bluuebunny/crossref_metadata_2025_split huggingface dataset:
1713-P: Adipocyte O-GlcNAc Transferase Regulate Adipogenesis through De Novo Lipogenesis in Mice
Authors: MORINO KATSUTARO , TSUJI AKIKO , OHASHI NATSUKO , IDA SHOGO , PERRY RACHEL J. , UGI SATOSHI , FUJITA YUKIHIRO , SHULMAN GERALD I. , MAEGAWA HIROSHI 
Published: June 2020

O-linked N-acetylglucosamine (O-GlcNAc) modification is one of the post-translational modifications which modulates protein fate and function, and it is mediated by O-GlcNAc transferase (OGT). The substrate of OGT, UDP-GlcNAc, is biosynthesized through the branch of glycolysis. Thus O-GlcNAcylation has been regarded as a nutrient sensor. Metabolic regulation in white adipose tissues (WAT) is dramatically changed in the process of obesity. We previously reported that the deletion of Ogt in adipose tissues (Ogt-FKO) decrease WAT mass without affecting glucose tolerance in mice under normal condition. However, the role of O-GlcNAcylation in WAT in the process of being obesity remains unknown. In this study, we investigated the role of O-GlcNAcylation in WAT under diet induced obesity. Despite no significant differences in food intake, body weight gain by high-fat diet was suppressed in Ogt-FKO mice along with the significant decrease of WAT mass. However, Ogt-FKO mice were severely impaired glucose tolerance and decreased insulin sensitivity in liver, which was confirmed by hyper-insulinemic euglycemic clamp. Histologically, we observed smaller adipocytes and fibrosis in WAT of Ogt-FKO mice. In addition, gene expression of F4/80, CD11c, MCP-1 and Col1a1 were significantly higher in Ogt-FKO mice, suggesting increased inflammation and fibrosis. Also, the expression of genes associated to fatty acid synthesis such as SREBP-1c, FAS, SCD1 and SCD2 were reduced in Ogt-FKO mice. Furthermore, Ogt-FKO mice showed lower serum concentration of adiponectin and leptin (46.43 ± 3.62 vs. 8.42 ± 1.53ng/ml) along with their gene expression, which is consistent with severe atrophy of WAT in Ogt-FKO mice.
In conclusion, loss of O-GlcNAcylation in WAT exhibited obesity resistance and impaired glucose tolerance because of lipoatrophy under diet induced obesity, and the results suggest that O-GlcNAcylation in WAT plays important role for fatty acid synthesis and functional adipocyte formation.

Disclosure
K. Morino: None. A. Tsuji: None. N. Ohashi: None. S. Ida: None. R.J. Perry: Research Support; Self; AstraZeneca. S. Ugi: None. Y. Fujita: None. G.I. Shulman: Advisory Panel; Self; AstraZeneca, Janssen Research & Development, LLC, Merck & Co., Inc. Advisory Panel; Spouse/Partner; Merck & Co., Inc. Consultant; Self; Novo Nordisk A/S. Consultant; Spouse/Partner; Novo Nordisk A/S. Other Relationship; Self; Gilead Sciences, Inc., iMetabolic Biopharma Corporation. Other Relationship; Spouse/Partner; iMetabolic Biopharma Corporation. Other Relationship; Self; Maze Therapeutics. H. Maegawa: Speaker’s Bureau; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo, Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Sanofi K.K., Takeda Pharmaceutical Company Limited.

Funding
Japan Society for the Promotion of Science (18K16226)
1714-P: Regulation of Phosphorylation Status in Insulin Signaling via a4 Is Necessary for Adipocyte Maintenance and Lipid Dynamics
Authors: SAKAGUCHI MASAJI , OKAGAWA SHOTA , OKUBO YUMA , KITANO SAYAKA , IGATA MOTOYUKI , KONDO TATSUYA , ARAKI EIICHI 
Published: June 2020

