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Objective: To estimate the prevalence of protein-energy malnutrition in people admitted for a diabetic foot ulcer (DFU) and to assess the relationship between malnutrition and DFU severity and outcome. Methods: This prospective, observational cohort study included individuals consecutively admitted for a DFU between July 2016 and September 2019. The Global Leadership Initiative on Malnutrition (GLIM) criteria determined the prevalence of malnutrition. The SINBAD score reflected DFU severity. Outcome was evaluated at discharge and at 6 months. The independent contribution of nutritional status on DFU severity and outcome was investigated using logistic regression analysis. Results: A total of 110 patients were included. Malnutrition, as defined by the GLIM criteria, was diagnosed in 26 cases; malnutrition was moderate in 9 and severe in 17. DFU severity differed significantly between subjects with malnutrition versus without malnutrition (SINBAD: 3.85 vs. 3.81, p = 0.012). Logistic regression analysis showed that severe malnutrition (p = 0.015) and hemoglobin level (p = 0.003) were independently linked to DFU severity. At 6-month follow-up, 39 DFU were healed, 36 patients had undergone an amputation (32 minor, 4 major) and 8 had died. No differences were noted in outcome at discharge or at 6 months according to nutritional status. Conclusions: In 24% of patients, malnutrition was diagnosed. Severely malnourished individuals presented with more severe ulcers. However, malnutrition had no impact on the short-term outcome of a DFU. (C) 2021 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.

Objective: Data on switching from traditional mealtime insulin analogs to fast-acting insulin aspart (Fiasp) in routine clinical practice are sparse. The aim was to evaluate the efficacy and safety of this switch in a “real-world” clinical practice setting in adult people with type 1 diabetes (PWD1) who were using intermittent or real-time continuous glucose monitoring (iCGM or rtCGM) in Belgium. Research Design and Methods: Data from 438 adult PWD1 (60% men, age 44.6±16.1 y, duration of diabetes 21.5±14.0 y, iCGM/rtCGM: 391/47, multiple daily injections/pump: 409/29), who initiated Fiasp between January 2018 and May 2020 were retrospectively analyzed. The primary endpoint was the evolution of time in range (TIR, 70-180 mg/dl) at 6 (n=416) and 12 months (n=380). Secondary endpoints included change in HbA1c, BMI, insulin doses, time below range (T180 and T>250 mg/dl). Results: TIR improved from 50.3±15.6% to 54.3±15.1% at 6 months and 55.5±15.2% at 12 months (p180 mg/dl decreased from 42.3±16.7% to 38.1±16.5% and to 37.7±16.9% (p250 mg/dl evolved from 16.5±12.8% to 13.8±11.8% and to 13.1±12.5% (p Conclusions: In a Belgian real-world setting of adult PWD1, switching to Fiasp resulted in a 5% increased TIR, corresponding to 75 min/day, in combination with less time spent below and above range. Disclosure L. Billion: None. F. W. Peiffer: None. K. P. Van dessel: None. C. Mathieu: Advisory Panel; Self; Novo Nordisk, Sanofi, Merck Sharp and Dohme Ltd., Eli Lilly and Company, Novartis, AstraZeneca, Boehringer Ingelheim, Roche, Medtronic, ActoBio Therapeutics, Pfizer, Insulet and Zealand Pharma, Research Support; Self; Medtronic, Novo Nordisk, Sanofi and ActoBio Therapeutics, Speaker’s Bureau; Self; Novo Nordisk, Sanofi, Eli Lilly and Company, Boehringer Ingelheim, AstraZeneca and Novartis. P. Gillard: None. C. De block: Advisory Panel; Self; A. Menarini Diagnostics, Abbott Diagnostics, AstraZeneca, Boehringer Ingelheim , Eli Lilly and Company, MSD, Novartis AG, Novo Nordisk, Roche Diagnostics, Sanofi, Research Support; Self; AstraZeneca, Novo Nordisk, Speaker’s Bureau; Self; A. Menarini Diagnostics, Abbott Diagnostics, Boehringer Ingelheim , Eli Lilly and Company, Novo Nordisk, Sanofi. S. Charleer: None. L. Verbraeken: None. M. Sterckx: None. K. Vangelabbeek: None. N. De block: None. C. Janssen: None. N. Bolsens: Advisory Panel; Self; Medtronic. E. L. Dirinck: None.

