bluuebunny/crossref_metadata_2025_split huggingface dataset:
817-P: Late Postprandial Hypoglycemia Is Reduced with Ultrarapid Insulin—An Insulclock Connected Cap-Based Real-World Study
Authors: GOMEZ-PERALTA FERNANDO , VALLEDOR XOÁN , LOPEZ-PICADO AMANDA , ABREU CRISTINA , PUJANTE ALARCÓN PEDRO , FERNÁNDEZ-RUBIO ELSA , GARCÍA ELENA , AZRIEL SHARONA , CORCOY ROSA , CERQUEIRA CRISTINA , PÉREZ JESUS , RUIZ-VALDEPEÑAS LUIS 
Published: June 2023

Background: Reaching optimal postprandial glucose dynamics is a daily challenge in T1D people. The study aimed to analyze the postprandial hyperglycemia excursion (PHE) and late postprandial hypoglycemia (LPH) risk according to time and type of insulin.
Methods: Real-world (RW), retrospective study in T1D using multiple daily injection (MDI) insulin. Five hours of paired CGM and automatically tracked insulin injections collected with the connected cap Insulclock®. Meal events were identified using the ROC detection methodology. Postprandial glucometrics and LPH (glucose &lt;70mg/dL 2-5 hours after a meal) were evaluated according to insulin injection time and type: rapid (RI) or ultrarapid analog-Fiasp®- (URI).
Results: Meal glycemic excursions (n= 2488), RI: 1211, 48.7%; UR: 1277, 51.3%, in 82 people. In 63% insulin was injected after the meal started. URI use was associated with lower LPH risk URI vs RI, n(%): Early (-45-15 min): 20 (9,5) vs 11 (8,0); Optimal (-15-0 min): 18 (6,4) vs 29 (8,8); Delayed (0+45 min) 71 (9,1) vs 100 (13,4); (p 0.012). Lower PHE (Glucose peak-baseline; mg/dL) was observed with URI vs RI (mean±SD): Early: 102.23 ±32.19 vs 101.2 ±36.73; Optimal: 96.62 ±29.63 vs 99.89 ±29.93; Delayed 111.6 ±40.2 vs 118.13 ±43.3; (p &lt;0.001).
Conclusion: Ultrarapid analog use reduces postprandial hyper- and hypoglycemia, even in the case of delayed injections.

Disclosure
F.Gomez-peralta: Advisory Panel; Abbott Diabetes, Insulcloud S.L., Speaker's Bureau; A. Menarini Diagnostics, Boehringer Ingelheim and Eli Lilly Alliance, Lilly Diabetes, Novartis, Novo Nordisk. C.Cerqueira: Employee; Insulcloud S.L. J.Pérez: Employee; Insulcloud S.L. L.Ruiz-valdepeñas: Employee; Insulcloud S.L., Stock/Shareholder; Insulcloud S.L. X.Valledor: Employee; Insulcloud S.L. A.Lopez-picado: Employee; Insulcloud S.L.. C.Abreu: Speaker's Bureau; Lilly, Novo Nordisk. P.Pujante alarcón: None. E.Fernández-rubio: Speaker's Bureau; Lilly Diabetes, Novo Nordisk, AstraZeneca. E.García: Advisory Panel; Airliquide, Speaker's Bureau; Abbott Diabetes, Dexcom, Inc., Boehringer Ingelheim and Eli Lilly Alliance, Novo Nordisk, Sanofi, Airliquide. S.Azriel: Advisory Panel; Boehringer-Ingelheim, Novo Nordisk, Medtronic, Speaker's Bureau; Dexcom, Inc., Lilly Diabetes, AstraZeneca, Sanofi. R.Corcoy: Advisory Panel; Novo Nordisk, Other Relationship; Novo Nordisk, Lilly, Sanofi, Abbott, Speaker's Bureau; Sanofi, Roche Diabetes Care.
819-P: Impact of Meal Bolus Timing and Bedtime Snacking on Glycemic Control in Hospitalized Patients
Authors: ALEXANIAN SARA , CHENEY MICHAEL C. , BELLO RAMOS JENNY , SPARTANO NICOLE L. , WOLPERT HOWARD , STEENKAMP DEVIN W. 
Published: June 2023

