bluuebunny/crossref_metadata_2025_split huggingface dataset:
Deep Phenotyping of a Spontaneous Nonhuman Primate Model of Diabetic Macular Edema
Authors: CHIA SER MIEN , GONG LI , TIU SARAH , ANNAMALAI SARAYU PARIMAL , LI NINA X. , PAN LINGZHEN , HONG LEWIS , BAKAR ALI ASAD ABU , CHIN CHIH-LIANG , ZENG WEN 
Published: June 2018

Diabetic retinopathy (DR) is a diabetic complication involving damages to blood vessels in the retina that, if left untreated, can lead to blindness. It is estimated that over 93 million people suffer from DR worldwide and in fact the disease accounts for 12% of all new cases of blindness each year in the United States. Diabetic macular edema (DME) is one of the manifestations of DR, in which fluids leak from the blood vessels into the centre of the macula, causing pain, swelling, and blurred vision. However, the underlying pathogenesis of DR/DME is complex and not well understood, thus impeding the development of effective treatment. Consequently, the use of animal models of DR is of critical importance for better understanding of the underlying pathogenesis of DME, as well as developing new drugs. Non-human primate (NHP) models of diabetes are known to be the most clinically translatable animal models, where the animals develop major clinical phenotypes along the disease progression, including DR. As such, in this study we phenotyped a cohort of type 2 prediabetes/diabetes NHPs (n=123, weight: 11.5±2.0kg, age: 15.5±2.9years) using clinically relevant circulating and imaging biomarkers. Specifically, spectral domain optical coherence tomography (OCT) was first used to identify a subgroup of the animals with significantly thickened retina (329 ± 6.77µm) with an accumulation of hard exudates and inter-retinal cysts (n= 59). Fundus fluorescein angiography (FA) imaging further confirmed the presence of retinal vascular leakage into the cystoid spaces during the late-phase FA. Levels of vascular endothelial growth factor (VEGF) in both plasma and vitreous fluid were also measured and the results appear to correlate with retina thickness (vs. aged-matched controls). Taken together, our findings demonstrate a clinically translatable NHP model for DR/DME that allows characterization of disease progression in vivo, investigation of co-morbidities, and evaluation of novel therapeutics.

Disclosure
S. Chia: Employee; Self; Merck Sharp & Dohme Corp.. L. Gong: None. S. Tiu: Employee; Self; Merck & Co., Inc. S. Annamalai: Employee; Self; Merck Sharp & Dohme Corp. N.X. Li: Employee; Self; Merck & Co., Inc.. L. Pan: None. L. Hong: Employee; Self; Merck Sharp & Dohme Corp.. Employee; Spouse/Partner; Illumina, Inc. A. Abu Bakar Ali: Employee; Self; Merck & Co., Inc. C. Chin: Employee; Self; Merck & Co., Inc.. W. Zeng: None.
FoxK1/K2 Are New, Important Components of IR and IGF1R Signaling and Control of Cell Proliferation and Metabolism
Authors: SAKAGUCHI MASAJI , CAI WEIKANG , WANG CHIH-HAO , BATISTA THIAGO M. , ARAKI EIICHI , KAHN C. RONALD 
Published: June 2018

Insulin and IGF-1 are regulators of cell growth and metabolism. Despite considerable progress in understanding the molecular mechanisms underlying these effects, except for members of the FoxO family, many regulators of the transcriptional effects of these hormones remain poorly understood. To identify new components of IR/IGF1R signaling, we created brown preadipocyte lines in which both endogenous IR and IGF1R genes had been deleted and then reconstituted these cells with normal IR, IGF1R or chimeric receptors containing the extracellular domain of IR fused to intracellular domain of IGF1R and vice versa. Mass spectroscopic proteomic analysis revealed a number of proteins co-precipitated with each receptor construct, in both ligand stimulation-dependent and -independent manners. Among the proteins that associated with both receptors and chimeric receptors in a ligand-dependent manner was FoxK1. In contrast to FoxO1, the transcription factor FoxK1 was translocated from the cytoplasm to the nucleus after insulin stimulation, a pattern that is reciprocal to that of FoxO1 after insulin stimulation. We show that FoxK1 and FoxK2 are phosphorylated in two major domains and that translocation to the nucleus is dependent on the Akt-mTOR mediated phosphorylation, while their localization to the cytoplasm in the basal state is dependent on GSK3 phosphorylation. Knockdown of FoxK1 and FoxK2 in a mouse hepatocyte cell line causes marked alteration of the transcription of genes associated with apoptotic pathway and down-regulation of genes involved in control of cell cycle and metabolism. This resulted in decreased cell proliferation and altered mitochondrial fatty acid metabolism in these cells. Thus, insulin stimulates the reciprocal translocation of FoxKs and FoxO1 between the cytoplasm and nucleus turning off FoxO1-regulated genes and turning on FoxK-regulated genes resulting in an elaborate balance in insulin regulation of metabolism, growth and cell survival.

