bluuebunny/crossref_metadata_2025_split huggingface dataset:
1410-P: Changes in Circulating MicroRNA-193b and Long-Term Successful Weight Loss in Response to Dietary and Lifestyle Interventions: The POUNDS Lost and CENTRAL Trials
Authors: HEIANZA YORIKO , XUE QIAOCHU , ROOD JENNIFER , KROHN KNUT K. , MEIR ANAT YASKOLKA , BLÜHER MATTHIAS , KOVACS PETER , SHAI IRIS , BRAY GEORGE , SACKS FRANK , QI LU 
Published: May 2022

Circulating microRNAs (miRNAs) have been implicated in controlling whole-body metabolism through intercellular communications. MicroRNA-193b (miR-193b) plays essential roles in white and brown adipocyte adipogenesis and regulating adipokine secretion. We tested whether changes in circulating miR-193b were associated with reductions of adiposity and various fat depots in response to weight-loss dietary and lifestyle interventions in two independent trials. This study included participants of a 2-year weight-loss diet intervention trial (POUNDS Lost) with data on changes in circulating miR-193b-5p from baseline to 6 months after interventions (n=509) . We also assessed changes in circulating miR-193b-5p over 18 months in the CENTRAL weight-loss lifestyle intervention trial (n=111) . At baseline, higher miR-193b was associated with greater adiposity, energy expenditure, ectopic fat depots, and lower adiponectin levels. In response to the interventions, decreases in miR-193b were associated with larger reductions of weight (p &lt;.0001) , waist circumference (p &lt;.0001) , and whole-body total % fat mass (p=0.03) at 6 months in the POUNDS Lost trial. In the CENTRAL trial, decreases in miR-193b were associated with larger reductions of weight (p=0.03) , total (p=0.002) and visceral adipose tissue (p=0.004) , and different fat depots (deep and superficial subcutaneous, and hepatic fat; p &lt;0.for all) . In both trials, every 1 SD decrease of miR-193b was associated with an increased probability for the achievement of successful weight loss (-5% or more weight loss) at the end of interventions (odds ratio [OR]: 1.4; p=0.0in POUNDS Lost; OR 1.9; p=0.02 in CENTRAL) .
In conclusion, changes in circulating miR-193b in response to weight-loss diet/lifestyle interventions were significantly associated with the long-term successful weight loss and reductions of fat depots closely related to the risk of diabetes.

Disclosure
Y.Heianza: None. F.Sacks: None. L.Qi: None. Q.Xue: None. J.Rood: None. K.K.Krohn: None. A.Yaskolka meir: None. M.Blüher: Consultant; AstraZeneca, Lilly, Novo Nordisk A/S, Pfizer Inc., Sanofi, Speaker's Bureau; Bayer AG, Boehringer Ingelheim International GmbH, Novartis AG. P.Kovacs: None. I.Shai: None. G.Bray: None.

Funding
NIH (DK091718, DK100383, DK115679)
1412-P: Preexisting Nonalcoholic Steatohepatitis Attenuates Improvement of Adipose Tissue OXPHOS Capacity after Weight-Loss Surgery
Authors: KAHL SABINE , STRASSBURGER KLAUS , GANCHEVA SOFIYA , SAATMANN NINA , GRANATA CESARE , HERDER CHRISTIAN , PAFILI KALLIOPI , PUETZER-FURMANCZAK JENNIFER , SARABHAI THERESIA , HEILMANN GERONIMO , ESPOSITO IRENE , SCHLENSAK MATTHIAS , RODEN MICHAEL 
Published: May 2022