Insulin and IGF1 signaling through the PI3K/AKT and MAPK/ERK pathways are essential for maintenance of brown and white adipose tissues (BAT and WAT), as shown by our previous results using adipocyte-specific and inducible IR/IGF1R knockout mice (Ai-DKO). Here, through a research to screen the genes essential for adipose tissues maintenance in WAT and BAT using Ai-DKO mice, we identified a reduction of α4, a protein phosphatase protector which regulate phosphorylation state, in Ai-DKO BAT. shRNA-mediated α4 knockdown (KD) altered insulin-stimulated phosphorylation status in BAT; decreased IRβ (Y1162/1163), IRS1 (Y612) and Akt (S473), with a mild change in ERK1/2 (T202/Y204) but increased ribosomal S6 protein (S235/236), suggesting α4 reduces S6 phosphorylation state via a unique pathway. Next, to investigate the impact of α4 in vivo, we created inducible adipocyte-specific α4 KO (Ai-α4 KO) mice with tamoxifen-inducible Cre-ERT2 transgene. Once induced α4 KO in adipocytes, the mice revealed extensive losses of adipocytes in SC-WAT and BAT depots with increased apoptotic cell death. Ai-α4 KO mice showed cold intolerance, severe diabetes, ectopic lipid accumulation in the liver, and pancreatic islet hyperplasia. RNA-seq showed a marked reduction of genes associated with mitochondrial fatty acid oxidation and increases with inflammatory cytokine pathways in Ai-α4 KO SC-WAT and BAT. WAT and BAT mass can recover after a few months in Ai-α4KO. Interestingly, lipidomics analysis displayed that the regenerated adipocytes showed unique lipid content in the Ai-α4KO. Thus, our model demonstrates that the tuning of phosphorylation status for insulin-dependent signaling by α4 is critical for maintaining and regeneration of white and brown adipose tissues.

Disclosure
M. Sakaguchi: None. S. Okagawa: None. Y. Okubo: None. S. Kitano: None. M. Igata: None. T. Kondo: None. E. Araki: Advisory Panel; Self; Abbott. Speaker’s Bureau; Self; ARKRAY, Astellas Pharma Inc., AstraZeneca, Eli Lilly Japan K.K., Merck & Co., Inc., Novo Nordisk Inc., WebMD LLC. Other Relationship; Self; Kowa Company, Ltd., Mitsubishi Tanabe Pharma Corporation, Novartis Pharma K.K., Sumitomo Dainippon Pharma Co., Ltd., Takeda Pharmaceutical Company Limited.

Funding
Japan Society for the Promotion of Science; Merck Sharp & Dohme Foundation; Takeda Foundation; Boehringer Ingelheim; Eli Lilly and Company
1716-P: L-PGDS Inhibition Reduces Adiponectin Levels and Insulin Sensitivity in 3T3-L1 Adipocytes
Authors: SRIVASTAVA ANKITA , PALAIA THOMAS , LEE JENNY , HALL CHRIS , STEVENSON MATTHEW , FERNANDO ANNE G. , RAGOLIA LOUIS 
Published: June 2020

The prevalence of obesity has increased steadily over the last few decades and is a major risk factor for type 2 diabetes and cardiovascular disease. Obesity is associated with alterations in adipose tissue functioning leading to metabolic dysfunction. In previous studies, we have reported the role of lipocalin-type prostaglandin D2 synthase (L-PGDS) in glucose intolerance and atherosclerosis. More recently, we demonstrated that L-PGDS KO mice develop NAFLD even on a low fat diet. Our present study explored the role of L-PGDS in adipose tissue. We found decreased expression of L-PGDS in insulin resistant 3T3-L1 adipocytes. Enzymatic inhibition of L-PGDS in 3T3-L1 adipocytes using AT56 impaired insulin signaling by reducing the phosphorylation of AKT protein and the expression and translocation of GLUT4 to plasma membrane. Furthermore, we found that inhibition of L-PGDS reduces the expression of adiponectin and AMPK phosphorylation in 3T3-L1 adipocytes. Rosiglitazone treatment in insulin resistant 3T3-L1 adipocytes significantly increased L-PGDS expression. Treatment with rosiglitazone restored the expression of adiponectin and phosphorylation of AMPK in AT56 treated 3T3-L1 adipocytes. Correspondingly, we found decreased L-PGDS expression in visceral fat of obese humans. Cumulatively, these data confirm that the absence of L-PGDS results in decreased insulin sensitivity via impaired insulin signaling and reduced adiponectin levels in 3T3-L1 adipocytes. Thus, our findings suggest that L-PGDS plays a significant role in maintaining the insulin sensitivity in 3T3-L1 adipocytes and provides a novel opportunity for therapeutic intervention of obesity-associated metabolic syndrome.