AIM: To evaluate the efficacy and safety of switching from traditional mealtime insulins to fast-acting insulin aspart (Fiasp) in a "real-world" clinical practice setting in adult people with type 1 diabetes (PWD1) who were using intermittently scanned or real-time continuous glucose monitoring (isCGM or rtCGM, respectively). MATERIALS AND METHODS: Data from 438 adult PWD1 (60% men, age 44.6 ± 16.2 years, diabetes duration 21.5 ± 14.0 years, isCGM/rtCGM: 391/47, multiple daily injections/continuous subcutaneous insulin infusion: 409/29), who initiated Fiasp from January 2018 to May 2020, were analysed. The primary objective was the evolution of time in range (TIR; 70-180 mg/dL) at 6 and 12 months. Secondary objectives included change in HbA1c, body mass index (BMI), insulin doses, time below range (180 and >250 mg/dL). RESULTS: TIR improved from 50.3% ± 15.6% to 54.3% ± 15.1% at 6 months (n = 425) and to 55.5% ± 15.2% at 12 months (n = 385) (P

International audience; Background: Non-alcoholic fatty liver disease (NAFLD) is the most important cause of chronic liver disease in the western world. Steatosis can be accompanied by inflammation and cell damage (non-alcoholic steatohepatitis, NASH), and even liver fibrosis. Sphingolipids are a heterogeneous class of lipids and essential components of the plasma membrane and plasma lipoproteins. The atypical class of deoxy-sphingolipids has been implicated in the metabolic syndrome and type 2 diabetes.Aim: To determine if circulating (deoxy)sphingolipids are associated with NAFLD and its different entities, steatosis, inflammatory changes (inflammation and ballooning) and fibrosis.Methods: Sphingolipids were analysed by LC-MS after hydrolysing the N-acyl and O-linked headgroups in plasma of obese adults who underwent a liver biopsy in suspicion of NAFLD.Results: Two-hundred and eighty-eight patients were included. There was no association between typical sphingolipids and NAFLD and its different entities. There was a significant association between the presence of steatosis and the concentrations of deoxy-sphinganine [exp(B) 11.163 with CI (3.432, 36.306) and p < 0.001] and deoxy-sphingosine [exp(B) 8.486 with CI (3.437, 20.949) and p < 0.001]. There was no association between these deoxy-sphingolipids and activity of the steatohepatitis, nor was there any association with fibrosis. Differences in deoxy-sphingolipids also correlated independently with the presence of the metabolic syndrome, but not diabetes.Conclusion: Deoxy-sphingolipids are elevated in patients with steatosis compared to those without fatty liver, but not different between the different NAFLD subtypes, suggesting that deoxy-sphingolipid bases might be involved in steatogenesis, but not in the further progression of NAFLD to NASH nor in fibrogenesis.

Background Malnutrition has a detrimental effect on wound healing; hence, it might influence the outcome in people with a diabetic foot ulcer (DFU). The aim of this manuscript is to overview studies that describe the prevalence of malnutrition in DFU patients and assess the relation between malnutrition, DFU severity, and outcome. Methods A literature review was performed. Malnutrition had to be defined by anthropometry and/or validated screening and assessment tools. Results Five papers were included: one RCT, three prospective cohort studies and one retrospective observational study. A substantial number of patients were at risk for malnutrition (49%-70%) or were malnourished (15%-62%). In one study, nutritional status was related to DFU severity. Three authors demonstrated a negative influence of malnutrition on outcome. Two studies examined the prevalence of malnutrition after six months, but did not detect a decline in malnutrition rates. Conclusions Despite a large heterogeneity, all papers indicated that malnutrition is highly prevalent among DFU patients. Notwithstanding the lack of unequivocal evidence, malnutrition might have a negative influence on DFU outcome. Therefore, clinicians should pay attention to the nutritional status of people with a DFU.

Objective To evaluate the glucose and insulin profiles during an oral glucose tolerance test (OGTT) after Roux-en-Y gastric bypass (RYGB) in symptomatic and asymptomatic patients. Research design and methods This retrospective study consisted of two groups that had undergone RYGB. The symptomatic (S) group (n = 27) had an OGTT at presentation, whereas the asymptomatic (A) group (n = 99) had an OGTT 1 year after RYGB. Each group was subdivided into two groups, namely, those with glycaemia 54 mg/dL (S2/A2) during OGTT. Most of the patients underwent OGTT preoperatively. Results Preoperatively, the glucose and insulin levels, as well as the speed of increase and decrease, were similar in all groups. Postoperatively, the minimum glucose levels during the OGTT did not differ between the symptomatic and asymptomatic groups (55 +/- 19 vs. 54 +/- 17 mg/dL) or between the S1 and A1 subgroups (39 +/- 7 vs. 43 +/- 8 mg/dL). The peak glucose values were higher in the symptomatic versus the asymptomatic group (236 +/- 52 vs. 189 +/- 43 mg/dL;P