Impaired adipose tissue (AT) function closely associates with obesity, type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) . Mitochondrial oxidative phosphorylation (OXPHOS) capacity of AT improves after weight loss surgery. However, it is not clear if the improvement is affected by the presence of NAFLD before surgery. We examined 52 severely obese people exhibiting no histological liver disease (OBE_CON) , simple steatosis (OBE_NAFL) or steatohepatitis (OBE_NASH) before (0 weeks) , 12 and 52 weeks after bariatric surgery. Whole-body insulin sensitivity was measured by hyperinsulinemic euglycemic clamps. OXPHOS capacity of subcutaneous AT was assessed by high-resolution respirometry. Transcript levels of TNFα in AT were quantified by RT-PCR. Before surgery, OBE_NASH presented with lower insulin sensitivity and higher HbA1c compared to OBE_CON and OBE_NAFL (all p&lt;0.05) whereas OXPHOS capacity in AT was comparable between the groups. Maximum coupled respiration declined at week 12 by 17% from week 0 in OBE_CON only (p&lt;0.05) . From 12 to 52 weeks, AT maximum coupled respiration markedly increased by 82 and 49% in OBE_CON and OBE_NAFL (both p&lt;0.001) but only by 28% in OBE_NASH (p=0.05; maximum coupled OXPHOS at week 52: OBE_CON vs. OBE_NASH p&lt;0.05) . The changes in AT maximum coupled respiration from 12 to 52 weeks correlated negatively with changes in AT TNFα levels in OBE_CON (β=-0.83, p&lt;0.001) and negatively with changes in systemic C-reactive protein levels in OBE_NASH (β=-0.34, p&lt;0.05) . Maximal noncoupled OXPHOS yielded similar changes and correlations.
In conclusion, in severe obesity, weight loss-related improvements in AT OXPHOS capacity may be mediated to a great extent by reduced AT inflammation in people without liver disease; however, with pre-surgery manifestation of NASH and worsening of metabolic control, residual systemic subclinical inflammation may attenuate the improvement of AT OXPHOS capacity after bariatric surgery.

Disclosure
S.Kahl: None. G.Heilmann: None. I.Esposito: None. M.Schlensak: None. M.Roden: Advisory Panel; Eli Lilly and Company, Research Support; Boehringer Ingelheim International GmbH, Nutricia, Speaker's Bureau; Novo Nordisk. K.Strassburger: None. S.Gancheva: None. N.Saatmann: None. C.Granata: None. C.Herder: Research Support; Sanofi. K.Pafili: None. J.Puetzer-furmanczak: None. T.Sarabhai: None.

Funding
German Federal Ministry of Health; Ministry of Culture and Science of the State North Rhine-Westphalia;German Federal Ministry of Education and Research;European Funds for Regional Development (EFRE-0400191) ;EUREKA Eurostars-2 (E!113230DIA-PEP) ;German Science Foundation (CRC/SFB1116/2 B12; RTG/GRK 2576 vivid, Project 3) ;Schmutzler Stiftung
1419-P: Insulin Resistance Predicts Severe Acute COVID-and Long COVID
Authors: AYHAN EKREM M. , CAO SHU , RAEBER OLIVIA , CHINTHRAJAH SHARON , NADEAU KARI , MCLAUGHLIN TRACEY 
Published: May 2022

Background: Obesity and diabetes are known risk factors for severe acute COVID-19. About half of individuals with obesity have insulin resistance (IR) , which may potentiate severe acute disease and/or predispose to long COVID.
Methods: We identified 596 adults from Stanford hospital or clinics confirmed COVID-19+ by rtPCR and categorized according to severity of illness based on the NIH categories1. Pre-COVID predictors including BMI, fasting plasma glucose (FPG) , and triglyceride/HDL-cholesterol ratio (TG/HDL) as a surrogate2 for IR were abstracted from the EMR using the Stanford Research Repository Tools software. Follow-up surveys were administered via REDCap 2-4x in the first month and 1x per month for 1 year thereafter to assess symptom type and duration. Long COVID was defined as symptom duration &gt; 30 days. Metabolic predictors of acute COVID-severity (BMI, FPG, TG/HDL) were evaluated via multiple linear regression adjusted for sex, age, ethnicity, and other metabolic predictors. A logistic regression to predict long COVID included all metabolic predictors along with age, sex, and ethnicity. Models were repeated with a stepwise approach to increase statistical power given the smaller number of participants with complete data.
Results: Participants were 51±18 years of age, 49% female, and 62% racial and ethnic minorities. Mean BMI was 29.5±7.9 kg/m2. NIH illness severity was 7.9% asymptomatic, 37.2% mild, 25.9% moderate, 15.1% severe, and 13.9% critical. Diabetes, lung disease, and hypertension prevalence were 27%, 18%, and 34%, respectively. Mean follow-up was 94±99 and incidence of long COVID was 47.1%. BMI, FPG, and TG/HDL were independently associated with acute COVID-severity in the cohort as a whole (r=0.187, P&lt;0.001; r=0.180, P=0.002; r=0.180, P=0.009) , while only TG/HDL was associated with long COVID (r=0.173, p=0.013) .
Conclusions: Findings suggest that IR, independent of sex, age, ethnicity, obesity and hyperglycemia, confers increased risk for both severe acute COVID-and long COVID.

