bluuebunny/crossref_metadata_2025_split huggingface dataset:
1230-P: Isolation of Functional Endothelial Progenitor Cells from Human Adipose Tissue
Authors: CACCIOPPOLI CRISTINA , PERRINI SEBASTIO , GENCHI VALENTINA ANNAMARIA , DORIA ROSSELLA , PALMA GIUSEPPE , CIGNARELLI ANGELO , NATALICCHIO ANNALISA , LAVIOLA LUIGI , GIORGINO FRANCESCO 
Published: June 2021

Endothelial progenitor cells (EPCs) are key for angiogenic responses in multiple tissues and mediate a coordinate augmentation of the capillary network as adipose tissue (AT) expands in response to positive energy balance. However, isolation and culture of EPCs from human AT has been difficult. Here we describe a new method for obtaining well-characterized EPCs from human AT. Subcutaneous and visceral AT specimens (approximately 1-2 g) were obtained from 10-20 obese subjects by needle biopsy of abdominal subcutaneous AT and removal of omental AT fragments during abdominal surgery, respectively. Human EPCs were isolated from both the digested (SVCI) and undigested (SVCII) stromal vascular fractions of AT by anti-CD31 beads. After 5 days of in vitro culture, EPCs from SVCII exhibited an endothelial-like cobblestone morphology as compared to EPCs from SVCI. Flow cytometry analysis showed that the percentage of CD31+ and CD144+ cells was much higher in the SVCII compared to SVCI fraction (SVCII: CD31 97.9±2.9%, CD144 93.3±4.7%; SVCI: CD31 4.0±1.2%, CD144 3.8±0.7%). Immunofluorescence staining demonstrated that CD31+ EPCs from SVCII expressed Von Willebrand Factor (vWF) and VE-cadherin. Additionally, significantly higher mRNA and protein levels of CD31, E-selectin, e-NOS, VEGFR, and CD34 were found in CD31+ EPCs from SVCII than in control cells (CD31- cells from SVCI). EPCs from SVCII maintained the expression of endothelial markers (CD144 mRNA and protein levels) up to the fourth cell passage. Lastly, CD31+ EPCs from SVCII, but not control cells, were able to form tubes in 3D scaffolds (Matrigel) resembling capillary structures, as well as to incorporate acetylated LDL in vitro. Thus, we have successfully isolated EPCs with high proliferative potential and specific functional properties from the human AT. This will potentially increase our understanding of AT biology particularly in relation to altered expansion of distinct AT depots in human obesity.

Disclosure
C. Caccioppoli: None. S. Perrini: None. V. Genchi: None. R. Doria: None. G. Palma: None. A. Cignarelli: None. A. Natalicchio: Speaker’s Bureau; Self; AstraZeneca, Boehringer Ingelheim International GmbH, Lilly Diabetes, Sanofi. L. Laviola: Advisory Panel; Self; A. Menarini Diagnostics, Abbott, AstraZeneca, Lilly Diabetes, Novo Nordisk Inc., Roche Diabetes Care, Sanofi-Aventis, Speaker’s Bureau; Self; Boehringer Ingelheim International GmbH, Medtronic. F. Giorgino: Consultant; Self; AstraZeneca, Boehringer Ingelheim International GmbH, Lilly Diabetes, Novo Nordisk, Roche Diabetes Care, Sanofi, Research Support; Self; Lilly Diabetes, Roche Diabetes Care.
124-LB: Development of IDG-16177, a Selective and Safe GPR40 Agonist for the Treatment of Type 2 Diabetes
Authors: YOON JONGMIN , SONG HAENGJIN , KIM JUNG HO , LEE SEOLHEE , SHIN CHORONG , JUN YEARIN , HONG DAHAE , LEE DON-GIL , JANG EUNHYE , KIM JISU , AN KYUNGMI , HONG CHANG-HEE , KWAK HYUN-JUNG , JE IN-GYU , SONG HYO-JUNG 
Published: June 2021