Background/objectives To study the importance and clinical usefulness of the 1-h plasma glucose (1hPG) in a Caucasian obese population with regard to the presence of prediabetes, diabetes, and metabolic syndrome (MetS). Subjects/methods We conducted a cross-sectional study of 2439 overweight or obese subjects. All received an oral glucose tolerance test (OGTT) using the American Diabetes Association criteria. ROC-curves were used to compare the sensitivity and (1-specificity) of 1hPG versus FPG and 2hPG to diagnose prediabetes and diabetes. Results Of 2439 patients (72.1% female) (age 43 ± 13 years, BMI 37.9 (34.6–41.6) kg/m2), 1262 (51.7%) had a 1hPG ≥ 155 mg/dL. The prevalence of prediabetes was 33.8% and of diabetes 9.8%. In these 240 diabetic patients, only 1.6% (four patients) did not show a 1hPG ≥ 155 mg/dL. Subjects with 1hPG ≥ 155 mg/dL were more insulin resistant (p p p p p p p p p p = 0.008), VAT (p p p = 0.001). Compared to 1hPG Conclusions This study supports the role of 1hPG value as a valuable tool in the detection of obese subjects at high risk for T2DM and MetS.

Introduction: Type 2 diabetes mellitus (T2DM) is increasingly prevalent and associated with increased morbi/mortality. In Caucasian obese subjects we investigated a possible link between 1-hour plasma glucose (1HrPG), diabetes and the metabolic syndrome (MetS). Methods: Overweight and obese patients were consecutively included from the obesity clinic. ROC-curves were used to compare the diagnostic sensitivity and specificity of 1HrPG vs. fasting plasma glucose (FPG), 2HrPG, and HbA1c to diagnose diabetes, using American Diabetes Association criteria. Results: We included 2439 patients (72% female) [mean age 43±13 years, median BMI 37.3 (33.7-41.3) kg/m²]. Diabetes was diagnosed in 9.8% and prediabetes in 33.8% of subjects. Exactly 1262 (51,7%) had a 1HrPG ≥155 mg/dL. These subjects were more insulin-resistant (p Conclusion: This study supports the need for detection of subjects with higher 1HrPG values. being at risk for development of T2DM, MetS and cardiovascular disease. Disclosure L. Haverals: None. K.P.S. Van Dessel: None. A. Verrijken: None. E.L. Dirinck: None. F.W. Peiffer: None. L. Van Gaal: Advisory Panel; Self; Astra Zeneca, Boehringer Ingelheim, Eli Lilly, Janssen J & J, Merck MSD, Novo Nordisk, Sanofi and Servier/Intarcia. Speaker's Bureau; Self; Astra Zeneca, Boehringer Ingelheim, Eli Lilly, Janssen J & J, Merck MSD, Novo Nordisk, Sanofi and Servier/Intarcia. Research Support; Self; EU (Hepadip & Resolve consortium) and National Research Funds. C. De Block: None.

ObjectiveIn this study, we hypothesized that mutations in the resistin encoding gene, RETN, may cause a monogenic form of obesity.Design/methodsWe screened the coding region of RETN in 81 morbidly obese adults, 263 overweight and obese children/adolescents, and 116 healthy lean subjects. In vitro experiments include qPCR, ELISA, and western blot for WT and mutant resistin transfected into 3T3-L1 adipocytes.ResultsMutation analysis identified five sequence variants in our patient populations: 3′-UTR +87 G/A, 3′-UTR +100 A/G, T73T, IV3-61 C/A, and C78S. In our control population, we only found the 3′-UTR +87 G/A variant. We started functional experiments for the C78S mutation that was found in a 20-year-old obese male (body mass index (BMI)=39.7 kg/m2) and his obese mother (BMI=31.9 kg/m2). In vitro testing demonstrated that the mutation does not impair mRNA expression. We identified a 100-fold lower extracellular protein concentration for mutant resistin compared with WT levels using a resistin ELISA on cell culture medium (P=4.87×10−6). We also detected a decreased intracellular concentration for the mutant protein (tenfold lower relative levels, P=0.007). The plasma resistin levels of the proband and his mother, however, did not differ significantly from lean control individuals.ConclusionsIn conclusion, we identified the first missense mutation in resistin in a morbidly obese proband and his obese mother. Functional testing of the mutant protein suggests that the C78S mutant protein is degraded, possibly resulting in a decreased extracellular concentration, which may predispose to obesity.