Disclosure
E.M.Ayhan: None. S.Cao: None. O.Raeber: None. S.Chinthrajah: Advisory Panel; Alladapt Therapeutics, Novartis, Other Relationship; Aimmune, Astellas, Consortium of Food Allergy Research (CoFAR) , DBV Technologies, FARE, MCHRI , NIAID, Regeneron. K.Nadeau: None. T.Mclaughlin: Board Member; January, Inc., Research Support; Merck & Co., Inc., Novo Nordisk, Stock/Shareholder; Eiger BioPharmaceuticals.

Funding
National Institutes of Health (28291) National Institutes of Health (198537) National Institutes of Health (196111) Stanford Diabetes Research Center (128573)
1421-P: Long-Term Type 2 Diabetes Remission after Bariatric Surgery in Patients with and without Liver Steatosis
Authors: LAUTENBACH ANNE , WERNECKE MARIE , MEYHÖFER SEBASTIAN M. , MEYHÖFER SVENJA , STOLL FABIAN D. , ABEREL JENS 
Published: May 2022

Background: Nonalcoholic steatohepatitis (NASH) is considered the hepatic manifestation of insulin resistance. Therefore, we aimed to assess the association between biopsy-proven liver steatosis and long-term remission of type 2 diabetes (T2D) 8 years following different bariatric procedures.
Methods: In a retrospective cohort study including 249 patients with and without T2D, the association between biopsy-proven NASH and long-term remission of T2D 8 years following sleeve gastrectomy (SG) and Roux-enY-gastric bypass (RYGB) has been assessed.
Results: Out of 249 patients, 15.3% showed NASH and T2D at the time of surgery. 8 years after surgery, T2D remission was achieved in 44.7% of patients with NASH compared to 76.0% without NASH. Patients with T2D remission were younger, had higher BMI, displayed lower HbA1c and lower preoperative insulin use (p&lt;0.001) . Patients without remission of T2D showed higher steatosis scores (p&lt;0.05) . In a multivariate logistic regression, higher preoperative HbA1c (OR 0.41) , insulin use (OR 0.16) and preexisting liver fibrosis (OR 0.19) decreased the probability of long-term T2D remission (p&lt;0.05) . Liver steatosis, hepatocyte ballooning or lobular inflammation were not significantly associated with T2D remission. Patients without T2D were predominantly female, of younger age (p&lt;0.001) and displayed lower scores of steatosis, hepatocyte ballooning and lobular inflammation (p&lt;0.05) . With regard to type of surgery, there was no significant difference in T2D remission.
Discussion and Conclusion: Our data suggest that long-term remission of T2D after bariatric surgery (BS) is associated with lower preoperative insulin use and lower biopsy-proven steatosis scores in patients with NASH. Furthermore, T2D remission might be less likely in patients with liver fibrosis. Type of surgery did not affect T2D remission. Our results might help identify patients with NAFLD who benefit most from BS with regard to glycemic outcomes long-term.

Disclosure
A.Lautenbach: Advisory Panel; Novo Nordisk, Speaker's Bureau; Boehringer Ingelheim International GmbH, Novo Nordisk. M.Wernecke: None. S.M.Meyhöfer: None. S.Meyhöfer: None. F.D.Stoll: None. J.Aberel: Advisory Panel; Novo Nordisk, Speaker's Bureau; Novo Nordisk.
1428-P: Monocyte Cholesterol Metabolism during Weight Loss and Glycemic Improvement
Authors: DING JINGZHONG , LOHMAN KURT , KRITCHEVSKY STEPHEN B. , PARKS JOHN S. , HOESCHELE INA , NICKLAS BARB J. , DEMONS JAMEHL , LIU YONGMEI 
Published: May 2022