Background: Basal-bolus insulin is the standard of care to treat hyperglycemia in hospitalized patients in the non-ICU setting. Matching insulin with food is a barrier to achieving blood glucose (BG) goals. The glycemic impact of a snack at bedtime without prandial insulin and delayed meal-time bolus in the hospital has not been previously explored.
Methods: The InFi study is an ongoing randomized controlled open-label trial comparing Fiasp vs aspart in hospitalized patients using the Dexcom G6 PRO CGM to assess postmeal glycemic outcomes. We performed an interim analysis of 100 subjects to assess the impact of bedtime snacks on fasting POC glucose (FG) and the impact of delayed meal bolus on postprandial sensor glucose (PPSG) time in range (TIR) 70-180 mg/dL. Meal intake was determined by a CGM heuristic, insulin bolus time by barcoded EMR.
Results: Four hour post-meal TIR was 54% for on-time boluses (n=119) vs 25% with bolus delay of &gt;5 minutes (n=86), p &lt;0.001. Evening snacking (9pm-12am) was associated with higher FG levels, 201 vs 158 mg/dL (N=30, 50), p = 0.03.
Conclusion: Delayed meal-time insulin bolusing is common in hospitalized patients and results in a significant reduction in post-meal TIR. Evening snacking is a significant cause of overnight hyperglycemia. Given the importance of BG control, hospitals should work to optimize meal insulin delivery and develop strategies to address bedtime food intake.

Disclosure
S.Alexanian: Research Support; Novo Nordisk. M.C.Cheney: None. J.Bello ramos: None. N.L.Spartano: Research Support; Novo Nordisk. H.Wolpert: Consultant; Abbott Diabetes, Employee; Eli Lilly and Company. D.W.Steenkamp: Research Support; Abbott Diabetes, Novo Nordisk.

Funding
Novo Nordisk (ISS-001295)
82-OR: NRF2 Regulates Neonatal ß-Cell Mass Expansion
Authors: BAUMEL-ALTERZON SHARON , KATZ LIORA S. , LAMBERTINI LUCA , GARCIA-OCANA ADOLFO , SCOTT DONALD 
Published: June 2023

The pediatric population suffers from increased incidence of both major types of diabetes in recent decades, highlighting the urgent need for discovering mechanisms that regulate functional β-cell mass. We found that the master antioxidant regulator, Nrf2, is required for adaptive adult β-cell expansion under hypercaloric conditions via regulation of β-cell proliferation, β-cell survival, and maintenance of β-cell identity. Additionally, we found that Nrf2 expression in β-cells of 7-day-old mice is 15-fold higher of that in adult β-cells (p&lt;0.0001, n=6). Based on these observations, we hypothesized that Nrf2 regulates β-cell proliferation and survival at early stages of life and contributes to the maintenance of normal β-cell mass later in life. To test this, we deleted Nrf2 in β-cells by crossing InsCre with Nrf2lox/lox mice (βNrf2KO). βNrf2KO mice at 28 days of age exhibited a 65% reduction of β-cell mass compared to control mice (p&lt;0.0005, n=6). Importantly, at 7 days of age, βNrf2KO mice displayed a 65% reduction of β-cell proliferation (p&lt;0.0001, n=6), a 22% reduction of nuclear Pdx1 levels (p&lt;0.0001, n=6), a 5.84-fold increase in β-cell death (±0.04, p&lt;0.001, n=6) and a 2.93-fold increase in β-cell oxidative stress (p&lt;0.001, n=6) compared to control mice. Surprisingly, daily administration of antioxidant NAC to 7-day-old βNrf2KO mice only partially restored β-cell proliferation but completely blunted oxidative stress compared to control mice. This suggests that neonatal β-cell proliferation induced by Nrf2 relies on additional mechanisms beyond oxidative stress. Interestingly, RNAseq of isolated islets from 7-day-old βNrf2KO mice showed decreased expression of mitochondrial encoded genes and upregulation of stress-responsive genes. This suggests that Nrf2 controls β-cell proliferation by regulating mitochondrial bioenergetics. We conclude that Nrf2 is required for β-cell mass expansion in neonatal ages by controlling β-cell proliferation, identity, and survival.

Disclosure
S.Baumel-alterzon: None. L.S.Katz: None. L.Lambertini: None. A.Garcia-ocana: Consultant; Sun Pharmaceutical Industries Ltd. D.Scott: None.