Current treatment guidelines highlight the increased cardiovascular risk associated with type 2 diabetes and identify the need for intensive risk factor management. Dyslipidaemia characterised by elevated serum triglycerides, low levels of high-density lipoprotein cholesterol (HDL-C) and an increase in small, dense low-density lipoprotein cholesterol (LDL-C) particles (the lipid triad), is one of the most important modifiable cardiovascular risk factors in patients with type 2 diabetes. Statins, which are effective in reducing LDL-C, are currently considered the foundation of lipid-lowering treatment in type 2 diabetes, in addition to lifestyle modification. Increasingly, guidelines also identify low HDL-C as an important secondary priority for treatment. Of the available treatment options, both fibrates and nicotinic acid are effective in treating dyslipidaemia associated with type 2 diabetes, although the latter has greater potency in raising HDL-C. Based on its profile of activity, addition of nicotinic acid to primary statin therapy would be a logical strategy in the treatment of diabetic dyslipidaemia. Outcome data from large prospective studies are awaited to confirm the potential morbidity and mortality benefits of this approach.

Objective: To study the relationship between elevated liver tests and high sensitive C-reactive protein (hs-CRP), as potential markers of liver inflammation and non-alcoholic steatohepatitis (NASH), with anthropometric and laboratory parameters in overweight patients, especially the relationship with visceral adipose tissue (VAT). Methods: Patients presenting to the obesity clinic were prospectively included. Detailed anthropometry, computed tomography (CT)-measured VAT, liver tests (aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT)) and hs-CRP were assessed, along with an extended series of biochemical parameters. Results: All 480 patients (gender distribution male (M)/female (F) (10/90%)) with complete data were included. Mean age was 39±13 years, mean BMI 34.5±6.0 kg m−2. In 37.3% of the patients one or more of the liver tests were elevated. VAT was positively related to AST (r=0.18, P

Interactions between leptin and insulin have been shown previously, in vitro and in vivo. In this study, we evaluate the associations of leptin levels with insulin secretion and insulin sensitivity in type 2 diabetes. Fasting leptin levels, HbA 1c, glucose, insulin, C-peptide, intact and des-31,32-proinsulin were measured in 100 non-insulin-treated type 2 diabetic patients. Glucose, insulin and C-peptide were measured 2 hours after an oral glucose load. Insulin resistance and beta-cell function were calculated using HOMA. Leptin levels were found to be associated with all measures of beta-cell secretion: with fasting and 2 hours insulin and C-peptide, with intact and des-31,32-proinsulin concentrations, and with beta-cell secretion estimated with HOMA. This association was independent of age and body fat in women, but in men, associations with insulin and C-peptide weakened after controlling for fat mass, whereas those with intact and des-31,32-proinsulin disappeared. Fasting insulin and C-peptide levels were also significant in multiple regression analyses, besides gender and fat mass. Insulin resistance, as assessed by HOMA, was strongly correlated with leptin, also after correction for age and fat mass in both genders. We conclude that, besides fat mass and gender - the main determinants for leptin levels in type 2 diabetic subjects as in healthy subjects - insulin secretion and the degree of insulin resistance also seem to contribute significantly to leptin levels.

Weight gain is a known risk factor for the development of type 2 diabetes and even modest weight reduction can reduce the risk of developing diabetes, so controlling body weight is an important public health goal in the fight against diabetes and its comorbidities. Weight reduction is also a cornerstone of diabetes management, improving glycaemic control and reducing other risk factors associated with this disease. Pharmacotherapies such as sibutramine contribute to the management of type 2 diabetes in overweight and obese patients.

Plasminogen activator inhibitor type 1 (PAI-1), an inhibitor of fibrinolysis and an important and independent cardiovascular risk factor, has been shown to be elevated in obesity and type 2 diabetes. Recent study results have suggested that adipose tissue - visceral fat in particular - could play an important role in the fibrinolytic process. In order to assess the specific role of this fat distribution, we measured PAI-1 activity (AU/ml) and visceral fat (CT-scan at level L4-L5) in 2 groups of 30 overweight and obese diabetic and overweight and obese non-diabetic women. Subjects were matched for age, weight, body mass index, fat mass and total abdominal fat. Visceral adipose tissue and PAI-1 were significantly higher in diabetic women (p = 0.022 and p = 0.004 respectively) than in non-diabetic patients. Visceral fat correlated significantly with PAI-1 activity, even after correction for insulin and triglycerides (r = 0.28, p = 0.034). Stepwise regression analysis showed visceral fat as the most important determinant factor for PAI-1 in the whole group and in the non-diabetic group. In the diabetic group, fasting insulin was the most important determinant. These results show that visceral fat is more important than BMI or total body fat in the determination of PAI-1 levels. Furthermore, the increased amount of visceral fat in type 2 diabetics may contribute to the increase of PAI-1 activity levels and the subsequent increased risk for thrombovascular disease, regardless of BMI and total fatness.