GPR40 has been considered a potential therapeutic target for type 2 diabetes because activation of GPR40 stimulates insulin secretion when glucose levels increased. Fasiglifam, a GPR40 agonist, was withdrawn from clinical development in Phase III due to DILI. Therefore, we evaluated the safety profiles of IDG-16177, a novel GPR40 agonist. The potential for IDG-16177 to have off-target effects was assessed in a panel of 173 binding assays. 10 μM IDG-16177 demonstrated activity (&gt;50% inhibition) against DP, EP2, EP3 and EP4 with 81, 83, 57 and 67 % inhibition, respectively. In a functional assay against the same targets, IDG-16177 was inactive in agonist and antagonist mode except for DP with 62.2% activity inhibition at a concentration of 10 μM. IDG-16177 and fasiglifam showed the similar level of hepatotoxic response in HμRELToxTM assay. Formation of reactive metabolite and covalent binding to proteins was evaluated in human hepatocytes. IDG-16177 shows lower covalent binding burden at expected human efficacious dose (0.3~1 mg) than fasiglifam. Transporter inhibitory potential of IDG-16177 was assessed in hepatic transporter-expressing membrane vesicles. IDG-16177 and fasiglifam showed the similar inhibition level of BSEP, MRP2, MRP3, and MRP4. But clinically predicted plasma concentration of IDG-16177 is lower than that of fasiglifam, so the safety margin of IDG-16177 is wider than that of fasiglifam. A core battery of safety pharmacology was evaluated and IDG-16177 did not induce adverse effect in all studies. A 4-week toxicity study was conducted in rats and monkeys, and the liver was determined as the target organ in monkeys. The NOAEL was over 60-fold than in vivo efficacy dose. IDG-16177 was not genotoxic in Ames test, in vitro and in vivo micronucleus test. And no phototoxicity was observed in in vitro 3T3 NRU study. These results shows that the potential for IDG-16177, a safe and effective GPR40 agonist, to treat patients with type 2 diabetes.

Disclosure
J. Yoon: None. J. Kim: None. K. An: None. C. Hong: None. H. Kwak: None. I. Je: None. H. Song: None. H. Song: None. J. Kim: None. S. Lee: None. C. Shin: None. Y. Jun: None. D. Hong: None. D. Lee: None. E. Jang: None.
1242-P: Defining the Nkx6.1 Interactome in Beta Cells Reveals a Novel Interaction with Pdx1
Authors: LITTLEFIELD CONNOR C. , JENSEN NATHANAEL C. , HILL JONATHON T. , PRICE JOHN C. , TESSEM JEFFERY S. 
Published: June 2021

The beta cell transcription factor Nkx6.1 plays a critical role in pancreatic progenitor cell differentiation, mature beta cell proliferation and insulin secretion. The pathways regulated by Nkx6.1 that results in these phenotypes are still being defined. Given that transcription factors generally function in complexes, we sought to determine proteins that interact with Nkx6.1 and may be harnessed to expand functional beta cell mass. INS-1 832/13 beta cells were transduced with AdCMV-Nkx6.1-BioID, AdCMV-GFP-BioID or left untreated. Biotinylated proteins were isolated and the Nkx6.1 interactome was defined using liquid chromatography-tandem mass spectrometry (LC-MS/MS). We defined 176 biotinylated proteins in cells transduced with AdCMV-Nkx6.1-BioID that were not observed with AdCMV-GFP-BioID or naturally biotinylated proteins from untreated lysates (P≤0.05, n=9). These 176 proteins are enriched in terms of nucleotide binding (P=3.6E-5), ribosomal proteins (P=9.1E-4), and transcription factors (P=4.3E-4). Among the enriched transcription factors, we validated that Pdx1, Mef2d and Nr2c2 were biotinylated in response to transduction with AdCMV-Nkx6.1 using biotin-targeted immunoprecipitation and western blot. To examine if these transcription factors are likely to interact with Nkx6.1 on the genome, we analyzed the frequency of proximal binding sites for Nkx6.1 and our candidate genes. Nr2c2 and Pdx1 binding sites in close proximity to Nkx6.1 binding sites were statistically overrepresented in the genome (P≤0.01). Given the role of Pdx1 on functional beta cell mass, we further characterized the interaction of endogenous Nkx6.1 and Pdx1 by co-immunoprecipitation (Co-IP). Our data demonstrates a significant Pdx1 binding by Nkx6.1 Co-IP, as compared to Co-IP with the IgG control (P=0.015, n=3). These data define potential Nkx6.1 binding partners in INS-1 832/13 cells, as well as a novel interaction between two essential beta cell transcription factors, Nkx6.1 and Pdx1.

Disclosure
C. C. Littlefield: None. N. C. Jensen: None. J. T. Hill: None. J. C. Price: None. J. S. Tessem: None.

