bluuebunny/crossref_metadata_2025_split huggingface dataset:
1907-P: GLP-1RA and iSGLT2 Combination Treatment Effects over Fatty Liver Index
Authors: CARRETERO GÓMEZ JUANA , AREVALO LORIDO JOSE CARLOS , GÓMEZ-HUELGAS RICARDO , SEGUÍ-RIPOLL JOSÉ MIGUEL , TEMBRA MANUEL SUAREZ , CASAS JOSÉ MANUEL , CARRASCO JAVIER , DIABETES OUP ,   OBESITY AND NUTRITION SPANISH WORKING GR
Published: June 2019

Aim: To analyze changes in Fatty Liver Index (FLI) in obese and T2DM patients under treatment with GLP-1RA - SGLT2i combination.
Methods: Observational, prospective, multicenter study. Patients were stratified according to predetermined treatment schedule groups (successively vs. simultaneously).
Results: We included 142 patients (59.1% men, mean age 60.8±8.9 years). 76.7% had hypertension and 81.7% dyslipidemia. The BMI was 36.9 ±.7.1 kg/m2, FLI was 97±11, A1C was 8.0% ±1.5%, Triglyceride (Tg) was 158±102 mg/dl, Waist circumference (WC) 120.3 cm and gamma-glutamyl-transferase (GGT) was 43±45 UI/L. At 26 weeks follow-up we found a significant reduction in FLI (-5 points; p&lt;0.0000), A1C (-1.1%; p&lt;0.0001), BMI (-2.1 kg/m2; p&lt;0.00003), GGT (-11 UI/L; p&lt;0.0003), WC (-6.7 cm; p&lt;0.000) and Tg (-28.5; p&lt;0.01). Table 1 expands results in predetermined groups.
Discussion: Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of fat in the absence of other causes of steatosis. FLI is an accurate algorithm which can be used as a surrogate marker of steatosis; it combines measures of Tg, GGT, WC and BMI. GLP-1RA have direct effects on hepatocytes improving liver histology and reducing GGT levels. However, data on SGLT2i over the liver fat are scarce. Our study demonstrated that the combination of GLP-1RAs-SGLT2i reduces liver fat in patients with T2DM being positively correlated with improvement in A1C, BMI, WC and GGT.

Disclosure
J. Carretero Gómez: None. J. Arevalo Lorido: None. R. Gómez-Huelgas: None. J. Seguí-Ripoll: None. M. Suarez Tembra: None. J. Casas: None. J. Carrasco: None.
1910-P: SOCS3 Deficiency on a High-Fat Diet Accelerates Systemic Inflammation and Results in Lethal Myeloid Hematopoiesis without Obesity and Adiposity
Authors: CHO KAORI , USHIKI TAKASHI , ISHIGURO HAJIME , KATAGIRI TAKAYUKI , SUWABE TATSUYA , HIRAI HIDEYO , NAKAGAWA YOSHIMI , MASUKO MASAYOSHI , ALEXANDER WARREN , SHIMANO HITOSHI , SONE HIROHITO 
Published: June 2019

Introduction: Suppressors of cytokine signaling (SOCS) are negative regulators of cytokine signaling; SOCS3 controls myeloid hematopoiesis by suppressing G-CSF. SOCS3 haploinsufficiency attenuates diet-induced obesity by enhanced leptin sensitivity while improving insulin resistance. We established SOCS3 conditional knock-out (KO) mice to elucidate how high fat diets (HFD) affect inflammation and obesity in complete SOCS3 deficiency.
Methods: Embryonic lethality of complete SOCS3 deficiency was overcome using a conditional Socs3 allele inactivated by tamoxifen (TAM)-inducible cre-recombinase with SOCS3fl/flRosa26-CreERT2T/+ mice. They were fed HFD (60 kcal% fat) or control chaw (10 kcal% fat) starting at 4 weeks of age and TAM or vehicle administration was done at 8 weeks.
Results: Although insulin resistance improved and obesity and fatty liver were not confirmed in SOCS3-KO with HFD (S3HFD), the S3HFD group looked moribund around day 30 post-TAM by systemic inflammation; their mean survival was 62.5 days after TAM. Other groups did not look moribund. Significant granulopoiesis was also observed in S3HFD (peripheral blood neutrophil counts 29301 ± 20581/mm3). This myeloid hematopoiesis occurred in the spleen and not the bone marrow. S3HFD exhibited the progression of various granulocytes from progenitor cells (c-kitint∼highLy6G-) to mature granulocytes (c-kit-Ly6G+).Hematopoietic infiltration was confirmed in the liver in S3HFD with granulocytes, monocytes, and macrophages. Inflammasome-associated genes (IL-1β and Caspase1) were elevated in the liver at day 65 post-TAM in S3HFD.
Conclusion: SOCS3 deficiency showed myeloid proliferation under HFD without obesity and adiposity. SOCS3-KO may help in the clarification of the specific mechanism of myeloid proliferation and invasion in HFD-induced inflammation.

