bluuebunny/crossref_metadata_2025_split huggingface dataset:
1627-P: Real-World Comparison of Acute Complications in Adult Patients with Type 1 Diabetes in U.S. and European Registries
Authors: ZHOU FANG L. , HERMANN JULIA , PETTUS JEREMY , KERNER WOLFGANG , MILLER KELLEE , STECHEMESSER LARS , EDELMAN STEVEN , IBALD-MULLI ANGELA M. , HOLL REINHARD W. 
Published: June 2020

The study compares acute complications among adults with type 1 diabetes (T1D) by glycemic control in a U.S. Electronic Health Record database (T1PCO) with the German/Austrian Prospective Diabetes Follow-up (DPV). T1PCO included 31,430 and DPV 5,190 individuals in the analysis (age ≥18 years, T1D duration ≥2 years). During baseline (12 months prior to index date), ≥1 HbA1c and ≥1 insulin prescription was required. Baseline demographics, severe hypoglycemia (SH) and diabetic ketoacidosis (DKA) were analyzed for overall populations, by age group, and glycemic control (HbA1c categories). In both databases, incidence of DKA was highest in those with HbA1c ≥9.0%. Additionally, the incidence of DKA (per year) increased with deteriorating control (HbA1c&lt;8%: 1.3% vs. 1.7%, HbA1c≥10%: 19.9% vs. 22.9%; DPV and T1PCO respectively). In contrast, incidence of SH patterns differed between the databases. While in the T1PCO cohort SH increased with poorer glycemic control, the trend was reversed in DPV cohort (Figure). Real-world comparisons demonstrate the challenges in diabetes care across many countries around the world. Different patterns of incidence of SH by HbA1c may be related to differences in the capture of SH in databases, it may also reflect important differences in diabetes management including access to different types of insulin, CGM, pumps, education and type 1 savvy health care providers.

Disclosure
F.L. Zhou: Employee; Self; Sanofi. Stock/Shareholder; Self; Sanofi. J. Hermann: None. J. Pettus: Consultant; Self; Diasome Pharmaceuticals, Inc., Lexicon Pharmaceuticals, Inc., MannKind Corporation, Novo Nordisk Inc., Sanofi. W. Kerner: None. K. Miller: None. L. Stechemesser: None. S. Edelman: Advisory Panel; Self; Brightsight, InPen, Lexicon Pharmaceuticals, Inc., Lilly Diabetes, Novo Nordisk A/S. Board Member; Self; Senseonics. Speaker’s Bureau; Self; AstraZeneca, MannKind Corporation, Merck & Co., Inc., Sanofi. A.M. Ibald-Mulli: Employee; Self; Sanofi-Aventis. R.W. Holl: None.

Funding
Sanofi
1633-P: Women with Type 1 Diabetes (T1D) Experience a Shorter Reproductive Period Compared with Nondiabetic Women: The Pittsburgh Epidemiology of Diabetes Complications (EDC) Study and the Study of Women’s Health Across the Nation (SWAN)
Authors: YI YAN , EL KHOUDARY SAMAR R. , MILLER RACHEL G. , RUBINSTEIN DEBRA , MATTHEWS KAREN A. , ORCHARD TREVOR J. , COSTACOU TINA 
Published: June 2020

Evidence suggests that insulin deficiency and hyperglycemia may disrupt the normal function of the female reproductive system, leading to delayed menarche and premature ovarian aging. We compared the length of the reproductive period of women with T1D and women without diabetes. We assessed age at menarche and natural menopause in women with childhood-onset T1D (diagnosed in 1950-80) who participated in the Pittsburgh EDC study’s 2010-16 follow-up (where reproductive history was assessed) and nondiabetic participants from the Pittsburgh site of the SWAN study. Women who had not yet reached natural menopause, had a hysterectomy/oophorectomy before menopause or received sex hormone therapy during the menopausal transition were excluded from analyses. In EDC, covariate data were selected from the follow-up visit where chronological age was closest to the baseline age in SWAN. Reproductive history was self-reported. The Women’s Ischemia Syndrome Evaluation historical and hormonal algorithms were also used to assess menopause status. Women with T1D (n=105) were younger (42.8 vs. 46.0 yrs, p=.0003), more likely to be white (96.2% vs. 68.3%, p&lt;.0001), never smokers (67.3% vs. 48.1%, p=.002), with lower BMI (25.2 vs. 26.5 kg/m2, p=.002) and higher HDL-C (61.0 vs. 53.0 mg/dl, p&lt;.0001) compared with women without diabetes (n=341). Women with T1D were also older at menarche (13.3 vs. 12.6 yrs, p&lt;.0001) but younger at natural menopause (50.1 vs. 51.9 yrs, p&lt;.0001). Adjusting for age, race, smoking status, BMI, HDL, and number of pregnancies, T1D was associated with 3.3 (95% CI: 2.5-4.0) fewer reproductive years. The length of the reproductive period of women with T1D is shorter, having delayed menarche and earlier natural menopause, compared with women without diabetes. Factors that could be related to a shorter reproductive period in T1D should be investigated.