Disclosure
A. Srivastava: None. T. Palaia: None. J. Lee: None. C. Hall: None. M. Stevenson: None. A.G. Fernando: None. L. Ragolia: None.

Funding
American Heart Association (15GRNT22420001); George Link, Jr. Foundation, Inc.
1725-P: Viral Insulins as Agonists and Antagonists on Insulin/IGF-1 Receptors
Authors: MOREAU FRANCOIS , BRANDAO BRUNA ,   ESQ., CEDERQUIST CARLY , BATISTA THIAGO M. , DIMARCHI RICHARD , ALTINDIS EMRAH , KAHN C. RONALD 
Published: June 2020

Recently, we identified four insulin/IGF-1 like peptides (VILPs) in the sequence of viruses belonging to the Iridoviridae family. These VILPs show up to 50% homology with the sequence of the human insulin/IGF-1. Moreover, the predicted tertiary structures and major receptor binding residues are conserved between the VILPs and insulin/IGF-1. Although these viruses are known to infect primarily fish, sequences of VILPs have been found in human blood and feces. VILPs can interact with the human and murine insulin and IGF-1 receptors and induce the activation of their downstream signaling. Functionally, VILPs are able to induce glucose uptake and cell proliferation.
VILPs can be synthesized as a single-chain (SC) or double-chain (DC) peptides, i.e., more IGF-1 like or more insulin like structures. In the present study, we show that SC and DC forms of lymphocystis disease virus (LCDV-1) VILP interact differently with the human insulin and IGF-1 receptor. Competition binding assay reveals that SC is more potent than DC in binding to the IGF-1 receptor. In vivo, following i.p. injection in mice both LCDV-1 SC and DC produced similar mild decreases in blood glucose compared to insulin, even at a 166-fold excess. In vitro, however, DC LCDV1-VILP acts as a weak agonist to stimulation of IGF1R, whereas SC LCDV-VILP serves as a strong antagonism effect on the IGF-1 receptor. Thus, the activation of the IGF1R by IGF-1 is strongly repressed by the SC LCDV-1 VILP, even at equal concentrations. This antagonistic action of SC VILP is restricted to the IGF1R and does not affect insulin receptor. As a functional consequence of IGF1R blockade, SC LCDV-1 VILP inhibits IGF-1 stimulated migration of a cervical cancer cell line.
In summary, we have shown that SC VILP may provide a novel inhibitor of IGF1R signaling and IGF-1 action on tumor cell migration, with minimal effects on glucose metabolism, thus providing a potentially unique reagent for treatment of IGF-1 sensitive tumors.

Disclosure
F. Moreau: None. B. Brandao: None. C. Cederquist: None. T.M. Batista: None. R. DiMarchi: Employee; Self; Novo Nordisk Inc. E. Altindis: None. C. Kahn: Advisory Panel; Self; ERX Pharmaceuticals, Kaleido Biosciences. Consultant; Self; AntriaBio, Flagship Pioneering, Sana-Cobalt.
1727-P: Mice Deficient in Myeloid Cell-Derived Interleukin-1a Are Protected from Diet-Induced Obesity and Insulin Resistance
Authors: SUK SUJIN , FRIEDLINE RANDALL H. , NOH HYE LIM , HU XIAODI , TRAN DUY A. , TAUER LAUREN A. , KIM ALLISON M. , KIM LAUREN H. , KIM JASON K. 
Published: June 2020

Interleukin (IL)-1α is a major mediator of inflammation, and functional polymorphism of IL-1α is associated with human obesity. We have recently generated mice with genetic ablation of IL-1α selectively in myeloid cells. On chow diet, Lyz-IL-1α KO mice showed normal metabolic phenotypes. In contrast, when male Lyz-IL-1α KO mice were fed a high-fat diet (HFD), whole body fat mass was markedly reduced in these mice (Figure 1; *P&lt;0.05). Metabolic cage study found that this was mostly due to a 2-fold increase in physical activity in Lyz-IL-1α KO mice (Figure 2). Food intake and energy expenditure were not affected in these mice. We performed a hyperinsulinemic-euglycemic clamp to measure insulin sensitivity in awake mice (n=7). HFD-fed Lyz-IL-1α KO mice were more insulin sensitive than HFD-fed wild type (WT) mice with a 2-fold increase in glucose infusion rates (Figure 3). Whole body glucose turnover and glycolysis were significantly increased in HFD-fed Lyz-IL-1α KO mice (Figure 3). Basal hepatic glucose production (HGP) was not altered, but clamp HGP was reduced by 40% in Lyz-IL-1α KO mice. As a result, hepatic insulin action was markedly increased in HFD-fed Lyz-IL-1α KO mice (Figure 4).
In conclusion, these results indicate that Lyz-IL-1α KO mice are protected from diet-induced obesity and insulin resistance, and our findings identify IL-1α as a novel therapeutic target in obesity and type 2 diabetes.