Disclosure
K. Cho: None. T. Ushiki: None. H. Ishiguro: None. T. Katagiri: None. T. Suwabe: None. H. Hirai: None. Y. Nakagawa: None. M. Masuko: None. W. Alexander: None. H. Shimano: None. H. Sone: Research Support; Self; Astellas Pharma Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Kowa Pharmaceutical Europe Co. Ltd., Kyowa Hakko Kirin Co., Ltd., Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Teijin Pharma Limited.
1918-P: Carbohydrate and Fat Oxidation Fasting and in Response to a Hyperinsulinemic Clamp is Similar in Obese Youth Regardless of PCOS Status
Authors: WIROMRAT PATTARA , RYNDERS COREY A. , NADEAU KRISTEN J. , CREE-GREEN MELANIE 
Published: June 2019

Whole-body metabolic flexibility (MF), i.e., switching substrate oxidation between fasting and fed states often becomes abnormal with insulin resistance (IR). Data regarding MF in women with PCOS, whom often have IR, are mixed and confounded by varied diets and habitual physical activity. No study has assessed MF in response to a multi-phase hyperinsulinemic-euglycemic clamp in PCOS females relative to non-PCOS with similar habitual physical activity and controlled diet. Adolescent girls with obesity and PCOS (age 14.9 ± 1.5 years; BMI 35 ± 4 kg/m2), 10 obese controls (age 13.5 ± 1.3; BMI 32 ± 2) and 13 normal BMI PCOS (age 16.2 ± 1.5; BMI 22.8 ± 2) were included. All girls were sedentary per questionnaire and 7 day accelerometry. A 4-phase hyperinulinemic-euglycemic clamp (basal, 10, 16 and 80 mU/m2/min of insulin) including glucose and glycerol tracers was performed. Glucose rate of disappearance (Rd), glycerol rate of appearance (Ra) and respiratory quotient (RQ) were assessed during each clamp phase. MF was defined as a change in RQ from baseline to each phase (ΔRQ). Basal RQs were not different between groups. Lean PCOS had higher ΔRQ at phase 10 compared to obese PCOS (p=0.005) and obese controls (p=0.003). All groups had similar ΔRQs at 16 and 80 phases. In multivariable regression models, Δ 10 glycerol Ra (Δ from baseline to 10 phase) was associated with phase 10 ΔRQ, independent of age and BMI (p=0.04); Δ 80 glycerol Ra and Δ 80 glucose Rd were associated with phase 80 ΔRQ, independent of age and BMI (p=0.048). Sedentary obese adolescents regardless of PCOS status have lower MF compared to lean PCOS during the low insulin dose which was associated with whole body lipolysis. However, this difference is not found during the high insulin dose, suggesting obese girls have only subtle defects in MF. Further, PCOS is not associated with lower MF once diet and habitual activity are matched.

Disclosure
P. Wiromrat: None. C.A. Rynders: None. K.J. Nadeau: None. M. Cree-Green: None.

Funding
American Diabetes Association (7-11-CD-08 to K.J.N.); American Heart Association (13CRP14120015); Thrasher Research Fund; National Center for Research Resources Colorado (TL1TR002533); Pediatric Endocrinology Society; National Institute of Diabetes and Digestive and Kidney Diseases (T32DK063687, K23DK107871)
192-LB: Serum Magnesium Levels and Its Relationship with Alterations of Glucose Metabolism during Pregnancy
Authors: LÓPEZ CASTRO ALICIA , ZAVALZA GOMEZ ANA BERTHA , HERNANDEZ GONZALEZ SANDRA OFELIA , ESPINEL-BERMUDEZ MARIA CLAUDIA , ORTIZ HERNANDEZ JOSE RICARDO 
Published: June 2019

