2Ds than in IGTs. Glycemic variability seems to play a greater role than mean glucose and long-term hyperglycemia on peripheral microcirculation, mostly in patients with IGT. Lipid parameters cluster with glycemic variability and are associated with lower vasomotricity. [ABSTRACT FROM AUTHOR]

Introduction Nous avons montré que l'activité parasympathique cardiaque est souvent altérée chez les patients obèses non diabétiques et de la même façon chez les obèses métaboliquement sains. Cette étude avait pour but d'examiner l'influence de l'activité vago-sympathique sur la fréquence cardiaque (FC) et la réponse insulinique à l'hyperglycémie provoquée orale (HGPO) chez les patients obèses métaboliquement sains. Patients et Méthodes Nous avons inclus 24 patients, âgés de 34 ± 13 ans, IMC 42,2 ± 6,9 kg/m 2 , n'ayant aucun ou un seul critère du syndrome métabolique en plus d'un large tour de taille. L'activité parasympathique cardiaque (HF-FC) a été évaluée par analyse spectrale des variations de fréquence cardiaque en respiration contrôlée (Finapress®). Une HGPO (75 g de glucose) a été réalisée. Des index d'insulinosécrétion, l'index insulinogénique (IGI = Δinsulinémie (T0-T30)/Δglycémie (T0-T30)) et l'index de disposition orale (DIO = IGI/insuliné-mie) ont été calculés. Les taux sériques d'adrénaline et de noradrénaline ont été mesurés. Résultats Les patients ont été séparés en deux groupes selon leur activité para-sympathique à jeun. Les patients ayant une forte activité parasympathique à jeun (HF-FC supérieure à la médiane) maintenaient une plus forte activité parasympathique durant l'HGPO ( p < 0,001). La réponse de l'adrénaline et de la noradrénaline ne différait pas entre les deux groupes. FC augmentait durant l'HGPO dans les deux groupes ( p = 0,002), mais était plus faible à jeun et durant l'HGPO de 10 battements/minute en moyenne chez les patients ayant une forte activité parasympathique ( p = 0,03). Les patients avec forte activité parasympathique avaient un DIO plus élevé ( p = 0,035). Conclusions Parmi les patients obèses métaboliquement sains, ceux dont l'activité parasympathique est plus forte à jeun conservent cette activité plus élevée après l'ingestion de glucose. Ce profil rend compte d'une plus faible fréquence cardiaque à jeun et après HGPO et semble contribuer à une meilleure réponse insulinique. [ABSTRACT FROM AUTHOR]

Introduction La variabilité glycémique peut jouer un rôle dans les complications microangiopathiques du diabète. Nous avons récemment montré que la variabilité glycémique était plus marquée chez les patients obèses non diabétiques ayant des valeurs d'HbA 1c légèrement élevées. L'objectif était d'examiner les relations entre la variabilité glycémique et le flux sanguin microcirculatoire évalué au niveau cutané (FSC) chez des patients intolérants au glucose (IGT) et diabétiques (DT2). Patients et Méthodes Nous avons inclus 34 patients, 19 avec IGT (HbA 1c 5,46 ± 0,61 %) et 15 DT2 sous traitement oral (HbA 1c 7,14 ± 0,74 %), ayant une pression artérielle normale et sans antécédent cardio-vasculaire. Le FSC (moyenne et déviation standard, DS) a été mesuré par laser doppler (Périflux®) sur l'avant-bras pendant 3 minutes au repos une heure après un petit-déjeuner standard apportant 75 g de glucides. La variabilité glycémique en période post-prandiale a été évaluée en calculant moyenne glycémique, déviation standard, CONGA et J index sur les 3 heures suivant le petit-déjeuner (CGMS). Résultats Comparativement aux IGT, les DT2 avaient moyenne glycémique, déviation standard de la glycémie, CONGA et J index plus élevés et moyenne et déviation standard du FSC plus basses ( p < 0,03 à p < 0,0001). Dans la population totale, la moyenne du FSC (mais non la DS du FSC) était corrélée négativement à la DS glycémique et au J index (r = − 0,41, p < 0,01 ; r = − 0,34, p < 0,05) mais non à la glycémie moyenne. Conclusions Le flux sanguin cutané microcirculatoire périphérique est plus faible chez les DT2 que chez les IGT. La variabilité glycémique semble jouer sur la microcirculation périphérique un rôle plus important que la glycémie moyenne, du moins au stade du prédiabète et dans le DT2 bien contrôlé. [ABSTRACT FROM AUTHOR]

Introduction La variabilité glycémique (VG) peut jouer un rôle dans les complications diabétiques. Nous avons récemment montré que la VG était plus marquée chez les patients obèses non diabétiques ayant des valeurs d'HbA 1c légèrement élevées. L'objectif était d'examiner les relations entre la VG, l'hémodynamique cardio-vasculaire et la fonction autonome cardiaque chez des obèses intolérants au glucose (IGT). Patients et Méthodes Nous avons inclus 19 obèses avec IGT, pression artérielle normale et sans histoire cardio-vasculaire. Au cours d'une période de 6 minutes de respiration contrôlée, les activités vagale (HF-FC) et sympathique (LF-FC) ont été évaluées par l'analyse spectrale des variations de la fréquence cardiaque (pléthysmographie digitale, système Task Force Monitor®), le débit moyen d'éjection systolique (MSER), le débit cardiaque (DC) indexé et le volume d'éjection ventriculaire gauche (VE) par impédance thoracique. Le flux sanguin cutané (moyenne et déviation standard, DS) a été mesuré par laser doppler (Périflux®). La VG a été évaluée en calculant CONGA et J index sur 24 heures (CGMS). Résultats Le CONGA était corrélé à DC indexé, VE et MSER ( p < 0,05 pour tous les paramètres) mais non au flux sanguin cutané. Les patients ont été séparés en 2 groupes : G1 < médiane et G2 > médiane de HF-FC. Les patients G2 étaient plus jeunes que les patients G1 (35 ± 9,7 vs 54,8 ± 7,1 ans). Dans G2, la moyenne glycémique des 24 h, le CONGA et le J index étaient plus élevés que dans G1 ( p < 0,03 à p < 0,002), ainsi que DC indexé, VE, MSER ( p < 0,0001 pour tous) et LF-FC ( p < 0,01), même après ajustement sur l'âge. Conclusions Chez les obèses intolérants au glucose, la VG est associée à une hyperkinésie cardiaque. Ceux avec une bonne activité vagale ont une glycémie plus élevée, une VG et une hyperkinésie plus marquées, probablement liées à une plus forte activité sympathique concomitante. [ABSTRACT FROM AUTHOR]