Disclosure
Y. Yi: None. S.R. El Khoudary: None. R.G. Miller: None. D. Rubinstein: None. K.A. Matthews: None. T.J. Orchard: None. T. Costacou: None.

Funding
National Institutes of Health (DK34818); Rossi Memorial Fund; National Institute on Aging; National Institute of Nursing Research; Office of Research on Women’s Health
1663-P: Gene Editing of the Human T-Cell Receptor Locus Enables Optimized In Vitro Testing of Autoreactive T-Cell Function in Type 1 Diabetes
Authors: PETERS LEEANA D. , POSGAI AMANDA L. , BRUSKO TODD M. 
Published: June 2020

Gene editing of the human T cell receptor locus enables optimized in vitro testing of autoreactive T cell function in type 1 diabetes.
The generation of antigen specific T cells and subsequent implementation as “living drugs” has garnered great interest in the immunotherapy space. One of the main caveats to this approach is the potential for heterologous chain pairing between the α- and β-chains of the endogenous and de-novo T cell receptors (TCRs). The consequences of chain mispairing can range from reduced antigen specific functionality to off-target autoimmune reactivity. The latter is an important consideration when designing therapies for autoimmune and inflammatory diseases, specifically with regards to the introduction of regulatory T cells (Treg) adoptive cell therapy. To date, infusions of polyclonal Tregs have demonstrated safety but have failed to reverse established type 1 diabetes (T1D). This demonstrates the need for the generation of safe and effective antigen-specific Tregs capable of recognizing β-cells in T1D. We have previously shown the ability to generate GAD-specific Tregs which maintain lineage stability and suppressive phenotype. To extend this work, we deleted the endogenous TCR α-chain gene (TRAC) via CRISPR/cas9 in CD8+T cells. We achieved &gt;90% editing efficiency through ribonucleoprotein (RNP) complex mediated single guide RNA delivery. Moreover, we found TRAC-KO CD8+ T cells displayed increased peptide MHC-dextramer staining, CD69 and CD25 upregulation after stimulation with cognate antigen, and increased antigen-specific killing of β-cell lines when compared to mock guide treated T cells. We believe this workflow can be applied to generate antigen specific Tregs, which we expect to provide increased suppressive capacity. Hence, we present a TCR-gene editing protocol in primary human T cells that results in efficient deletion of the endogenous TCR α-chain and robust enhancement of antigen-specific T cell function.

Disclosure
L.D. Peters: None. A.L. Posgai: None. T.M. Brusko: Board Member; Self; OneVax, LLC. Consultant; Self; Caladrius Biosciences, Inc., Sanofi-Aventis. Speaker’s Bureau; Self; CSL Behring.

Funding
National Institutes of Health (P01AI42288, R01DK106191, T325T32DK108736-03HIRN, UC4 P0063595)
1672-P: Characterization of Immune Checkpoint Inhibitor–Mediated Hyperglycemia: Beyond Insulin-Dependent Diabetes
Authors: LEITER AMANDA , CARROLL EMILY , BROOKS DANIELLE C. , SHIMOL JENNIFER BEN , EISENBERG ELLIOT , GALSKY MATTHEW , GALLAGHER EMILY 
Published: June 2020