Intracellular magnesium contributes in the regulation of the effects of insulin and glucose uptake; its deficits strongly associated with hyperglycemia, hypertriglyceridemia and insulin resistance (IR). Studies in healthy, hypertensive, and diabetes mellitus type 2 (DM2) subjects have shown a lower concentration of intracellular magnesium, higher glucose increase. It is unknown if there is hypomagnesemia related to hyperglycemia and insulin resistance during pregnancy. Analytical cross-sectional study in pregnant women who signed consent, ≥18 years old, any trimester of pregnancy. Patients with chronic diarrhea, alcohol intake (≥30 g/day), use of diuretics and/or calcium channel blockers, reduced renal function, or supplemented with magnesium for at least six months prior to the study were not included. Clinical variables were determined, anthropometry, vital signs, serum magnesium levels, fasting glucose and 2-h plasma glucose (2-h PG) value during a 75-g oral glucose tolerance test (OGTT), lipid profile and glycosylated hemoglobin (A1C) were measured. We analyzed 84 patients with whom the 3 study groups were formed: healthy pregnant women, with IR (TyG index) and gestational diabetes (GD) (Table). Hypomagnesemia was found in all 3 groups without a clear relationship between low magnesium levels and alterations in glucose status.

Disclosure
A. López Castro: None. A. Zavalza Gomez: None. S. Hernandez Gonzalez: None. M.C. Espinel-Bermudez: None. J.R. Ortiz Hernandez: None.
1920-P: Coingestion of Glucose and Fructose Has Synergistic Effects on Lipoprotein Risk Factors for Cardiovascular Disease in Healthy Young Adults
Authors: HIERONIMUS BETTINA , MEDICI VALENTINA , LEE VIVIEN , NUNEZ MARINELLE , HAVEL PETER J. , STANHOPE KIMBER L. 
Published: June 2019

Global sugar consumption is at an all-time high. In previous studies, we and others have demonstrated that, compared with glucose (Gluc), consumption of fructose (Fruc) increases risk factors for cardiovascular disease (CVD), diabetes and metabolic syndrome. However, humans almost exclusively consume Fruc in combination with Gluc. Our aim was to study effects of Gluc, Fruc and their combination - high fructose corn syrup (HFCS) - and identify effects on metabolic risk factors.
We performed a parallel-armed, double blinded intervention study wherein the subjects consumed beverages sweetened with 25% of their energy requirement (Ereq) as Gluc, Fruc or HFCS, or 17.5% Ereq as Fruc or HFCS, or Aspartame (ASP) for two weeks with their usual diet. Procedures, which included fasting and postprandial blood draws, were conducted over a 48-h period at baseline and at the end of intervention while subjects consumed standardized meals containing 30% Ereq as fat, 15% protein, 55% carbohydrate (mainly complex during baseline; complex + sweetened beverage during intervention). As expected, the increases for 24h triglyceride area under the curve (AUC), 24h uric acid AUC, and postprandial apoCIII were highest in both Fruc groups (all P&lt;0.01 versus ASP), next highest in both HFCS groups (all P&lt;0.05 25% Ereq HFCS versus ASP), and lowest in the Gluc group (all P&gt;0.05 versus ASP). Unexpectedly, the increases of LDL- and non-HDL-cholesterol (C) and ApoB were highest in the HFCS groups (all P&lt;0.001 25% HFCS versus ASP, P&lt;0.01 versus Gluc). Re-analyzing the outcomes based on the amounts of Fruc and Gluc contained in the beverages revealed significant interactions between Fruc and Gluc on fasting and postprandial concentrations of LDL-C, non-HDL-C and ApoB (all P&lt;0.01).
While sole consumption of Fruc leads to increases of metabolic risk factors, those increases are exacerbated for several risk factors when Fruc is co-ingested with Gluc as HFCS.

Disclosure
B. Hieronimus: None. V. Medici: None. V. Lee: None. M. Nunez: None. P.J. Havel: Research Support; Self; Arrowhead Research, Bristol-Myers Squibb Company, Magnamosis Inc. K.L. Stanhope: None.