Funding
Thomas J. Beatson, Jr. Foundation (2019-003)
1246-P: Microcirculatory Circuit of Pancreatic Islets in Diabetic Fetopathy and Congenital Hyperinsulinism
Authors: PROSHCHINA ALEXANDRA , GUBAEVA DILIARA , KRIVOVA YULIYA , OTLYGA DMITRY , MELIKYAN MARIA 
Published: June 2021

The main cause of diabetes is the loss or dysfunction of beta cells that leads to insulin deficiency and hyperglycemia. However, there are some opposite pathologies, in which insulin secretion results in hypoglycemia. Data on the islets morphology in such diseases may be useful for understanding of the pathogenesis of diabetes. Diabetic fetopathy (DF) is a complication of gestational diabetes or preexisting maternal diabetes mellitus, which is characterized by the accelerated fetal growth and neonatal hypoglycemia. These complications mainly develop due to fetal hyperinsulinemia as a compensatory response to the increased delivery of the glucose to the fetus. Congenital hyperinsulinism (CHI) is a severe genetic disease, in which hypoglycemia is caused by excessive insulin secretion. There are two main CHI forms based on histology: diffuse and focal. Pancreatic samples of 4 newborns with DF from mothers with diabetes, 7 infants with diffuse CHI, and 7 infants with focal CHI were compared to 6 control infants without hypoglycemia. The diagnosis of CHI and histological form were established based on increased insulin level during hypoglycemia, presence of pathologic mutations in ABCC8/KCNJ11 genes, and immunohistochemistry results. All pancreatic samples were examined by immunohistochemistry with antibodies against insulin, glucagon, and vimentin. Histological changes such as nuclei enlargement in some beta-cells, islets hypertrophy, and prominent islets vascularization were observed in the endocrine pancreas of infants with DF as well as in patients with CHI. Swelling of the perivascular space was the distinguishing feature, which was revealed only in newborns with DF. In children with CHI, the abundant vascularization in large islets was not accompanied by swelling. We assume that a long-term increase of blood glucose in fetuses with DF leads to vasodilatation, which subsequently causes impaired endothelial permeability and swelling.

Disclosure
A. Proshchina: None. D. Gubaeva: None. Y. Krivova: None. D. Otlyga: None. M. Melikyan: None.
1250-P: Reg3g Mediates Sex-Specific Islet Dysfunction in Offspring of Obese Mice via Heparan Sulfate Glycan Polymerization
Authors: JARRELL JAMES C. , CASASNOVAS JOSE , KUA LIM 
Published: June 2021

Human offspring of obese mothers suffer higher risk of developing type 2 diabetes due to insufficient islet insulin secretion. Preclinical maternal obesity models demonstrated the sex-differences in offspring islet function, but the mechanistic targets are unknown. We found that a higher islet Regenerating Islet Derived Protein 3-Gamma (Reg3g) is associated with the maintenance of islet function in female offspring of obese dams. Reg3g binds to EXTL3 glycosyltransferase that polymerizes heparan sulfate glycosaminoglycan (HSG). To date, the role of Reg3g mediated HSG polymerization in modulating β-cell health in offspring of obese mice is unclear. We hypothesize that the upregulation of Reg3g-mediated HSG polymerization protects offspring of obese mice from glucose intolerance and islet dysfunction. We evaluated islet GSIS, islet Reg3g gene/protein, and pancreatic HSG with SAX-HPLC in offspring born to chow-fed mice (Con) and diet-induced obese mice (MatOb) on postnatal day 21 (P21). To define the causality of Reg3g, wildtype (WT) and heterozygous Reg3g mutant (Reg3g+/-) offspring of Con and MatOb were generated. Lastly, we tested the therapeutic effect of intraperitoneal recombinant Reg3g (rReg) and heparan sulfate analogue (HS) from P14-20 in male MatOb pups. Compared to same-sex controls, P21 female MatOb pups had higher islet Reg3g gene/protein* (n=3-6), higher islet (n=3/3) and pancreatic (n=6/6) HSG*, and unchanged GSIS. Male MatOb pups had unchanged islet Reg3g and a lower pancreatic HSG* (n=8/8). Male MatOb pups also had a lower glucose tolerance* (n=9-19) and 30% decrease in GSIS* (n=5/5). The sex-difference in glucose tolerance was ablated in Reg3g+/- mice, where female MatOb Reg3g+/- pups had significantly impaired GTT. Lastly, rReg3g or HS improved glucose tolerance in male MatOb pups* (n=3-7). *p&lt;0.05.
In conclusion, our findings supported the role of Reg3g as an amenable mechanistic target mediating islet dysfunction in MatOb offspring.