Immune checkpoint inhibitors (ICIs) treat cancer by augmenting patients’ (pts) immune responses against cancer. The immune activation from ICIs is associated with immune-related adverse events. Inflammation has a known association with hyperglycemia (HG) and insulin resistance. Little is known about the prevalence of post-ICI HG (pIHG) beyond autoimmune diabetes (DM). We hypothesized that: (1)Pts with pIHG are more likely to have steroid exposure, pre-existing DM, and obesity (body mass index ≥30kg/m2); (2)A subset of pts have pIHG that cannot be explained by autoimmune DM or steroid use. We analyzed a cohort of 411 cancer pts on ICIs between 2011 and 2017 at our institution. We included pts who had ≥3 post-ICI glucose measurements. We defined pIHG as a random glucose &gt;200mg/dL from ICI initiation up to 6 months after cessation. We recorded DM diagnosis and steroid exposure as documented in the medical record. We compared pts with and without pIHG using the Fisher’s exact test. 385 pts had post-ICI glucose data. 105 (27.3%) had pIHG. Compared to those without pIHG, pIHG pts were more likely to be male (71% vs. 59%, p=0.04), to have pre-existing DM (54% vs. 10%, p&lt;0.01) and to be obese (31% vs. 18%, p&lt;0.01). Of the 105 pts with pIHG, 59(56%) had pre-ICI HG, 9(8.6%) had no pre-ICI glucose data, and 37(35.2%) had new onset pIHG. Of these 37 pts, 25(67.6%) had steroid-related HG and none had antibody-confirmed autoimmune DM. Of the remaining 12 pts, 3 had worsening of pre-existing DM. No obvious precipitant of HG was detected in the remaining 9 pts apart from ICI therapy. Timing of HG after ICI initiation ranged from 4 to 107 weeks (median 12.3 weeks). HG in 5 of these pts resolved without intervention.
In conclusion, pIHG occurred in over a quarter of pts. Risk factors for pIHG included pre-existing DM and obesity. The majority of new pIHG was related to steroid use. However, a subset of pts had new HG that may be related to ICI therapy, suggesting that ICIs may have a role in immune-related insulin resistance.

Disclosure
A. Leiter: None. E. Carroll: None. D.C. Brooks: None. J. Ben Shimol: None. E. Eisenberg: None. M. Galsky: Advisory Panel; Self; AstraZeneca, Bristol-Myers Squibb, Genentech, Inc., Merck & Co., Inc., Pfizer Inc. E. Gallagher: Advisory Panel; Self; Novartis Pharmaceuticals Corporation.

Funding
National Cancer Institute (P30CA196521, K08CA190770)
1674-P: Stearate Potentiates MIP-1a Production with TNF-a via TLR4/TBK1/IKKe /IRF3 Signal Axis: Significance for Insulin Resistance
Authors: AHMAD RASHEED , KOCHUMON SHIHAB P. , AREFANIAN HOSSEIN , ALMULLA FAHD 
Published: June 2020

Increased levels of plasma free fatty acids (FAs) are an important contributor to chronic inflammation, insulin resistance and other obesity-related complications. However, the molecular mechanisms by which individual FAs contribute to obesity-associated inflammation and disorders remain incompletely understood. Here we report that dietary saturated FAs specifically stearate led to a profound production of macrophage inflammatory protein (MIP)-1α (CCL3) in the presence of TNF-α in monocytes, macrophages and adipose tissues. Using pharmacologic and genetic approaches, we identified the involvement of TLR4/TBK1/IKKε/IRF3 signal axis in this production of MIP-1α in response to stearate and TNF-α. Consistent with this, cultured adipose tissues from TLR4 knockout (KO) mice revealed that stearate and TNF-α treatment did not induce MIP-1α compared with TLR2 KO or wild type (C57BL/6) mice. Moreover, C57BL/6 mice fed a high fat diet (HFD) for 16 weeks showed elevated levels of plasma fatty acids, TNF-α and MIP-1α along with insulin resistance. MIP-1α was significantly correlated with TNF-α. Our human data shows that expression of TLR4/p-IRF3 was elevated in the PBMCs of obese individuals as compared to lean. Furthermore, elevated MIP-1α expression levels in obese fat tissues were significantly correlated with TNF-α and macrophage markers.
In conclusion, these findings provide a mechanistic link between stearate and TNF-α for the overproduction of obesity associated MIP-1α, which could be used as a new target for the treatment of obesity-related chronic inflammation/insulin resistance.

Disclosure
S.P. Kochumon: None. F. Almulla: None.