Funding
National Institutes of Health (DK128387, DK114338)
828-P: Identification of Novel Protein Biomarkers as Predictors of Type 1 Diabetes Development and Progression, and as Indicators of Treatment Efficacy
Authors: CHHABRA PREETI , MA MINGYANG , BRAYMAN KENNETH L. 
Published: June 2023

The aim was to identify novel protein biomarkers as predictors of Type 1 diabetes (T1D) development and progression in NOD mice, and as indicators of treatment efficacy. Heparin plasma was obtained from 6-weeks old NOD mice divided into Control, Prehyperglycemic, Diabetic, and IgM-treated groups. Plasma samples were analyzed using SomaScan Proteomic platform. 7288 somamers were evaluated. Cyclic Loess normalized Log2 signal was used to analyze the ADAT files (Boulder BioConsulting). Linear regression models were fit and ANOVA performed. Extracted pairwise contrasts, coefficients and predictions were used for downstream analysis in R. BH FDR correction was performed for p values. Differentially expressed (DE) somamer selection was based on p value or q value &lt;0.05 and/or &gt;2 absolute fold-change criteria. GSEA v4.2.2 and Cytoscape v3.9.1 EnrichmentMap pipeline v1.1.0 was used for Pathway analysis, and enrichment results mapped as a network of gene sets. Our studies identified four significant DE proteins in the prehyperglycemic stage and seven in diabetes, with an overlap of two. 17 enriched pathways were downregulated and two upregulated with diabetes. IgM group formed a distinct cluster in principal component analysis suggesting a global effect of the treatment. IgM-treated vs. Diabetic contrast found 418 DE proteins, many associated with the treatment itself. IgM-treated vs. Prehyperglycemic + Diabetic contrast identified 386 DE proteins in a second model. IgM-treated vs. healthy controls had 334 DE proteins. 33 DE proteins in the diabetic group were maintained at normal levels with IgM therapy. Venn diagrams comparing contrasts involving IgM-treated samples showed a significant overlap of unique DE proteins. IgM downregulated ~46 pathways. To conclude, novel proteins have been identified with significant clinical potential as predictors for T1D development and progression, and for monitoring treatment efficacy.

Disclosure
P.Chhabra: None. M.Ma: None. K.L.Brayman: None.

Funding
Manning Family Foundation (GF006791)
83-LB: Simplifying Insulin Treatment in Persons with T2 DM over 65 Years—Interim Report of the STOP Study
Authors: MAZZIERI ALESSIO , DE FANO MICHELANTONIO , MANCINETTI FRANCESCA , XENOS DIONYSIOS , BOCCARDI VIRGINIA , FANELLI CARMINE G. , PORCELLATI FRANCESCA 
Published: June 2023

This is an interim evaluation of the STOP study, a proof-of-concept observation, whose aim is to test effectiveness and safety of IDegLira in deintensifying diabetes therapy in insulin-treated persons with T2DM aged &gt;65 years. The study, retrospective observational, gathered so far data related to 93 consecutive persons with T2 DM, in whom IDegLira was introduced in therapy, and for whom clinical data were available for at least 6 months after the switch. The 93 persons (42 F, age 76±8 yrs, diabetes duration 20±10 yrs, duration of insulin treatment 13±12 yrs, BMI 28.6±4.9 kg/m2, A1C 7.4±0.9), were for the 75% in basal/bolus insulin therapy. Sixteen % of them, needed caregiver, whereas 53% were in follow up at the Geriatric Clinic for mild/severe cognitive impairment. After 3 months, fasting plasma glucose (PG) decreased (from 138±38 to 117±24 mg/dl, p=0.000036 vs baseline), similarly A1C (from 7.4±0.9 to 7.0±0.6%, p=0.000126). All results showed additional improvement at 6 month (p&lt; 0.005 vs baseline). Rates of hypoglycemia at any time of day (PG &lt;70 mg/dl) were lower after 3 months (0.35±0.94 vs 1.15±2.61, episodes/pt/month, p=0.0057). Episodes with PG &lt;54 mg/dl decreased from 0.56±1.71 to 0.03±0.25, p=0.0093). Accordingly, the proportion of patients with at least one episode of PG &lt;70 mg and 54 mg/dl, felt down from baseline to 3 month (23.7 to 14%;16.1 to 11%, respectively), being zero at 6 months. Rapid acting insulin dose decreased by 80 % at 3, up to 95% at 6 months (from 0.18±0.13 to 0.04±0.06 at 3, and 0.01±0.04 U/kg at 6 months, p&lt; 0.0001). Nearly all patients interrupted it. IDegLira was initiated at a mean dose of 17±5.4 U/die to further increase to 23±9.6 after 6 months. BMI did not change significantly (p=ns). According to our preliminary results, IDegLira seems to offer a relevant option, to more complex insulin regimens, in terms of effectiveness and safety, in a population in whom preventing hypoglycemia and improving quality of life are mandatory and clinical inertia is often present.