Funding
National Heart, Lung, and Blood Institute (1R01HL09133, 1R01HL107256); National Center for Research Resources (UL1RR024146); Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD051958); Office of Research on Women’s Health; Office of Dietary Supplements; National Institute on Aging (to K.L.S.)
1921-P: The Role of BCAA Catabolism in Glucose Homeostasis
Authors: NISHI KIYOTO , ABELL LAUREN , MCMILLEN TIMOTHY , TIAN RONG 
Published: June 2019

The rate limiting step of BCAA (Branched-chain amino acid; Valine, Leucine and Isoleucine) catabolism is regulated by the branched-chain keto acid dehydrogenase complex (BCKDC). PPM1K is a phosphatase which regulates BCAA catabolism by activating BCKDC through dephosphorylation. We and other groups have reported impaired BCAA catabolism and elevated blood BCAA levels in PPM1K-defiient mice (KO). Several studies have shown that elevated blood BCAA levels are associated with obesity and glucose intolerance. In addition, PPM1K expression is reduced in obesity model animals (leptin-deficient mice, etc.) and GWAS data shows loss-of-function SNP of PPM1K gene is associated with diabetes. Based on these findings, loss/reduction of PPM1K is thought to induce glucose intolerance. However, no previous study has directly analyzed the role of PPM1K in obesity and glucose metabolism. Therefore, in this study, we analyzed KO and wild type mice (WT) with diet-induced obesity. Firstly, KO and WT were fed with either normal chow diet (NCD) or high-fat diet (HFD; 60% of kcal from fat). KO showed normal body weight gain in both NCD and HFD condition. Next, KO and WT underwent intra-peritoneal glucose tolerance test (ipGTT). NCD-fed KO showed normal glucose tolerance. Surprisingly, HFD-fed KO showed significantly better glucose tolerance (AUC WT 58192±7828 vs. KO 47526±6646 min*mg/dL, p&lt;0.05). As impaired BCAA catabolism leads to both decreased BCAA catabolite and increased BCAAs, to distinguish the effect of these two factors, we did ipGTT in WT fed with BCAA-restricted diet (LB; the amount of BCAA were reduced to one-third of control), which has decreased BCAA catabolite without increased BCAAs. LB showed improved glucose tolerance (AUC Cont 38639±5748 vs. LB 32087±5072 min*mg/dL, p&lt;0.05), indicating that decreased BCAA catabolite rather than increased BCAAs may cause better glucose tolerance in KO.
In summary, these results suggest the critical role of PPM1K and BCAA catabolism in the regulation of glucose homeostasis.

Disclosure
K. Nishi: None. L. Abell: None. T. McMillen: None. R. Tian: None.

Funding
Japan Heart Foundation; National Institutes of Health
1926-P: Regulation of Soluble Epoxide Hydrolase by Gut Bacteria and Acetate
Authors: YOUN JANG , OH YOUNG-TAEK 
Published: June 2019

Epoxyeicosatrienoic acids (EETs) are lipid mediators with beneficial effects on metabolic and cardiovascular (CV) health. EETs are metabolized to biologically less active diols by soluble epoxide hydrolase (sEH). Inhibition of sEH, which increases EETs, has been shown to improve glucose homeostasis, blood pressure, and CV health in insulin-resistant or diabetic animals and proposed as an effective strategy to treat diabetes and CV diseases. Despite its importance to metabolic and CV health, little is known about mechanisms by which sEH is regulated in vivo. Our recent study demonstrated that in vivo sEH activity, assessed from plasma oxylipin levels, profoundly (3-fold) decreased after a meal in rats. Interestingly, this effect was completely abolished in rats with gut bacteria depleted by antibiotic treatment, suggesting that a gut-bacteria-derived factor(s) may be responsible for the postprandial effect. Gut bacteria produce short chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, from nutrients, and plasma SCFA levels rise during feeding. In the present study, we tested the possibility that SCFAs may be involved in the postprandial inhibition of sEH activity. For this, we examined the effects of SCFAs on sEH activity in vitro by measuring EET conversion to diol in liver homogenates. Acetate showed a profound effect to inhibit sEH activity (up to 91%) with EC50 of 39 ± 3 µM (n = 4). In contrast, propionate and butyrate had no significant effects (n = 4 and 5, respectively). The acetate effect occurred at physiological concentrations, suggesting acetate may be an endogenous inhibitor of sEH, and the postprandial inhibition of sEH activity may be mediated by acetate produced by gut bacteria after a meal. Because acetate is produced in vivo predominantly by gut bacteria, these data may explain why the postprandial effect to inhibit sEH was absent in gut-bacteria-depleted rats. Taken together, our data suggest sEH activity may be regulated in vivo by gut bacteria through the production of acetate.