Disclosure
S. Suk: None. R.H. Friedline: None. H. Noh: None. X. Hu: None. D.A. Tran: None. L.A. Tauer: None. A.M. Kim: None. L.H. Kim: None. J.K. Kim: None.

Funding
National Institutes of Health (5U2CDK093000)
1728-P: Oral Consumption of a PI3K P110a Inhibitor Perturbs Glucose Homeostasis without Affecting the Physical or Cognitive Function of Adult Mice
Authors: HEDGES CHRISTOPHER , BOIX JORDI , MERRY TROY L. 
Published: June 2020

Advances in medicine have contributed to an ageing population, and various age-associated pathologies contribute to loss of independence and quality of life. Calorie restriction and genetic inhibition of insulin signalling pathway intermediates such as phosphatidylinositol-3-kinase (PI3K), have shown promise in improving lifespan but are difficult to implement clinically. Therefore, we sought to test whether pharmacological inhibition of PI3K using an orally ingested p110α-selective inhibitor, BYL-719, promotes changes in glucose homeostasis and physical function in adult (8-month old) male and female mice. Three days of exposure to a standard chow diet containing 0.30 g/kg BYL-719 elevated blood glucose in response to a meal challenge, however, following four weeks of BYL-719 diet consumption blood glucose response to a meal was normalised in females, but not males. Despite this, both male and female mice fed the BYL-719 diet were glucose intolerance and had impaired insulin sensitivity compared to mice fed a control diet. There was no difference between groups in measures of physical performance (treadmill, rotarod or hang time performance) or stress/anxiety behaviour assessed through open field test. However, female mice fed the BYL-719 diet showed greater exploratory behaviour in an object recognition test. Collectively, these data indicate that short-term pharmacological inhibition of PI3K p110α alters glucose homeostasis, but has only mild effect with respect to the physiological stimulus of a meal, and without deterioration of physical or cognitive function in adult mice. This indicates BYL-719 is safely tolerated in adult mice, and longer-term study is warranted to test the efficacy of BYL-719 in prolonging lifelong health in an aged population.

Disclosure
C. Hedges: None. J. Boix: None. T.L. Merry: None.

Funding
Health Research Council of New Zealand
1738-P: The Role of Adipocyte YAP in Glucose Homeostasis and Insulin Resistance In Vivo
Authors: HAN DANIEL JONG JIN , ASLAM RUKHSANA , OJHA TANVI , YUEN DARREN , LUK CYNTHIA T. 
Published: June 2020

Adipose tissue is a dynamic metabolic organ that is essential for the regulation of whole-body glucose homeostasis. Adipose tissue hypertrophy with obesity is associated with glucose intolerance and insulin resistance underlying type 2 diabetes. Furthermore, studies suggest fibrosis formation is increased in adipose tissue of mice fed with a high-fat diet (HFD) and results in metabolically dysfunctional adipose tissue. Yes-associated protein 1 (YAP) is a transcription cofactor that promotes fibrosis in the lung, liver, and kidney. However, the role of YAP in adipose tissue and glucose homeostasis is unknown. To understand the role of YAP in vivo under metabolic stress conditions, we assessed how HFD impacts YAP protein levels. We have found that YAP protein levels increase in adipose tissue with weight gain. This suggests that YAP signaling may contribute to adipocyte dysfunction and insulin resistance under metabolic stress conditions. To further investigate the role of YAP in adipose tissue and glucose homeostasis in vivo, we developed adipose tissue-specific YAP knockout (adipose tissue YAP-KO) mice and placed them on both chow and HFD for 12 weeks. On an HFD, adipose tissue YAP-KO mice show improved glucose tolerance compared to controls. While blood glucose levels were lower, adipose tissue YAP-KO mice did not show improvements in insulin sensitivity. Together, these data indicate that YAP increases in adipose tissue with weight gain and disruption of YAP in adipocytes improves glucose tolerance; suggesting that adipocyte YAP plays an important role in modulating glucose homeostasis under metabolic stress conditions.