Funding
Kuwait Foundation for the Advancement of Science (RA-AH-2016-007)
1678-P: Insulin Peptide Reactive T-Cells May Reflect Disease Activity in Ketosis-Prone Type 2 Diabetes
Authors: SATOMURA ATSUSHI , SUZUKI SEIYA , HAISA AKIFUMI , OIKAWA YOICHI , SHIMADA AKIRA 
Published: June 2020

Ketosis-prone type 2 diabetes with autoantibody negative and beta cell function positive group (KPD) is recognized as atypical diabetes characterized by the onset of disease at a relatively young age, obesity, sudden onset of ketosis and a transient decrease in insulin secretion. Previously we have reported that insulin peptide reactive T cells are detected in KPD patients (2017, ADA meeting). In this study, we examined the correlation between insulin peptide reactive T cells and clinical background such as C-peptide, HbA1c, and HLA types especially focusing on class I region to assess the significance of insulin peptide reactive T cells detected in KPD subjects. Peripheral blood was obtained from enrolled subjects with informed consent, and stimulated with insulin peptides (insulin B9-23, B10-24, B11-25, B12-26) for 24 hours, then interferon (IFN)-gamma spots were counted. Maximum spots more than 2.5 were considered as positive based on the data from control subjects. Seven out of 21 (33.3%) KPD participants (21 males, 0 females, mean age 40.3 years) showed positive result, and this frequency was similar to that in acute-onset type 1 diabetes (17 out of 50; 34.0%) (22 males, 28 females, mean age 44.5 years); these results were consistent with our previous observation. Only 1 out of 35 (2.9%) showed positive result in controls (26 males, 9 females, mean age 61.8 years). In KPD participants, serum C-peptide level was significantly lower in the ELISpot positive group than in the negative group (1.40±0.55 ng/mL vs. 2.35±0.76 ng/mL; p &lt;0.05). Moreover, there was a significant positive correlation between the spot number and HbA1c at onset in the positive group (rs= 0.6232, (p &lt;0.05 by Spearman correlation test). Furthermore, HLA A*02:01 or A*24:02 positive rate was significantly higher in the ELISpot positive group (n=7) than the negative group (n=14) (86% vs. 36%; p &lt;0.05). These findings suggest that insulin peptide reactive IFN-gamma-producing T cells may reflect disease activity of KPD.

Disclosure
A. Satomura: None. S. Suzuki: None. A. Haisa: None. Y. Oikawa: None. A. Shimada: Advisory Panel; Self; Astellas Pharma Inc. Speaker’s Bureau; Self; Eli Lilly Japan K.K., Novo Nordisk Inc., Sanofi-Aventis.
1699-P: Mechanisms and Roles of Foxo1-Akt Negative Feedback Pathway in Adipocytes
Authors: OHNO TOMOHIRO , ONO HIRAKU , YOKOTE KOUTARO 
Published: June 2020

Objective: FoxO1 is a substrate of serine/threonine-kinase Akt. Although FoxO1 is phosphorylated by Akt and inactivated by insulin stimulation, constitutive activation of FoxO1 is reported to enhance Akt phosphorylation. Therefore, constitutive activation of FoxO1 may mimic insulin’s functions via Akt phosphorylation.
Methods: Constitutively-active FoxO1 (CA-FoxO1) in 3T3-L1 adipocytes is overexpressed by adenovirus and Changes in insulin signaling and downstream actions was studied.
Results: CA-FoxO1 induced Akt phosphorylation in differentiated 3T3-L1 adipocytes. Regarding downstream actions, CA-FoxO1 significantly enhanced glucose uptake (148.6% compared to controls, P =0.030), GLUT4 translocation (297.6%, P &lt;0.01), lipogenesis (175.9%, P =0.030) and tended to enhance glycogen synthesis (128.7%, P =0.154), while in contrast, under insulin-stimulated condition, significantly suppressed protein synthesis (56.5%, P &lt;0.01) and DNA synthesis (44.4%, P &lt;0.01). Regarding insulin signaling, CA-FoxO1 enhanced phosphorylations of GSK-3, PRAS40, and p70S6K. The enhancement of PI 3-kinase activity by 3nM insulin is larger than that by CA-FoxO1, while Akt phosphorylation by 3nM insulin is smaller than that by CA-FoxO1, suggesting the mechanism of FoxO1-Akt feedback is downstream of PI 3-kinase. In contrast to previous papers, protein amounts of IR-β, p110α subunit of PI 3-kinase, or Rictor were not significantly changed by CA-FoxO1.
Conclusion: Constitutive activation of FoxO1 induced Akt phosphorylation even in differentiated 3T3-L1 adipocytes, but FoxO1 activation mimicked only metabolic functions of glucose but not proliferative or oncogenic functions of insulin. This selective mimicking of insulin by FoxO1 activation in adipocytes may improve glucose metabolism with a low risk of tumorigenesis. The mechanisms of FoxO1-Akt feedback is suggested not to be the increase in IR-β or p110α subunit of PI 3-kinase as previously reported, but to be mainly downstream of PI 3-kinase.