Disclosure
J. Youn: None. Y. Oh: None.

Funding
American Diabetes Association (1-16-IBS-332 to J.Y.)
193-LB: Levels of Adherence to a Mediterranean Diet and Risk of Gestational Diabetes Mellitus: Modulation Effects of MTNRB1_rs10830963, TCFTL2_rs7903146, and MC4R_rs17782313 Gene Polymorphisms
Authors: BARABASH ANA , VALERIO DEOGRACIA JOHANNA , ASSAF-BALUT CARLA , DEL VALLE LAURA , DE LA TORRE NURIA GARCIA , BORDIU ELENA , DURAN ALEJANDRA , FUENTES MANUEL , INES JIMENEZ , CUESTA MARTIN , RUBIO MIGUEL A. , CALLE ALFONSO L. 
Published: June 2019

Background: A high adherence (adh.) to a MedDiet pattern was associated with a reduced GDM risk. Studies have shown associations between MTNR1B rs10830963, TCF7L2 rs7903146, MC4R rs17782313 SNPs and GDM risk. The conferring risk could be modified by a MedDiet. This study’s aim was to investigate if the association between the degree of adh. to a MedDiet and GDM incidence is modulated by MTNR1B rs10830963 C&gt;G, TCF7L2 rs7903146 C&gt;T and MC4R rs17782313 T&gt;C polymorphisms.
Methods and Findings: 874 women were stratified into 3 groups defined as high, moderate or low adh. according to late first-trimester (&gt;12 gestational weeks) compliance with 6 food targets: vegetables &gt;12 s/w, fruits &gt;12 s/w, juice &lt;2 s/w, nuts&gt; 3 s/w, consumption of extra virgin olive oil (EVOO) &gt;6 d/w and 40 mL/d EVOO. High adh. was defined as complying with 5-6 targets; moderate 2-4 targets and low 0-1 targets. Patients were genotyped for rs10830963, rs7903146 and rs17782313. Logistic regression analysis was adjusted for ethnicity, age, parity and BMI.
Results: There was a significant association between rs10830963 risk allele G and GDM risk (OR) 1.87(1.29-2.73); and fasting 1.77(0.88-2.66) and 1 h glycaemia 6.27 (1.72-10.83) during 75g OGTT (all p&lt;0.0001). Subjects with rs10830963 G allele who had low adh. had higher fasting glucose (mg/dL) compared to carriers with high adh. (88.24±0.93 vs. 84.59±0.85, p inter&lt; 0.05). For T carriers of rs7903146 and C carriers of rs17782313 the genetic risk for GDM was significantly lower in women with high adh. 0.43 (0.23-0.80) compared to low adh. 0.2 (0.14-0.99), p-inter &lt;0.01. The genetic risk score confirmed a significant gene-MedDiet interaction (p=0,05) for GDM. There was no effect in non-risk genotype carriers for the 3 SNPs.
Conclusions: MTNR1B, TCF7L2, MC4R genes modulate the effect of a DietMed on the development of impaired glucose metabolism and GDM.

Disclosure
A. Barabash: None. J. Valerio Deogracia: None. C. Assaf-Balut: None. L. Del Valle: None. N. Garcia de la Torre: None. E. Bordiu: None. A. Duran: None. M. Fuentes: None. J. Ines: None. M. Cuesta: None. M.A. Rubio: None. A.L. Calle: None.