Disclosure
A. Mazzieri: None. M. De fano: None. F. Mancinetti: None. D. Xenos: None. V. Boccardi: None. C. G. Fanelli: None. F. Porcellati: Board Member; Lilly Diabetes, Sanofi, Consultant; Novo Nordisk.
83-OR: Defining the Transcriptome and Epitranscriptome of the ß-Cell Compensation to Insulin Resistance
Authors: DE JESUS DARIO F. , ZHANG ZIJIE , WEI JIANGBO , BROWN NATALIE K. , HU JIANG , KAHRAMAN SEVIM , DIRICE ERCUMENT , KULKARNI ROHIT 
Published: June 2023

Type 2 diabetes (T2D) is characterized by decreased functional β-cell mass and poor compensation to insulin resistance. Thus, understanding of the mechanism(s) responsible for the physiological adaptation of β-cells to states of high metabolic demand is desirable. We aimed to dissect the transcriptome and m6A mRNA methylation landscape in the β-cell adaptation to insulin resistance. To this end we conducted RNA-sequencing in sorted β-cells and m6A-sequencing in whole islets from three mouse models: a) a dietary model (60% high-fat diet: Control-HF), b) a genetic model (liver-specific insulin receptor KO mouse on chow: LIRKO-C), and c) a superimposed dietary and genetic model of insulin resistance (LIRKO on a high fat diet: LIRKO-HF). These data were compared to littermate controls fed a chow diet (Control-C). Control-HF, LIRKO-C and LIRKO-HF each presented an increase in insulin resistance compared to Control-C. However, LIRKO-C and LIRKO-HF presented a robust insulin secretion capacity and a graded increase in β-cell proliferation and mass compared to Control-C. First, we correlated the transcriptome with surrogates of β-cell adaptation such as insulin secretion, β-cell mass or proliferation. Next, we intersected the genes that positively correlated with β-cell compensation with single-cell RNA seq datasets performed in islets from humans with or without T2D. This bioinformatics analyses identified extracellular matrix (ECM) as the most enriched pathway in the β-cell adaptation to insulin resistance. On the other hand, m6A-sequencing of Control-C, LIRKO-C and LIRKO-HF islets and the intersection of this dataset with the differentially methylated genes in human T2D islets, revealed enrichment in pathways associated with chromatin modifications. Together, these results point to ECM pathways as being important in the transcriptomic remodeling and that m6A acts on chromatin-modifying enzymes in the β-cell compensation to mammalian insulin resistance.

Disclosure
D.F.De jesus: None. Z.Zhang: Research Support; SinoVac. J.Wei: None. N.K.Brown: None. J.Hu: None. S.Kahraman: Employee; Boehringer Ingelheim Pharmaceuticals Inc. E.Dirice: None. R.Kulkarni: Advisory Panel; Novo Nordisk, Inversago, Biomea Fusion, Inc., REDD Pharma, Research Support; Inversago.

Funding
American Diabetes Association (7-21-PDF-140 to D.F.DJ.); National Institutes of Health (R01067536)
837-P: Improved Outcomes across Socioeconomically Advantaged and Disadvantaged Communities—A Real-World Study
Authors: MCKENZIE AMY L. , ATHINARAYANAN SHAMINIE J. 
Published: June 2023