Disclosure
M. Sakaguchi: None. W. Cai: None. C. Wang: None. T.M. Batista: None. E. Araki: Speaker's Bureau; Self; Astellas Pharma US, Inc., MSD K.K., Kowa Pharmaceuticals America, Inc., Sanofi, Novo Nordisk Inc.. Research Support; Self; Astellas Pharma US, Inc., MSD K.K., Ono Pharmaceutical Co., Ltd., Shionogi & Co., Ltd., Takeda Pharmaceuticals U.S.A., Inc., Daiichi Sankyo Company, Limited, Nippon Boehringer Ingelheim Co. Ltd., Novartis Pharma K.K., Novo Nordisk Inc., Sanofi, Mitsubishi Tanabe Pharma Corporation, Sumitomo Dainippon Pharma Co., Ltd., Taisho Toyama Pharmaceutical Co. C. Kahn: Advisory Panel; Self; CohBar, ERX Therapeutics, AntriaBio, Inc.. Board Member; Self; Kaleio Biosciences.
Hyperinsulinemia Invokes Greater Brain Perfusion in Reward and Motivation Regions in Obesity
Authors: GROSKREUTZ DEREK , SINHA RAJITA , LACADIE CHERYL , LAM WAI , HAMZA MUHAMMAD , SCHMIDT CHRISTIAN P. , SEO DONGJU , HWANG JANICE , BELFORT-DEAGUIAR RENATA , LEVENTHAL JESSICA , ROSENBERG SAMUEL , PARIKH LISA , CONSTABLE TODD , SHERWIN ROBERT , JASTREBOFF ANIA M. 
Published: June 2018

Elevated insulin levels are often observed in obesity, but the effects of hyperinsulinemia on cerebral blood flow (CBF) are not known. While insulin acts as a satiety factor in lean humans, it is unclear if this CNS effect is maintained in the setting of hyperinsulinemia in obesity. This study aimed to isolate the effects of elevated insulin levels during euglycemia in lean (LN: n=6, BMI 21.1 kg/m2, age 32 years) and obese (OB: n=8, BMI 32, age 30) humans. Participants underwent a 2 hour oral glucose tolerance test [mean 120-min insulin LN 41 mU/ml vs. OB 113 mU/mL (p=.49) and glucose LN 101 mg/dL vs. OB 112 mg/dL (p=.72)] and on 2 separate days received either a saline infusion (control) or underwent a euglycemic-hyperinsulinemic clamp (insulin 2 mU/kg/min, glucose 90 mg/dL) during functional magnetic resonance imaging (fMRI). Whole-brain analyses comparing neural responses on hyperinsulinemic vs. saline control days demonstrated increased CBF in the putamen, insula, anterior cingulate cortex, and middle temporal gyrus in the OB group, but not in the LN group (p=.01, whole-brain corrected; Figure). We conclude that obesity invokes different CBF responses to hyperinsulinemia, specifically in regions implicated in impulsivity, reward processing, and interoceptive signaling. Thus, while in lean humans increased insulin levels signal satiety and reduce food-seeking behavior, this may not be the case in obese humans.