Disclosure
J. C. Jarrell: None. J. Casasnovas: Employee; Self; Thermo Fisher Scientific. L. Kua: Stock/Shareholder; Spouse/Partner; Dexcom, Inc., Thermo Fisher Scientific.

Funding
Riley Children’s Foundation (to L.K.); Showalter Research Trust (EPAR1143 to L.K.); Center for Diabetes and Metabolic Diseases (P30DK097512)
1258-P: Il-1ß-Induced Transcription of Nf-kB Target Genes Is Repressed by Bet Bromodomain Inhibitors in Pancreatic ß-Cells
Authors: NORD JOSHUA , WYNIA-SMITH SARAH , SMITH BRIAN C. , LIPINSKI RACHEL JONES 
Published: June 2021

Autoimmune diabetes is characterized by chronic inflammation of pancreatic islets which ultimately destroys insulin-producing β-cells. In the islet, elevated proinflammatory cytokines lead to increased transcription of inducible nitric oxide synthase (iNOS) and its downstream product, nitric oxide (NO). Elevated levels of NO for prolonged periods lead to β-cell apoptosis. The exact causes of autoimmune diabetes are not well defined and, although genetic predisposition is a factor, low concordance rates of autoimmune diabetes among monozygotic twins indicates a role for epigenetic factors. Recent studies suggest that the bromodomain and extraterminal domain (BET) family of epigenetic regulatory proteins contribute to the onset and progression of autoimmune diabetes. BET proteins are epigenetic readers of sites of lysine acetylation found commonly on histones and have emerged as promising drug targets for a wide variety of diseases. We hypothesize that BET proteins increase proinflammatory cytokine-induced transcription in β-cells leading to β-cell damage and that selective inhibition of BET bromodomains with small molecules will prevent or reverse the progression of autoimmune diabetes. Here, we show that BET bromodomain inhibitors decrease the β-cell response to proinflammatory cytokines in an insulinoma β-cell line (INS832/13) and primary rat islets. BET inhibitors attenuated cytokine-induced transcription of inflammatory mediators, including iNOS. This decreased transcription is mediated through inhibition of the NF-κB signaling pathway by BET inhibitors. Using knockdown of individual BET proteins in a β-cell line, we identified the importance of individual BET family members in the altered transcriptional profile characteristic of autoimmune diabetes. This work uncovers important mechanisms of disease onset and progression of autoimmune diabetes, laying the groundwork for more targeted treatments with drug-like small molecules.

Disclosure
J. Nord: None. S. Wynia-smith: None. B. C. Smith: None. R. Jones lipinski: None.

Funding
American Diabetes Association (1-18-IBS-068 to B.C.S.); National Institutes of Health (R01DK119359, T32HL134643)
1260-PUB: Type 2 Diabetes and Congestive Heart Failure Are Mutually Independent Predictors of the Presence of Albuminuria
Authors: MAECHLER MAXIMILIAN , VONBANK ALEXANDER , LARCHER BARBARA , MADER ARTHUR , SPRENGER LUKAS , MUTSCHLECHNER BEATRIX , LEIHERER ANDREAS , MUENDLEIN AXEL , DREXEL HEINZ , SAELY CHRISTOPH H. 
Published: June 2021