Disclosure
T. Ohno: None. H. Ono: None. K. Yokote: Research Support; Self; Astellas Pharma Inc., Daiichi Sankyo, Eli Lilly Japan K.K., Kowa Company, Ltd., Kyowa Hakko Kirin Co., Ltd., Merck Sharp & Dohme Corp., Mitsubishi Tanabe Pharma Corporation, Mochida Pharmaceutical Co., Ltd., Nippon Boehringer Ingelheim Co. Ltd., Novartis Pharma K.K., Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Pfizer Japan Inc., Sanofi K.K., Shionogi & Co., Ltd., Sumitomo Dainippon Pharma Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Teijin Pharma Limited. Speaker’s Bureau; Self; Abbott, Astellas Amgen, AstraZeneca K.K., Bayer Inc., FUJIFILM Pharmaceuticals U.S.A., Inc., Kaken Pharmaceutical Co., Ltd., Sanwa Kagaku Kenkyusho.
170-LB: Predictors of Diabetes First Diagnosed in Pregnancy: A Machine-Learning Model
Authors: DE CAMPOS MARIA A. , OPPERMANN MARIA LUCIA R. , GENRO VANESSA K. , LEITAO CRISTIANE B. , HIRAKATA VÂNIA N. , REICHELT ANGELA J. 
Published: June 2020

Introduction: Pregestacional (PG) DM first diagnosed in pregnancy (diabetes in pregnancy, DIP) carries poor outcomes, which may be prevented by DM diagnosis before pregnancy. Aim: To identify risk factors (RF) for DIP that may help to diagnose DM before pregnancy.
Methods: Retrospective cohort, type 2 DM women; specialized prenatal care facility; public hospitals; Brazil. Data - age, ethnicity, schooling, DM family history (FH), previous obstetric history (number of pregnancies, GDM, preeclampsia (PE), macrosomia) - and PG BMI were collected from May 2005 to July 2019. Univariable analyses (student T and chi-square tests) with SPSS vs.18; two machine learning (ML) models (model 1: all variables; model 2: age, GDM, FH, number of pregnancies and PG BMI) with software Orange Data Mining vs. 3; random sampling statistics.
Results: Of the 466 women, 157 (33.7%, 95% CI 29-38%) had DIP. Baseline characteristics/main outcomes were similar between DIP and PG DM women. For model 1, AUC was 0.526 and precision, 0.566. For model 2 (Figure), AUC was 0.525 and precision, 0.556. Age was the most important RF, followed by previous macrosomia in women ≤ 28 years and by PG BMI in those &gt; 28 years.
Conclusion: In type 2 women, RF identified by ML with the algorithms used were poor predictors of DIP diagnosis. They were the same as for known pregestational type 2 DM. Age was the most important determinant, followed by previous macrosomia (for DIP) and BMI (for PG DM).

Disclosure
M.A. de Campos: None. M.R. Oppermann: None. V.K. Genro: None. C.B. Leitao: None. V.N. Hirakata: None. A.J. Reichelt: None.
1711-P: Dapagliflozin Promotes Adipose Beiging and Lipolysis and Reduces Adipocyte Size in the Obese Prediabetic Dog
Authors: KABIR MORVARID , BERGMAN RICHARD N. , PICCININI FRANCESCA , STEFANOVSKI DARKO , GOPAUL V. SASHI , YANG HSIU-CHIUNG , KOLKA CATHRYN M. 
Published: June 2020