Socioeconomic conditions of one's community have been attributed to disparities in diabetes outcomes and management practices. Among a random sample (n=19955) of people with type 2 diabetes receiving care at a nationwide telemedicine clinic utilizing a carbohydrate restricted nutritional approach and continuous remote care model (CR-CRCM), we explored A1c and medication utilization by area deprivation index quintile (Q). Upon enrollment, patients residing in more disadvantaged areas (Q4, Q5) had higher A1c compared to the least disadvantaged area (Q1; 7.8% vs 7.7%, p&lt;0.01), and insulin (INS) and sulfonylureas (SU), but not other medication classes, were prescribed to a greater proportion of patients living in Q5 (25% INS, 23% SU) compared to Q1 (18% INS, 18% SU) and Q2 (21% INS, 19% SU) after accounting for differences in age, sex, baseline BMI, baseline INS use (when appropriate), and race and ethnicity (p&lt;0.05). After one year in clinic, no differences in the prescription of medication classes between Q were observed, except for INS, where greater use remained only in Q5 than Q1 (14% vs 10%, p=0.011); among those remaining on INS, dose was reduced by 49-58% across all Q (p&lt;0.001). Differences in SU use were no longer present; 77-83% fewer SU were prescribed across Q. Differences in A1c between Q4 (6.6%) and Q5 (6.7%) vs Q1 (6.5%) remained (p&lt;0.001), though all groups achieved significant reductions in A1c of 1.1-1.2% (all p&lt;0.001) concurrent with reduced prescription of all diabetes medication (from 1.7-1.8 to 1.1-1.2 medication classes per person). Across all levels of socioeconomic disadvantage, patients achieved clinically and statistically meaningful reductions in A1c and medication. Higher rates of SU use among patients residing in more disadvantaged areas were mitigated through a CR-CRCM to improve glycemia. Further, these data suggest a CR-CRCM may overcome financial barriers to optimal diabetes management through reduced need for medication.

Disclosure
A.L.Mckenzie: Employee; Virta Health Corp., Stock/Shareholder; Virta Health Corp. S.J.Athinarayanan: Employee; Virta Health Corp.
84-LB: Intensification of Glucagon-Like Peptide-1 Receptor Agonists Therapy with Glargine 300 U/mL or IDegLira—The RESTORE-G Real-World Study
Authors: CANDIDO RICCARDO , NICOLUCCI ANTONIO , CHIARA ROSSI MARIA , LAROSA MONICA , NAPOLI RAFFAELE , STUDY GROUP RESTORE-G 
Published: June 2023

Combined use of basal insulin (BI) and glucagon-like peptide 1 receptor agonist (GLP1-RA) deserves consideration for the synergistic effects on glucose profile. Nevertheless, it is unclear if the addition of BI to the ongoing GLP1-RA therapy in free or fixed combination is associated with different outcomes. Aim of this RESTORE-G sub-study was to perform a propensity-score adjusted comparative effectiveness analysis of the two most innovative BIs for intensifying GLP1-RA therapy (±oral agents), i.e. Glargine 300 U/mL in free combination (Gla-300) vs. the fixed ratio combination of insulin degludec + liraglutide (IDegLira). Table shows sample sizes, patients characteristics and effectiveness results.

Compared to IDegLira, Gla-300 group had older age, worse metabolic control, and higher starting BI doses. After 6 months, statistically significant larger FBG reduction and BI dose increase were found in the free vs. fixed combination group. Trends of larger HbA1c and weight reductions with the free combination were also found, without reaching the statistical significance. In conclusion, higher benefits on FBG control in free vs. fixed combination has been found in people uncontrolled on GLP-1 RA, likely due to a better titration of the components. However, inertia in insulin initiation was documented in both groups.

Disclosure
R. Candido: None. A. Nicolucci: Board Member; AstraZeneca, Research Support; Novo Nordisk, Sanofi, Sobi, Shionogi & Co., Ltd., AlfaSigma, Speaker's Bureau; Boehringer Ingelheim and Eli Lilly Alliance. M. Rossi: Research Support; Sanofi, Novo Nordisk, Shionogi & Co., Ltd., AlfaSigma. M. Larosa: None. R. Napoli: Advisory Panel; Sanofi, Eli Lilly and Company, Novo Nordisk, Research Support; Novo Nordisk, AstraZeneca, Speaker's Bureau; Sanofi, Eli Lilly and Company, Novo Nordisk, AstraZeneca, MSD Life Science Foundation. Restore-g study group: n/a.