Immune cells drive chronic inflammation underlying obesity-related T2DM. We previously reported a cholesterol metabolism pathway as the top coordinated transcriptional module in human monocytes associated with both obesity and T2DM (FDR &lt;0.05) . To investigate whether this pathway is a modifiable link between obesity and T2DM, we randomly assigned 112 adults with obesity and prediabetes aged 40-70 years, 71% woman, 29% African American, to a weight loss intervention using Medifast meal replacement (N=63) or a weight stable control group (N=49) for 4 months. The outcome was a composite measure as the average of standard scores of cholesterol metabolism gene transcripts in monocytes. The intervention achieved 10% weight loss. The control group remained weight stable. Compared with the weight stable group, the weight loss group experienced reductions in both the composite measure and HbA1c (Table) . Changes in the composite measure and HbA1c were correlated (r=0.24, p=0.01) . For individual gene transcripts of this pathway, weight loss reversed obesity-associated upregulation in cholesterol synthesis (FDFT1 and SQLE) , fatty acid synthesis (SCD and FADS1) , and cholesterol uptake (LDLR and MYLIP) (p values &lt;0.05) .
In conclusion, weight loss induces beneficial changes in the cholesterol metabolism pathway in monocytes, a potential therapeutic target for obesity-related T2DM.

Disclosure
J.Ding: Research Support; Medifast, Inc. K.Lohman: None. S.B.Kritchevsky: None. J.S.Parks: None. I.Hoeschele: None. B.J.Nicklas: None. J.Demons: None. Y.Liu: None.

Funding
National Institutes of Health (R01DK103531)
1429-P: Metabolically Healthy Obese Is Actually Not Healthy but at Risk for Developing Diabetes Mellitus
Authors: MIZUSHIRI SATORU , DAIMON MAKOTO , KAMBA AYA , MURABAYASHI MASAYA , NISHIYA YUKI , ITO RYOMA , TAMURA AYUMI , ONO SHOMA , MATSUKI KOTA 
Published: May 2022

Objectives: Although obese individuals without obesity related metabolic abnormalities are often defined as metabolically healthy, risks for developing such abnormalities have not been evaluated well. Recently, a prospective study showed that metabolically healthy obese subjects were at higher risk of diabetes, stroke and cardiovascular disease than metabolically healthy subjects without obesity in UK. We here analyzed the association between metabolically healthy obesity and a risk for developing diabetes in a Japanese population.
Research Design and Methods: The participants were recruited from Iwaki study, a health promotion study of Japanese people aimed to prevent lifestyle-related disease. Among 1167 participants of Iwaki study held in 2014, 931 individuals attended at least one time in 2015 to 2019. We excluded 7 and 75 individuals without complete data sets and who were diagnosed with diabetes in 2014 respectively, thus 849 subjects were enrolled in this study. Obesity was defined as BMI &gt;25 kg/m2. We used the National Cholesterol Education Program ATP III Guideline to categorize metabolically unhealthy as participants meeting at least two criteria of metabolic abnormalities. Results: In 2014, the number of metabolically healthy subjects without and with obesity were 6 and 1 respectively. Cox proportional hazard model showed metabolically healthy subjects with obesity were at higher risk of diabetes compared with those without obesity (Hazard ratio 3.70, p=0.002) , even if after adjusted by age and sex (Hazard ratio 3.32, p=0.005) .
Conclusions: Our analysis suggest an importance of encouraging people with obesity to reduce body weight even though they are metabolically healthy. We are extending such analyses in association with other lifestyle-related diseases.

Disclosure
S.Mizushiri: None. M.Daimon: None. A.Kamba: None. M.Murabayashi: None. Y.Nishiya: None. R.Ito: None. A.Tamura: None. S.Ono: None. K.Matsuki: None.
1433-P: Comparative Weight Loss with GLP-1 Receptor Agonists vs. Bariatric Surgery in Obesity: A Systematic Review and Pair-Wise Meta-analysis
Authors: SARMA SHOHINEE , PALCU PATRICIA 
Published: May 2022