Albuminuria is a well-known characteristic of diabetic nephropathy and it is also present in a large portion of patients with congestive heart failure (CHF). However, the single and joint effects of type 2 diabetes mellitus (T2DM) and CHF on albuminuria are unknown. This issue therefore was addressed in the present study.
We investigated 180 patients with CHF, of whom 83 had T2DM (CHF+/T2DM+) and 97 did not have diabetes (CHF+/T2DM-) and 223 controls without CHF, of whom 39 had T2DM (CHF-/T2DM+) and 184 did not have diabetes (CHF-/T2DM-).
The prevalence of albuminuria was lowest in CHF-/T2DM- subjects (8.7%). When compared to this group it was significantly higher in CHF-/T2DM+ (23.1%, p=0.010), CHF+/T2DM- (38.1%, p&lt;0.001) and CHF+/T2DM+ patients (62.7%, p&lt;0.001). It was highest in CHF+/T2DM+ patients, in whom it was higher than in CHF-/T2DM+ (p&lt;0.001) and in CHF+/T2DM- (p=0.001) patients; a trend towards a higher prevalence of albuminuria in CHF-/T2DM+ patients vs. CHF+/T2DM- patients did not reach statistical significance (p=0.093). In logistic regression analysis, CHF and T2DM were mutually independent predictors of albuminuria, when adjusted for age, sex, body mass index, LDL cholesterol, history of smoking and hypertension, as well as for the use of statins and ACE inhibitors/angiotensin II receptor blockers (OR 2.57 [95% CI 1.47-4.51]; p=0.001 and OR 4.15 [2.18 - 7.88]; p&lt;0.001, respectively).
We conclude that T2DM and CHF are mutually independent predictors of albuminuria.

Disclosure
M. Maechler: None. C. H. Saely: None. A. Vonbank: None. B. Larcher: None. A. Mader: None. L. Sprenger: None. B. Mutschlechner: None. A. Leiherer: None. A. Muendlein: None. H. Drexel: None.
1266-PUB: Correlation of Sex Hormones Levels and Glycated Hemoglobin in Nondiabetic Middle-Aged and Elderly
Authors: BAO YUQIAN , XU YITING , CAO WEIJIE , SHEN YUN , TANG JUNLING , WANG YUFEI , MA XIAOJING 
Published: June 2021

Aims: Sex hormones are strongly linked to the occurrence and development of diabetes, and influence glycated hemoglobin (HbA1c) levels in diabetic population; but, the relationship between sex hormones and HbA1c in nondiabetic population remains unknown. This study aimed to explore the extent of influence of sex hormones on HbA1c levels in nondiabetic population.
Methods: A total of 1409 nondiabetic subjects, including 601 men and 808 postmenopausal women were recruited from Shanghai community. HbA1c was detected using high performance liquid chromatography, and hemoglobin level was determined by sodium lauryl sulfate colorimetry. Serum estradiol (E2), total testosterone (TT), and sex hormone binding globulin (SHBG) were measured by chemiluminescent microparticle immunoassays.
Results: The level of HbA1c was 5.6 (5.4-5.9) % in all subjects, with 5.6 (5.4-5.8) % in men and 5.7 (5.5-5.9) % in postmenopausal women. After adjusting for age, body mass index (BMI), and hemoglobin, E2 was positively correlated with HbA1c in men (r = 0.122, P = 0.003), and SHBG was inversely correlated with HbA1c (r = -0.125, P &lt; 0.001) in women. Other hormones were not correlated with HbA1c (all P &gt; 0.05). Multivariate linear regression analysis showed that, except for traditional factors, such as age, hemoglobin, and BMI, E2 was another determinant of HbA1c (standardized β = 0.137, P = 0.003) in men and the regression equation was HbA1c (%) = 0.001×E2 (pmol/ L) +5.465. In women, SHBG was another determinant of HbA1c (standardized β = -0.178, P &lt; 0.001), except for age and systolic blood pressure (SBP), and the regression equation was HbA1c (%) = -0.002×SHBG (nmol)/L) +5.772.
Conclusion: After controlling for confounding factors, E2 is positively correlated with HbA1c in men, and SHBG is inversely correlated with HbA1c in postmenopausal women. Sex hormones influence HbA1c levels in nondiabetic population, but it is very limited to affect the level of HbA1c in the diagnose of diabetes.

Disclosure
Y. Bao: None. Y. Xu: None. W. Cao: None. Y. Shen: None. J. Tang: None. Y. Wang: None. X. Ma: None.
1275-PUB: Call to Action: COVID-19 Pandemic Prompts Subcutaneous Treatment Option for Diabetes Ketoacidosis (DKA) in Hospital
Authors: MEEHAN DORIS , TALAVERA LAURA , PHILIS-TSIMIKAS ATHENA , FORTMANN ADDIE L. 
Published: June 2021