Disclosure
D. Groskreutz: None. R. Sinha: None. C. Lacadie: None. W. Lam: None. M. Hamza: None. C.P. Schmidt: None. D. Seo: None. J. Hwang: None. R. Belfort-DeAguiar: Research Support; Self; GlaxoSmithKline plc.. J. Leventhal: None. S. Rosenberg: None. L. Parikh: None. T. Constable: None. R. Sherwin: Other Relationship; Self; QuintilesIMS, MannKind Corporation. Research Support; Self; Regeneron Pharmaceuticals, Inc.. Other Relationship; Self; ICON plc. A.M. Jastreboff: Consultant; Self; Novo Nordisk Inc., Rhythm Pharmaceuticals Inc., Medtronic.
Regulation of Lipocalin 2 by Estrogen in Human Adipose Tissue—A Link between Erß Pathway and Insulin Resistance
Authors: KAMBLE PRASAD G. , PEREIRA MARIA J. , BOERSMA GRETHA J. , ALMBY KRISTINA E. , ERIKSSON JAN W. 
Published: June 2018

We recently showed that the adipokine lipocalin 2 (LCN2) causes insulin resistance in human adipose tissue (AT). Its expression is induced by dexamethasone (Dex) in AT from pre-menopausal women, but not from post-menopausal women or men. We also found that males had higher levels of LCN2 mRNA than females. Together, this proposes a regulation of LCN2 by glucocorticoids and sex steroids. Subcutaneous (SC) AT from post-menopausal women (n=29, 67±7 Y, BMI 28±5 kg/m2) was incubated ± 17 β-hydroxy estradiol (E2, 0.01-100 nM) and ± Dex (0.3 µM) for 24 h and LCN2 mRNA levels were measured. AT was co-treated with E2 (1 nM) and 100 nM and either estrogen receptor (ER) α or β antagonist, MPP or PHTPP, respectively, or with an ERβ agonist (DPN, 100 nM) for 24 h. E2 (1nM) increased LCN2 mRNA (p&lt;0.01) and protein (p&lt;0.05) levels by∼3 fold in AT, which was reversed by ERβ antagonist. Notably, E2 in presence of MPP induced LCN2 mRNA by 6 fold (p&lt;0.05) compared to control. Likewise, ERβ agonist also induced LCN2 mRNA by 3.5 fold (p&lt;0.05). Next, E2 induced ERβ mRNA by 1.8 fold (p&lt;0.05), but not ERα mRNA or protein levels. Dex alone did not change LCN2 mRNA levels in AT from post-menopausal females. Dex reduced ERα mRNA and protein levels by 20% (p&lt;0.001) and 35% (p&lt;0.01), respectively, but increased ERβ mRNA by 220% (p&lt;0.001). Dex-induced reduction in ERα mRNA levels was associated with BMI (r=0.569, p&lt;0.01), waist circumference (r=0.565, p&lt;0.01), fasting insulin (r=0.531, p&lt;0.05) and c-peptide (r=0.560, p&lt;0.01). In multivariate analysis BMI (std β coefficient = 0.626, p &lt; 0.01; model: r 2 = 0.392) remained as significantly associated variable.
In summary, E2 induced LCN2 expression in SCAT of postmenopausal women and this may be mediated via ERβ. Dex stimulation and inhibition of ERα and ERβ respectively implies a selective glucocorticoid mechanism to promote ERβ mediated transcriptional pathways. Overall, our data suggest that ERβ pathway may promote LCN2 expression and hence insulin resistance in AT.

Disclosure
P.G. Kamble: None. M.J. Pereira: None. G.J. Boersma: None. K.E. Almby: None. J.W. Eriksson: Employee; Spouse/Partner; Amgen Inc.. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Consultant; Self; Novo Nordisk A/S, Merck Sharp & Dohme Corp.. Research Support; Self; Bristol-Myers Squibb Company.
Real-World Risk Indicators of Severe Hypoglycemia in T2D—Results of the InHypo-DM Study
Authors: RATZKI-LEEWING ALEXANDRIA , HARRIS STEWART , MEQUANINT SELAM , AU NATALIE H. , BLACK JASON E. , REICHERT SONJA M. , BROWN JUDITH B. , RYAN BRIDGET L. 
Published: June 2018