Selective sodium glucose cotransporter-2 inhibition promotes urinary glucose excretion, thus reducing blood glucose. Previously we showed that 6 weeks of Dapagliflozin (Dapa) treatment improved insulin sensitivity and prevented weight gain in a canine model of mild type 2 diabetes. Little is known about the effects of Dapa on adipose tissue (AT) function. Eleven dogs were fed a high fat diet for 6 weeks, then received a single low dose of streptozotocin (18.5mg/kg) to induce mild type 2 diabetes. Animals were then exposed to Dapa (n=5, 1.25mg/kg) or placebo (n=6) once per day for 6 weeks, while remaining on the high fat diet. At the end of the study, subcutaneous (SC) and visceral (VIS) fat depots were obtained for adipocytes isolation and molecular studies and fasting plasma parameters were measured. Fasting plasma glucose and insulin levels were unaffected by Dapa treatment. Finite mixture modeling linear regression was used for adipocyte distributions. Dapa decreased adipocyte size and bimodal distributions in both SC and VIS by 10% (P&lt;0.001). Dapa increased UCP1, PGC1α and Prdm16 gene expression by 2.68, 2.34 and 2.16 folds (&lt;0.05) in SC and 2.5, 3.6 and 1.6 folds (&lt;0.05) in VIS depots respectively. Immunostaining of UCP1 in SC and VIS tissues confirmed beiging process. Primary adipocytes were cultured for 4 and 24h. Lipolysis, indicated by glycerol release into the media increased by 40% in SC and 43% in vis after 24h (P&lt;0.05). Adiponectin levels increased only in the SC adipocytes by 80% (P&lt;0.05) after 4 and 24h cultures. Leptin levels increased in SC (by 3 folds P&lt;0.05) and VIS by 2.6 P&lt;0.05) after 24h adipocyte cultures.
In conclusion, Dapa promotes AT beiging, lipolysis, adiponectin and leptin release by adipocytes and decreased adipocyte size and distributions. These changes were independent of glucose and insulin. Thus, for the first time we are beginning to identify mechanisms by which Dapa enhances AT function and improves energy homeostasis in mild type 2 diabetes canine model.

Disclosure
M. Kabir: None. R.N. Bergman: None. F. Piccinini: Employee; Self; Medtronic. D. Stefanovski: None. V. Gopaul: None. H. Yang: Employee; Self; AstraZeneca. C.M. Kolka: Research Support; Self; AstraZeneca.

Funding
AstraZeneca (D1690L00045-CSR212966)
1747-P: MicroRNA-30a Exerts Antifibrotic Effects in Subcutaneous White Adipose Tissue to Preserve Insulin Sensitivity in Obesity
Authors: CHERNIS NATASHA , SAHA PRADIP , FELIX JESSICA B. , MASSCHELIN PETER M. , LIAN LEQIN , COX AARON , KIM KANG HO , WU HUAIZHU , HARTIG SEAN M. 
Published: June 2020

White adipose tissue (WAT) is an endocrine organ that dynamically expands and contracts to meet the metabolic demands of the organism. However, prolonged excessive caloric intake overwhelms WAT depots, resulting in peripheral fat deposition, systemic glucose dysregulation, tissue fibrosis, insulin resistance, and type 2 diabetes mellitus. The chronic triggers that degrade WAT function remain undefined, hindering the development of effective strategies to treat obesity and prevent its co-morbidities. We have identified a microRNA, miR-30a, that potently stimulates subcutaneous adipose tissue metabolic flexibility and enhances systemic insulin sensitivity. In follow-up studies, we created a genetically engineered mouse model to conclusively show miR-30a expression in white adipocytes is antidiabetic. Obese mice modified to express miR-30a at elevated levels in adipose tissues maintain insulin sensitivity coupled with reduced hepatic steatosis. Proteomic profiling indicated that miR-30a targets Plasminogen Activator Inhibitor-1 (PAI-1) to limit pro-fibrotic programs that would otherwise restrict subcutaneous WAT expansion and decrease insulin sensitivity. While visceral WAT depots remain a site of significant fibrosis in mice, subcutaneous WAT fibrosis is epidemiologically linked to metabolic disease risk in adult humans. In obese humans, miR-30a expression negatively correlates with PAI-1 levels in subcutaneous WAT, supporting an anti-fibrotic role for miR-30a that ultimately defends insulin sensitivity. Collectively, our observations linking miR-30a expression to insulin sensitivity suggest a new method that restores WAT homeostasis.

Disclosure
N. Chernis: None. P. Saha: None. J.B. Felix: None. P.M. Masschelin: None. L. Lian: None. A. Cox: None. K. Kim: None. H. Wu: None. S.M. Hartig: None.

Funding
American Diabetes Association (1-18-IBS-105 to S.M.H.); National Institutes of Health (R01DK114356)