Funding
Sanofi
840-P: Dual Amylin and Calcitonin Receptor Agonist Treatment Improves Blood Pressure and Glucose Control in ZSF1 Rats
Authors: MELANDER SIMONE A. , LARSEN ANNA T. , ELHADY MOHAMED KHALED , KARSDAL MORTEN A. , HENRIKSEN KIM 
Published: June 2023

Long-acting dual amylin and calcitonin receptor agonists (DACRAs) are novel candidates for the treatment of type 2 diabetes and obesity due to their beneficial effects on both body weight, glucose control and insulin action. However, whether DACRAs affect hypertension, and diabetes-related cardiovascular complications remain unknown. In this study, the cardiovascular protective effect of the DACRA KBP-336 was evaluated in obese Zucker diabetic fatty-Spontaneously hypertensive heart failure F1 hybrid (ZSF1) rats. Obese ZSF1 rats were treated for 60 days with the KBP-336 (4.5 nmol/kg Q3D) and treatment efficacy on glucose control and blood pressure measured by tail cuff was evaluated. Furthermore, serum biomarkers of cardiovascular complications were evaluated. KBP-336 treatment significantly lowered fasting blood glucose levels compared to vehicle (P&lt;0.001). This was also illustrated in the HbA1c levels at study end, where KBP-336 resulted in significantly (P&lt;0.001) lower levels than vehicle. Importantly, KBP-336 significantly reduced both systolic (AUC levels reduced by 13.3%, P&lt;0.001) and diastolic (AUC levels reduced by 17.0%, P&lt;0.001) blood pressure compared to vehicle without affecting the heart rate. Notably, the beneficial effects on both glucose control and blood pressure were obtained independent of weight loss as KBP-336 only resulted in a small and transient weight reduction. Furthermore, serum levels of the marker of cardiovascular disease, rPRO-C6 (collagen type VI formation marker) were 6.4% lower in KBP-336 treated rats compared to vehicle, supporting improvement in cardiovascular parameters. In summary, we show for the first time that KBP-336 benefits blood pressure in a metabolic rat model suffering from hypertension. In addition, KBP-336 improved glucose control independent of weight loss. These data highlight KBP-336 as a promising candidate for treating obesity and related comorbidities including type 2 diabetes and hypertension.

Disclosure
S.A.Melander: None. A.T.Larsen: Employee; Nordic Bioscience A/S. K.Mohamed: Employee; Nordic Bioscience. M.A.Karsdal: Speaker's Bureau; Pfizer Inc. K.Henriksen: Employee; Nordic Bioscience A/S, Stock/Shareholder; Nordic Bioscience A/S.

Funding
Danish Research Foundation; Innovation Fund Denmark; European Union’s Horizon 2020 Research and Innovation Program (814244)
852-P: Duodenal Recellularization via Electroporation Therapy (ReCET) and GLP-1 RA to Replace Insulin in T2D Patients—EMINENT Study Six-Month Results
Authors: BUSCH CELINE B.E. , MEIRING SUZANNE , VAN BAAR ANNIEKE C.G. , HOLLEMAN FRITS , NIEUWDORP MAX , BERGMAN JACQUES J. 
Published: June 2023

Introduction: Re-Cellularization via Electroporation Therapy (ReCET™), a novel endoscopic procedure using electroporation to elicit apoptosis of the duodenal mucosa. In this study we aimed to eliminate insulin in T2D patients using a single ReCET procedure combined with GLP-1RA. Safety, feasibility, and efficacy of ReCET using the Endogenex system were assessed.
Methods: First in human study with 14 T2D patients on basal insulin (BMI 24-40 kg/m2; HbA1c ≤ 8.0%; C-peptide ≥ 0.2 nmol/l). All underwent ReCET after which semaglutide was titrated up to 1mg. Primary endpoints were: feasibility (technical success rate, procedure time [catheter in - out], % GLP-1RA tolerance); safety ((S)AE, hypoglycemic events); efficacy (off insulin at 6 mo; HbA1c ≤ 7.5%).
Results: ReCET showed 100% technical success rate. Procedure time was 58 (IQR 49-79) min. Maximum semaglutide dosage was tolerated by 13 patients. No device related SAEs were observed. One non-severe hypoglycemic event occurred. At 6 mo, 12 patients were off insulin. A significant improvement in several glycemic and metabolic parameters was observed (Table 1); HbA1c decreased (7.2 to 6.6% p=0.003) and TIR increased (72 to 91% p=0.022).
Conclusion: ReCET is safe and feasible. ReCET combined with semaglutide may effectively eliminate insulin in selected T2D patients, while improving glycemic control and metabolic health.

Disclosure
C.B.E.Busch: None. S.Meiring: None. A.C.G.Van baar: None. F.Holleman: None. M.Nieuwdorp: Advisory Panel; caelus health. J.J.Bergman: Consultant; Endogenex, Fractyl Health, Inc., Digma Medical, Research Support; Endogenex, Fractyl Health, Inc., Digma Medical.