Insight into the self-reported frequency of third-party assisted severe hypoglycemia (SH) is critical for the therapeutic optimization of type 2 diabetes (T2D). This study presents real-world epidemiological evidence on the self-reported incidence and related risk indicators of SH.
A validated questionnaire (InHypo-DMPQ) was administered to a population-based panel of adult Canadians with T2D treated with insulin and/or secretagogues. Questions pertained to respondents’ past hypoglycemia events as well as socio-demographic and clinical characteristics, including hypoglycemia unawareness. Univariable analyses (p≤0.20) followed by a multivariable zero-inflated negative binomial (ZINB) analysis were performed to explore the influence of potential risk indicators on the occurrence of any and repeated SH events.
The current evaluation is based on a cohort of 436 respondents (mean age: 53 years; male: 54%). Among these individuals, 37.8% (95% CI: 33.3%-42.4%) self-reported at least one SH event in the past year; the incidence rate was 2.4 events (95% CI: 2.26-2.55) per person-year. Based on the ZINB analysis, only non-severe (NH) hypoglycemia was independently associated with SH, holding other indicators constant. Among respondents who reported ≥1 (vs. zero) NH events, the odds of never experiencing an SH event decreased by 82% (95% CI: 39.3%-94.7%, p=0.006). Likewise, a history of NH, among those who had a chance of experiencing SH, increased the expected rate of SH by a factor of 4.29 (95% CI: 2.25-8.17, p&lt;0.001).
Real-world estimates of SH in T2D are often limited by sub-optimal reporting and gaps in clinical practice. To help clarify the true frequency of SH, this large, population-based study leveraged the value and clinical relevance of self-reported hypoglycemia data. The results of this study suggest that the burden of third-party assisted SH is substantial in people with T2D. Clinical strategies to prevent NH may reduce the risk of any/repeated SH events and resulting sequelae.

Disclosure
A. Ratzki-Leewing: None. S. Harris: Advisory Panel; Self; Novo Nordisk A/S, Sanofi, Merck, AstraZeneca, Amgen Inc., Lilly/Boehringer Ingelheim, Abbott, Janssen. Consultant; Self; Novo Nordisk A/S, Sanofi, Merck, AstraZeneca, Lilly/Boehringer Ingelheim, Abbott, Janssen. Research Support; Self; Novo Nordisk A/S, Sanofi, Merck, Abbott, AstraZeneca, Janssen. Other Relationship; Self; CIHR, CDA, The Lawson Foundation. S. Mequanint: None. N.H. Au: None. J.E. Black: None. S.M. Reichert: Other Relationship; Self; Novo Nordisk Inc., Sanofi, Abbott, AstraZeneca. Advisory Panel; Self; Servier. Speaker's Bureau; Self; Eli Lilly and Company. Other Relationship; Self; Boehringer Ingelheim Pharmaceuticals, Inc.. Speaker's Bureau; Self; Merck & Co., Inc., Janssen Pharmaceuticals, Inc.. J.B. Brown: None. B.L. Ryan: None.
Does Hypoglycemia Awareness Status on Gold and Clark Questionnaires Predict Hormonal and Symptomatic Responses to Hypoglycemia (HG) in Type 1 Diabetes (T1D)?
Authors: RUBIN NATHAN , MOHEET AMIR , EBERLY LYNN E. , KUMAR ANJALI , MANGIA SILVIA , SEAQUIST ELIZABETH R. 
Published: June 2018

Impaired awareness of hypoglycemia (IAH) is characterized by the diminished ability to perceive symptoms of HG. Gold and Clark questionnaires are commonly used in research to identify patients with IAH. However, the relationship between IAH status on questionnaires and the symptom and counterregulatory (CR) hormone responses to HG are not well understood. In this study, we examined data from 51 research subjects with T1D who completed both questionnaires and underwent a hyperinsulinemic hypoglycemic clamp (target glucose 50 mg/dL) on the same day. Clarke and Gold scores were highly correlated with one another (r = 0.78) and each had a similar relationship with epinephrine (EPI) response during HG (Clarke: r = -0.46, Gold: r = -0.53) and symptom response (Clarke: r = -0.60, Gold: r = -0.52). However, Clarke and Gold disagreed on classification of HG awareness status (misclassification=37%, Cohen’s κ=0.54). Clarke classifications were: 26 Aware (A), 13 Indeterminate (I), 12 Unaware (U), whereas Gold classifications were 16 A, 15 I, and 20 U. A mixture model based clustering identified 3 patterns in joint EPI and symptom responses. Cluster 1 subjects (n=10) had low symptom (&lt;5) and EPI responses (&lt;140) to HG and 8/10 were classified as U by one or both questionnaires. Cluster 3 subjects (n=9) had high symptom (20+) and EPI responses (450+) to HG and 8 of 9 were classified as A by one or both questionnaires. Cluster 2 subjects (n=22) had intermediate symptom and EPI responses to HG but concordance of classification by Clarke and Gold was true for only 11 of the 24. Clarke classified cluster 2 subjects as 12 A, 7 I, and 3 U whereas Gold classified the same subjects into 6 A, 7 I, and 9 U. IAH classification may be discordant between Clark and Gold questionnaires and may not always correlate with the CR responses during experimental HG. To ensure reproducibility, researchers must be rigorous and consistent in defining the awareness status of study subjects.