Background: One in three adults suffers from obesity.1 Glucagon-like peptide-1 (GLP-1) receptor agonists have been associated with 15-20% weight loss, a range previously only achieved with bariatric surgery.2,3,4 This systematic review and meta-analysis compares weight loss between GLP-1 receptor agonists and bariatric surgery.
Methods: MEDLINE, Medline-in-Process, Medline EPUBS Ahead of Print, EMBASE Classic + EMBASE (OvidSP) ; and Cochrane (Wiley) databases were searched from inception to April 21, 2021. We included randomized controlled trials (RCTs) and observational studies. Two independent reviewers extracted data, reported risk of bias, and graded certainty of evidence. Risk of bias was reported using Risk of Bias 2 (RoB 2) tool for RCTs and Risk of Bias in Non-randomized Studies- of Interventions (ROBINS-I) tool for observational studies. Data were pooled separately for RCTs and observational studies using random effects models. Change in weight, body mass index (BMI) , and glycated hemoglobin (HbA1C) were summarized.
Results: Seven included studies encompassed 11patients. Among RCTs, mean difference in weight between bariatric surgery and GLP-1 receptor agonist was −22.68 (95% CI: −31.41, −13.96) , mean difference in BMI was −8.18 (95% CI: −11.59, −4.77) , and mean difference in HbA1C was −1.28 (95% CI: −1.94, −0.61) . Among observational studies, mean difference in weight was −16.56 (95% CI: −36.53, 3.42) and mean change in BMI was −10.60 (95% CI:−17.22, −3.98) . These effects all favoured bariatric surgery.
Conclusion: In adults with obesity, bariatric surgery still confers highest reductions in weight and BMI compared to GLP-1 receptor agonists, but similar effects in glycemic control.
Word count: 248

Disclosure
P. Palcu: None.

Funding
Clinician Investigator Program, University of Toronto
144-OR: Adipose Modeling of FGF21 Signaling Mutations in a Severe Insulin Resistance Syndrome
Authors: PHAN NHUNG , ORNITZ DAVID M. , STONE STEPHEN I. 
Published: May 2022

Insulin-mediated pseudoacromegaly (IMPA) is a rare, severe insulin resistance syndrome characterized by tall stature, acanthosis nigricans, obesity, and acromegalic features. Patients with IMPA have normal growth hormone and IGF-1. However, they have markedly increased insulin levels. Our group previously described a patient with IMPA who carries digenic mutations in fibroblast growth factor receptor 1 (FGFR1) and beta-klotho (KLB) , which form the receptor complex for FGF21. FGF21 is a hepatokine that plays a critical role in adipose insulin sensitivity. To assess the pathogenicity of these mutations, we isolated iPSC from the proband with IMPA. We used CRISPR gene editing to correct the FGFR1 and KLB mutations and differentiated the iPSC lines into adipocytes. Both the uncorrected (mutant) and corrected (wild-type) lines were able to undergo successful differentiation to adipocytes. Western immunoblotting demonstrated that the uncorrected cells demonstrated decreased levels of FGFR1, pERK1/2, and p38-MAPK in response to insulin and/or FGF21. Additionally, the mutant adipocytes demonstrated significantly larger lipid droplets when stained with BODIPY (mean droplet size 62.6 μm2 uncorrected; 40.8 μm2 corrected; p= 0.00016) . To complement the iPSC work, a transgenic knock-in mouse line was created using CRISPR gene editing. Explants of gonadal white adipose tissue isolated from these mice demonstrated significantly decreased lipolysis (Max NEFA in mutant 0.mEq/L; wild-type 0.13 mEq/L; p=0.003) . Additionally, qRT PCR was performed in brown adipose tissue demonstrating decreased Ucp1 expression (mutant mice 37.2% of WT; p=4.0x10-5) . These results suggest that the FGFR1 and KLB mutations lead to decreased FGF21 signaling. Mutant adipose tissues are dysfunctional with impaired lipolysis and Ucp1 expression. Therefore these models are useful for determining the role of the FGF21 signaling in human insulin resistance syndromes.

Disclosure
N.Phan: None. D.M.Ornitz: None. S.I.Stone: Speaker's Bureau; Rhythm Pharmaceuticals, Inc.

Funding
NICHD (R21 HD098872) , NIDDK (KDK124574) , NCATS (UL1TR000448) , NIDDK (P30 DK020579) , NIDDK (P30 DK056341) , Burroughs Wellcome Fund Physician-Scientist Institutional Award, and Centene Precision Medicine Initiative
1445-P: Ogt Is Dispensable for Beta-Cell Development but Essential for Postnatal Beta-Cell Identity Maintenance via Pdx1
Authors: WONG ALICIA L. , AKHAPHONG BRIAN , LOCKRIDGE AMBER D. , ALEJANDRO EMILYN 
Published: May 2022