Disclosure
D. Han: None. R. Aslam: None. T. Ojha: None. D. Yuen: None. C.T. Luk: None.
1746-P: Obese Youth with Type 1 Diabetes (T1D) Have Worse Hepatic Insulin Resistance (IR) Than Youth with Type 2 Diabetes (T2D)
Authors: WIROMRAT PATTARA , CREE-GREEN MELANIE , BERGMAN BRYAN C. , TOMMERDAHL KALIE L. , BAUMGARTNER AMY , PYLE LAURA , NADEAU KRISTEN J. 
Published: June 2020

Background: The epidemic of obesity is growing in the U.S. due to changes in diet and lifestyle. Similar trends are also now occurring in T1D youth and may worsen IR and associated cardiovascular risk. However, the impact of obesity on IR in each tissue is unknown in T1D. Thus, we evaluated adipose, hepatic and muscle IR in obese youth with T1D, compared to BMI-similar control or T2D youth.
Methods: 20 youth with T1D (age 16.0±2.3 years; % female 55; BMI%ile 95th [97, 98]; HbA1c 8.7±1.6%), 20 youth with T2D (age 15.4±2.3; % female 52; BMI%ile 95th [98, 99]; HbA1c 8.5±2.4%) and 16 controls (age 14.8±1.8; % female 55; BMI%ile 97th [98, 99]) were included. In those with diabetes, glucose was controlled overnight by IV insulin to a target of ∼100 mg/dL. A 4-phase hyperinsulinemic-euglycemic clamp (basal, 10, 16 and 80 mU/m2/min of insulin [I]) with isotopic tracers was performed the following AM to assess adipose, hepatic and muscle IR, respectively. Free fatty acids (FFA), glucose rate of disappearance (Rd) and glycerol and glucose rate of appearance (Ra) and %suppression (basal to 80 phase) were calculated.
Results: Participant age, sex, BMI and Tanner stage were similar between groups. HbA1c was similar in groups with diabetes. During the basal phase, glycerol Ra/I and glucose Ra/I were similar between groups, but FFA/I was highest in obese controls (p&lt;0.001). At phase 10, glycerol Ra/I was similar between groups but FFA/I at phase 10 and 16 were similarly higher in T1D and T2D vs. controls (p=0.004, p&lt;0.001). At phase 16, glucose Ra/I and glycerol Ra/I were highest in T1D (p&lt;0.001, p&lt;0.001). At phase 80, T1D vs. T2D had similarly lower %glycerol Ra suppression than controls (p&lt;0.001) but higher glycerol Ra/I and glucose Rd in T1D vs. T2D (p=0.003, p=0.042). T1D youth and controls had similar glucose Rd (p=0.25).
Conclusion: Obese youth with T1D have similar to worse adipose, worse hepatic, and less muscle IR than those with T2D. Treatment targeting obesity and IR is critically needed in T1D youth.

Disclosure
P. Wiromrat: None. M. Cree-Green: Advisory Panel; Self; Novo Nordisk Inc. B.C. Bergman: Consultant; Spouse/Partner; Novo Nordisk Inc., Sanofi US. Research Support; Self; Eli Lilly and Company. Speaker’s Bureau; Spouse/Partner; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Janssen Pharmaceuticals, Inc., Merck & Co., Inc. K.L. Tommerdahl: None. A. Baumgartner: None. L. Pyle: None. K.J. Nadeau: None.

Funding
American Diabetes Association (7-11-CD-08 to K.J.N.); National Heart, Lung, and Blood Institute; National Institute of Diabetes and Digestive and Kidney Diseases; JDRF
1748-P: One Novel 7.2kb Deletion in Exon 8 of INSR Gene in Diabetic Qatari Female with Type A Insulin Resistance Syndrome: The 1000 Qatar-Omics Study Cohort
Authors: AKIL AMMIRA S. , YASSIN ESRAA A.M. , PADMAJEYA SUJITHA SUBASH , JERMAN LAILA A. , FADDA ABEER , AAMER WALEED H.O. , ALIYEV ELBAY E. , FAKHRO KHALID 
Published: June 2020