Disclosure
N. Rubin: None. A. Moheet: None. L.E. Eberly: None. A. Kumar: None. S. Mangia: None. E.R. Seaquist: Advisory Panel; Self; Eli Lilly and Company. Consultant; Self; Eli Lilly and Company, Sanofi, Zucera, InfoMed, 360 consulting. Other Relationship; Self; Novo Nordisk Inc..
A Prospective, Multicentric Study to Evaluate the Effects of Saroglitazar on Non-HDL Cholesterol and Small Dense LDL Particles in Patients with Diabetic Dyslipidemia
Authors: KAUL UPENDRA , JAIN PEEYUSH , KACHRU RANJAN , BHATIA VINEET , ARAMBAM PRIYADARSHINI , SHEKHAWAT SUDHIR , DIANA YUMNAM , RAWAT KAVITA , SINGH SHILPI , JAISWAL ASHOK 
Published: June 2018

Saroglitazar, a dual PPAR α/γ agonist, is approved in India for the treatment of diabetic dyslipidemia (DD) not controlled with statins. DD is highly atherogenic as it is associated with high triglycerides (TG), high small dense LDL (sdLDL) and low HDL-C. In this, prospective multi-centric study conducted in patients with type 2 diabetes and triglycerides (TG) ≥200 mg/dL after lifestyle and stable statin therapy for at least 3 months, efficacy and safety of saroglitazar has been evaluated. Total 104 patients (78% male) with mean age of 59.1 ± 11.4 years were enrolled. All subjects were given saroglitazar 4mg once daily for 24 weeks. The effects of saroglitazar were evaluated at 24 weeks by using paired t-test. Six months follow-up data is available from 73 patients. At 24 weeks the primary end point showed a significant reduction in non-HDL-C (from 138 ± 51 mg/dL to 113 ± 44 mg/dL; p&lt;0.001) and sdLDL (from 31.7 ± 11.8 mg/dL to 26.0 ± 11.9 mg/dL; p&lt;0.001). Of the secondary end points the values of TG, HDL-C, total cholesterol and HbA1c were also significantly improved at 24 weeks (Table). No major adverse event reported during the study period. This is the first study evaluating the effect of saroglitazar on sdLDL in patients with DD. The results indicate that saroglitazar is safe and well tolerated and effectively reduces sdLDL particles along with non-HDL-C.Change in laboratory parameters at 24 weeks follow-up (All values are Mean±SD)Laboratory parametersBaseline24 weeks follow-upP-valueNon HDL-C (mg/dL)138±51113±44&lt;0.001TG (mg/dL)351±360247±445&lt;0.001LDL-C (mg/dL)90±3882±240.074sdLDL (mg/dL)31.7±11.826.0±11.9&lt;0.001HDL-C (mg/dL)35.6±7.540.6±8.0&lt;0.001Total cholesterol (mg/dL)172±52154±43&lt;0.001HbA1c (%)7.98±1.666.95±0.71&lt;0.001

Disclosure
U. Kaul: None. P. Jain: None. R. Kachru: None. V. Bhatia: None. P. Arambam: None. S. Shekhawat: None. Y. Diana: None. K. Rawat: None. S. Singh: None. A. Jaiswal: Employee; Self; Zydus Cadila.
Insulin Sensitizing Effects of Vitamin D Mediated through Reduced Adipose Tissue Inflammation and Fibrosis
Authors: LONTCHI-YIMAGOU ERIC , KANG SONA , ZHANG KEHAO , GOYAL AKANKASHA , YOU JEE YOUNG , KISHORE PREETI , ROSEN EVAN , HAWKINS MEREDITH 
Published: June 2018