Funding
Instituto de Salud Carlos III of Spain; Fondo Europeo de Desarrollo Regional; Sociedad de Endocrinolog?a Nutrici?n y Diabetes de la Comunidad de Madrid (IPI/2017/NR2)
1933-P: Acute Hyperglycemia + Hyperinsulinemia Increases Carotid-Femoral Arterial Stiffness and Perfusion of Skeletal Muscle in Healthy Subjects
Authors: HORTON WILLIAM B. , JAHN LINDA , HARTLINE LEE , PATRIE JAMES T. , BARRETT EUGENE 
Published: June 2019

Introduction: Chronic hyperglycemia injures both micro-and microvasculature. Conversely, insulin stimulates vascular nitric oxide production and acts as a vasodilator. Whether acute hyperglycemia (AH) inhibits insulin’s vasodilator action in healthy vasculature is unknown. Here we tested whether AH interfered with insulin’s action to recruit microvasculature, enhance endothelial function, or diminish vascular stiffness.
Methods: Nine healthy, fasting subjects (ages 18-35 years; BMI 18-25 kg/m2) twice received a 1 mU/kg/minute 2-hour insulin clamp. On one occasion, subjects were euglycemic (EH); and on the second, were hyperglycemic (∼200 mg/dL) (HH) for 2 hours before and throughout the clamp. Octreotide infusion blocked endogenous insulin in both studies. We assessed endothelial function by flow-mediated dilation (FMD) and arterial stiffness with pulse wave velocity (PWV) and augmentation index (AI). We used contrast-enhanced ultrasound to measure insulin-mediated capillary recruitment in skeletal and cardiac muscle. Linear mixed model was used for statistical analysis, with Bonferroni correction for comparison between studies.
Results: Insulin increased carotid-femoral PWV (p=0.02 for Δ PWV) but decreased AI (p= 0.02) during HH, with AI significantly reduced in HH compared to EH (p=0.04). Insulin recruited microvasculature (p&lt;0.05) with either EH or HH, and microvascular blood volume (p=0.03) and blood flow (p=0.04) significantly increased in skeletal muscle after HH. No changes were observed in FMD or cardiac microvascular perfusion with either condition.
Discussion: This study provides evidence that 4 hours of AH evokes insulin-induced increases of carotid-femoral arterial stiffness in healthy subjects. Insulin’s ability to recruit microvasculature is preserved during AH.

Disclosure
W.B. Horton: None. L. Jahn: None. L. Hartline: None. J.T. Patrie: None. E. Barrett: Research Support; Self; AstraZeneca.

Funding
National Institutes of Health (F32HL142304-01)
194-OR: A Versatile Platform for Intravital Imaging of Biosensor-Labelled Beta Cells In Situ
Authors: REISSAUS CHRISTOPHER A. , TERSEY SARAH A. , DUNN KEN W. , LINNEMANN AMELIA K. , MIRMIRA RAGHAVENDRA 
Published: June 2019

The pancreatic islet is a complex system containing numerous cell types, including endocrine, immune, and endothelial. The pathologies of T1D and T2D originate in this organized, multicellular environment in vivo, and thus can only be fully understood in this context. We have developed several adaptable tools to generate a versatile platform combining intravital microscopy (IVM), virally-packaged biosensors, and abdominal imaging windows (AIW) allowing us to gather β cell specific measurements in vivo longitudinally. Here, we present characterization of in vivo physiology of mouse β-cells using two virally-packaged biosensors roGFP2 and GcAMP6s. To achieve in vivo expression of the biosensors, we used IP injected AAV8 to transduce in situ β cells. Using redox-sensitive roGPF2, we measured the response in biosensor signal after IV administration of the cytotoxic glucose analog alloxan from islets in situ (∼5-fold change vs. saline). To test the portability of the platform, we utilized Alox15 knockout mice (Alox15-/-), which show protection against oxidative stress. We observed a rapid 4.6-fold increase in biosensor signal ratio in WT mice, compared to a 3.3-fold increase in Alox15-/- mice after IV alloxan treatment. Using AAV8-GcAMP6s, we measured calcium activity of β-cells in situ after a glucose bolus and detected a small sub-population of β cells that oscillate at a 2x frequency compared to the entire islet. To overcome the endpoint nature of standard IVM, we next implanted AIWs over the pancreas of biosensor-labeled mice, which allows for stable, longitudinal imaging of islets in situ over for several weeks. Using IVM through AIW’s in AAV8-roGFP2 transduced mice, we monitored individual islets, before, during, and after streptozotocin-induced β cell ablation. We measured a ∼75% reduction in islet area by 10 days post ablation. Altogether, this versatile platform can lead to novel experiments examining β-cell physiology and signaling in vivo longitudinally in a variety of unique scenarios.

Disclosure
C.A. Reissaus: None. S.A. Tersey: None. K.W. Dunn: None. A.K. Linnemann: None. R. Mirmira: None.