T2D is associated with reduced pancreatic β-cell mass, in part, by increased apoptosis and identity loss as insulin-producing cells. Nutrient-sensor protein O-GlcNAc Transferase (Ogt) is a regulator of pancreas development and β-cell function. We hypothesized that Ogt also regulates postnatal β-cell identity maintenance, in part, by modulating the activity and localization of key β-cell transcription factors. We genetically ablated Ogt in endocrine progenitors in mice (Ngn3-cre;OgtKOEndo) . While phenotypically normal at birth, at postnatal (p) day 23, normoglycemic OgtKOEndo displayed aberrant islet architecture, along with a significant increase in Ins/Gcg-expressing bihormonal cells. Reduced levels of Pdx1 expression and increased incidence of cytoplasmic Pdx1 localization were observed in islets of OgtKOEndo mice compared to controls. All OgtKOEndo mice were diabetic by p60, with severe reductions in both α and β-cell mass. Next, we generated a β-cell Ogt-deficient mouse model (RIP-cre;OgtKOIns) . Like OgtKOEndo, OgtKOIns mice had increased incidence of bihormonal cells, with a trending increase in α-cell associated gene transcription. α-cell mass and β-cell mass were also reduced at p30 compared to controls. We hypothesized, mechanistically, that deletion of Ogt perturbed the activity of Pdx1, a transcription factor modified by Ogt and a key regulator of β-cell fate and insulin biogenesis. As expected, OgtKOIns islets display reduced Ins1/2 mRNA, total insulin content, and Pdx1 protein. Over-expression of Pdx1 in the OgtKO;PdxOEIns mice rescued islet insulin content, and O-GlcNAc modification of Pdx1 is positively correlated with insulin secretion. However, no rescue in β-cell mass was observed in OgtKO;PdxOEIns mice. Next, we will determine the role of the O-GlcNAc modification of Pdx1 in β-cell identity in vivo using the OgtKO;PdxOEIns mice and in vitro, using a proximity-directed nanobody technology to increase Pdx1 and Ogt interactions.

Disclosure
A.L.Wong: None. B.Akhaphong: None. A.D.Lockridge: None. E.Alejandro: None.

Funding
National Institutes of Health (DK115720)
1447-P: The Snd1 Coregulator Controls ß-Cell Function
Authors: KANOJIA SUKRATI , DAVIDSON REBECCA K. , SPAETH JASON , CASEY NOLAN 
Published: May 2022

The main function of the pancreatic β-cell is glucose-stimulated insulin secretion (GSIS) which serves to maintain whole body glucose homeostasis. Under type 2 diabetic conditions, a subset of β-cells fail and lose expression of key transcription factors (TFs) required for GSIS. Among these TFs is Pdx1, which requires the recruitment of a distinct set of transcriptional coregulators to modulate its activity. Recently, Pdx1 has been shown, through and IP-Mass Spec approach, to interact with numerous coregulators, including Snd1 (Staphylococcal nuclease and Tudor domain-containing protein) , which has been shown to facilitate protein-protein interactions and transcriptional control through the recruitment of chromatin modifying enzymes. Here, we first confirmed Pdx1 and Snd1 interact in the rodent β-cell lines by Co-IP, and in primary mouse β-cells and human EndoC-βH1 β-cell lines using proximity ligation assay. Next, we utilized CRISPR-Cas9 technology to generate Snd1-deficient mouse β-cell lines (Snd1KO) . Bulk mRNA-sequencing performed on Control and Snd1KO β-cell lines identified numerous differentially expressed genes linked to insulin secretion and cell proliferation. WST-1 cell proliferation assays revealed impaired proliferation in Snd1KO cell lines and high-glucose stimulated insulin secretion was blunted in INS-1 832/13 cells following siRNA-mediated knockdown of Snd1. As Snd1 has been shown to facilitate protein-protein interactions in other tissues, we found Snd1 interacts with numerous nuclear enriched proteins in the β-cell by IP-Mass Spec, including Stat3, Pax6, Ruvbl2 and Trim28. Future efforts are underway to characterize how Snd1 interactions with these proteins impact gene expression in vitro. Moreover, the role of Snd1 in modulating gene expression and β-cell function in vivo is being evaluated in a novel β-cell-specific (Ins1-Cre) Snd1 knockout mouse model.

Disclosure
S.Kanojia: None. R.K.Davidson: None. J.Spaeth: None. N.Casey: None.

Funding
K01DK115633Wells Center/Pediatric startupCDMD Pilot feasibility grant