Adipose tissue inflammation and fibrosis appear to be mediated by adipocytes and contribute to insulin resistance. Since vitamin D (25(OH)D) has anti-inflammatory and anti-fibrotic effects, expression of its receptor in adipocytes and macrophages suggests that 25(OH)D signaling could mediate paracrine effects within adipose tissue and improve insulin resistance. We performed a randomized, double-blinded placebo-controlled trial to examine the effects of repleting vitamin D in 25(OH)D-deficient (&lt;20 ng/ml), insulin resistant, overweight-to-obese humans (n=19). 25(OH)D repletion to &gt;30 ng/ml was associated with reductions in adipose tissue expression of inflammatory (0.6-0.7-fold decreased expression of TNF-α, IL-6, iNOS and PAI-1) and pro-fibrotic (0.4-0.8-fold decreased expression of TGF-β1, HiF1α, Collagen I, V, VI and MMP7) genes, decreased collagen VI immunofluorescence (19% reduction, p=0.02) and improved hepatic insulin sensitivity, assessed as suppression of endogenous glucose production (EGP) during hyperinsulinemic clamp studies (1.28 ± 0.20 vs. 0.88 ± 0.18 mg/kg/min, p=0.03).
To determine whether vitamin D’s effects are mediated through adipocytes, we studied an adipocyte-specific vitamin D receptor knockout mouse model (Adiponectin-Cre+VDR+/ fl) after 12 weeks on high fat diet. Despite no differences in body weight or adiposity, VDR KO mice exhibited increased adipose tissue expression of several pro-inflammatory (Tnf-α, iNos, Pai-1, Mcp-1 and F4/80; 4-10 fold) and pro-fibrotic genes (Tgf-β1, Collagen VI, and Tsp1; 2-4 fold), in concert with hepatic insulin resistance during 2h hyperinsulinemic (4 mU/kg/min)-euglycemic clamps (EGP 10 ± 3 vs. 3 ± 2 mg/kg/min in WT, p = 0.021).
These human and rodent studies establish a beneficial role of vitamin D in restraining adipose tissue inflammation and fibrosis as well as hepatic insulin resistance, and suggest that normalizing 25(OH)D levels could have metabolic benefits in targeted individuals.

Disclosure
E. Lontchi-Yimagou: None. S. Kang: None. K. Zhang: None. A. Goyal: None. J. You: None. P. Kishore: None. E. Rosen: None. M. Hawkins: None.
Hypoglycemia in Patients with Diabetes in an Australian Public Hospital Setting
Authors: PIYA MILAN K. , ZARORA REETU , FLETCHER THERESE , SIMMONS DAVID 
Published: June 2018

Background: Diabetes is a common co-morbidity among hospital inpatients, particularly in medical wards. Diabetes is linked to increased length of stay and mortality in hospital inpatients, and hypoglycemia (hypo) is considered a contributory factor. We sought to determine the prevalence of diabetes in medical wards and the prevalence and patterns of hypo during their hospital stay.
Methods: A daily census on three medical wards (79 beds) was conducted over a 4 month period from June 2017 in a 3bed tertiary Sydney hospital. Charts and medications for inpatients with diabetes were audited each Friday using a questionnaire based on the UK National Diabetes Inpatient Audit. Patients admitted under the care of the diabetes team were excluded. Readmissions were counted as separate episodes.
Results: The mean prevalence of diabetes was 27%, of which 2.4% had T1DM, with 212 patient episodes audited in 196 patients (16 readmissions). Mean age (SD) was 71 years (11.2), 54% male. Only 5.6% had a diabetes related admission. Insulin use was 34% on admission but 52% during hospital stay. There were 74 events of hypo (&lt;72 mg/dL) in 38 patients (18%), with 10 episodes of severe hypo (&lt;54 mg/dL) in 9 patients (4.3%). Within the first week of admission, 50 of these hypo events occurred (8 severe) in 29 patients. Insulin was prescribed in 82% of the patients who had hypo (31/38), and 89% of those who had severe hypo (8/9), with only 50% of them admitted on insulin. A smaller number of hypo events occurred 8am-5pm compared to 5pm-8am (29 vs. 45), with no significant difference between days of the week.
Conclusion: Hypoglycemia is a major burden in patients with diabetes in hospital, particularly in the first week of admission, even when patients are not admitted due to diabetes related problems. Insulin use was the major risk factor and many patients had multiple hypo events. We recommend early involvement of the diabetes inpatient team as well as centralized point of care testing of glucose to allow early identification of patients at risk.

Disclosure
M.K. Piya: None. R. Zarora: None. T. Fletcher: None. D. Simmons: Speaker's Bureau; Self; Roche Diabetes Care Health and Digital Solutions, AstraZeneca, Novo Nordisk Inc., Medtronic.