Background: A 46-year-old Qatari female with a BMI of 25kg/m2 presented with hyperglycemia (blood glucose 13.5 mmol/l), hyperinsulinemia (21µU/mL) with elevated levels of HbA1c (10.3mmol/l). Biochemical investigations showed raised serum C-peptide (2.02ng/ml) and triglycerides (2.07mmol/L) and uric acid (104mg/dL), with normal BP. The objective of this case study is to validate this variant found through WGS in insulin receptor (INSR) gene that play a major cause of insulin resistant syndrome with different spectrums.
Methods: Structural Variants discovered using custom multi-algorithm pipeline developed and optimized to run on HPC for short-read WGS data. In brief, 10 software packages applied (Breakdancer, Breakseq2, CNVnator, Delly, ERDS, Genomestrip, Manta, Speedseq, Svaba, WHAM), to existing short-read data. SVs annotated using AnnotSV and provides us functionally, regulatory and clinically relevant information. SVs analyzed based on their properties like pli-score, overlaps with known databases and OMIM annotations. This deletion was validated by ddPCR and the molecular docking performed by the autodock suit in order to understand the effect of deletion in the interaction between this receptor and insulin.
Results: The patient was identified with 7.2k heterozygous deletion in exon 8 of INSR gene which play an essential role in the formation of extracellular alpha subunits in insulin receptor. molecular docking proved the decrease of catalytic activity of INSR and, hence signaling. Considering this and the phenotypic data from Qatar biobank, the patient developed features of type A insulin resistant syndrome as consequence of persistence hyperinsulinemia. The patient also exhibits severe Deterioration of glucose tolerant even with medication and unfortunately developed nephropathy.
Conclusion: We highlighted the power of NGS in precise diagnosis and developing a potential and promising targeted therapeutics.

Disclosure
A.S. Akil: None. E.A.M. Yassin: None. S. Subash Padmajeya: None. L.A. Jerman: None. A. Fadda: None. W.H.O. Aamer: None. E.E. Aliyev: None. K. Fakhro: None.
175-OR: Impact of High-Deductible Health Plan Enrollment on the Timing of Diabetic Retinopathy Care and Vision Loss Diagnosis
Authors: WHARAM J. FRANK , ZHANG FANG , LU CHRISTINE , STRYJEWSKI TOMASZ , CALLAWAY KATHERINE , WALLACE JAMIE , NEWHOUSE JOSEPH P. , ROSS-DEGNAN DENNIS 
Published: June 2020

High-deductible health plans (HDHP) that require large out-of-pocket payments for retinopathy screening and ophthalmologist visits could delay retinopathy screening, retinopathy diagnosis, and vision loss diagnosis. We studied 2004-2014 data in a large commercial and Medicare Advantage claims database. We included a national sample of 39,798 HDHP members with diabetes enrolled for 1 year in a low deductible (≤$500) plan followed by up to 4 years in a HDHP (≥$1000) after an employer-mandated switch. We matched HDHP patients to 305,852 contemporaneous controls whose employers offered only low-deductible plans. Outcomes included time to first: (a) retinopathy screening, (b) diagnosis of mild-to-moderate and (c) severe non-proliferative diabetic retinopathy, and (d) vision loss diagnosis. We used Cox proportional hazards models adjusted for multiple baseline characteristics to estimate baseline and follow-up hazard ratios. At baseline, adjusted hazard ratios (aHRs) between HDHP members and controls were not statistically different. At follow up, HDHP members experienced delays in first retinopathy screening (aHR: 0.89 [085, 0.92]), diagnosis of mild-to-moderate non-proliferative diabetic retinopathy (aHR: 0.82 [0.76, 0.89]), diagnosis of severe non-proliferative diabetic retinopathy (aHR: 0.90 [0.81, 1.00]), and vision loss diagnosis (aHR: 0.93 [0.88, 0.99]). HDHP members with diabetes experienced delayed retinopathy screening, retinopathy diagnosis, and vision loss diagnosis compared with similar patients in more generous health plans. Reducing financial barriers to care might improve retinopathy outcomes.

Disclosure
J. Wharam: None. F. Zhang: None. C. Lu: None. T. Stryjewski: Other Relationship; Self; Aldeyra Therapeutics, Pykus Therapeutics. K. Callaway: None. J. Wallace: None. J.P. Newhouse: None. D. Ross-Degnan: None.

Funding
National Institute of Diabetes and Digestive and Kidney Diseases