COVID-19 challenges organizations to modify approaches to optimize diabetes management while reducing Personal Protective Equipment (PPE) use and nurse time, and maintaining patient safety. In April 2020, Scripps Health, a five-hospital health system in southern California created a subcutaneous Diabetes Ketoacidosis (DKA) treatment option for use with adults, admitted with mild to moderate DKA. Primary aims were to achieve DKA resolution and glycemic targets similar to the intravenous (IV) insulin treatment option, and no hypoglycemia &lt;70 mg/dL.
The new order set utilized weight-based dosing, with similar orders for labs, electrolyte and IV fluid replacement, and resolution criteria. Differences included automatic insulin dosing and basal/bolus insulin. Key changes were a reduced frequency of point of care testing (POCT) and ≤140 mg/dL hypoglycemia prevention orders. Post-implementation audits between April - July 2020 showed no hypoglycemia and resolution time similar to IV insulin. However, only 6% (N=17) of DKA cases were managed with subcutaneous, as compared to IV insulin. To help understand why there was such a limited uptake, a detailed retrospective chart review was undertaken on a subset of twenty-two DKA cases managed with IV insulin. Findings showed that 17 (77%) had type 2 diabetes, 5 (23%) had type 1 diabetes. 47% of cases had opportunities for subcutaneous management based on DKA classification and no contraindications for subcutaneous therapy.
Findings indicate organizations should consider a DKA subcutaneous option. Lack of knowledge of DKA severity may be a factor in low utilization, therefore an EHR DKA Classification tool was implemented to support providers. Research is needed to determine if this increases utilization of the subcutaneous treatment option and what other barriers exist.

Disclosure
D. Meehan: None. L. Talavera: None. A. Philis-tsimikas: Advisory Panel; Self; Bayer Inc., Lilly Diabetes, Medtronic, Novo Nordisk, Consultant; Self; Sanofi-Aventis, Employee; Spouse/Partner; Ionis, Other Relationship; Self; Merck & Co., Inc., Research Support; Self; Dexcom, Inc., Lilly Diabetes, Medtronic, Novo Nordisk, Sanofi-Aventis. A. L. Fortmann: None.
1277-PUB: Severe DKA in Adolescent at Onset of Type 2 Diabetes and COVID-19
Authors: BABY MERILYN , LITAO MELISSA KAORI S. , DAPUL HEDA R. , FRANKLIN BONITA , GALLAGHER MARY PAT 
Published: June 2021

Introduction: Obesity and type 2 diabetes (T2D) increase severity of SARS-CoV2 in adults. In one review of DKA and COVID-19 in adults, 77% had pre-existing diabetes while 10% were newly diagnosed. We report an adolescent with severe DKA and new onset T2D in the setting of COVID-19 infection, who had a complex hospital course.
Case: A 14-year old male with BMI of 43.7 kg/m2 and learning disabilities presented with decreased mental status and 4 day history of polydipsia, polyuria and emesis. Initial labs: glucose 546 mg/dl, BOHB 4.4 mmol/L, venous pH 6.94, HCO3 3mmol/L, serum osm 287 mOsm/kg, A1C 12.3%, pancreatic antibodies negative. C-reactive protein, d-dimer, ferritin, CPK, troponin, lipase (4,610 U/L), and amylase (839 U/L) were elevated. Patient received mannitol. No cerebral edema on head CT. Chest/Abd CT showed bilateral lower lobe consolidation of lungs and heterogeneous pancreas with no fluid collection. IV fluids and insulin were started. Nine hours after presentation, mental status declined further and patient required intubation for respiratory failure. At 19 hours, ketosis had resolved but acidosis persisted with arterial pH=7.05. SARS-CoV-2 nasopharyngeal swab PCR was positive. Course was complicated by multi-organ failure, rhabdomyolysis, and fluid refractory shock requiring vasopressors and renal replacement therapy (max creatinine 5.13 mg/dL). Patient started anticoagulant therapy, but on day 12 left femoral DVT was diagnosed. On hospital day 20 a retroperitoneal hemorrhage was noted. Inflammatory markers normalized by day 43. The patient had significant neurologic deficits and required prolonged rehabilitation after discharge on hospital day 46.
Conclusion: To our knowledge, this case of a morbidly obese adolescent with neurocognitive delays, is the first report of an adolescent with COVID-19 presenting with new onset T2D and DKA, who had a hospital course similar in severity to those reported in adult patients. Adolescents with T2D and SARS-CoV2 infection should be monitored for severe disease.

Disclosure
M. Baby: None. M. S. Litao: None. H. R. Dapul: None. B. Franklin: None. M. Gallagher: None.