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2015 ADA Posters 1930-2373.Indd ISLET BIOLOGY—APOPTOSISCATEGORY age 44.3 years), comprising 2,078 males (71.7%) and 822 females (28.3%) Multiple regression analysis(STATA 10SE) with leptin, adiponectin, resis- who underwent annual medical check-ups at our center between January tin and ASP as determinants of serum total 25 hydroxy vitamin D used a 2005 and December 2009, were recruited. The subjects were divided into model adjusted for age, gender, adjusted calcium, PTH , BMI, fasting insulin, four groups according to baseline serum triglyceride (TG) level and waist cir- smoking status, season of sampling and statin prescription. hs-CRP was re- cumference (WC): normal WC-normal TG level (NWNT), normal WC-high TG moved due to collinearity with leptin and resistin. level (NWHT), enlarged WC-normal TG level (EWNT) and enlarged WC-high Adiponectin determined circulating vitamin D concentration independent of TG level (EWHT). High serum TG level was defi ned as ≥150 mg/dL and en- other measured adipokines (β 0.39, 95% CI 0.14-0.63, p=0.003). Leptin, resistin larged WC was defi ned as ≥90 cm for men and ≥85cm for women. New cases and ASP did not infl uence vitamin D concentration (r2 of model 0.51, p=0.04). of diabetes were determined according to questionnaires fi lled in by partici- Serum adiponectin infl uences circulating vitamin D concentration inde- pants and the diagnostic criteria of the American Diabetes Association. Cox pendent of other adipokines. Resistin and ASP do not appear to be related to proportional hazards model analysis was used to assess the association of circulating vitamin D in our obese middle aged cohort. HTGW phenotype with the incidence of diabetes. A total of 101 (3.5%) new diabetes cases were diagnosed during the study period. The EWHT group had a higher incidence of diabetes (8.3%) compared with the NWNT group ISLET BIOLOGY—APOPTOSIS (2.2%). The adjusted hazard ratio (aHR) for diabetes for subjects with the EWHT phenotype at baseline was 4.113 (95% confi dence interval [CI] 2.397- 7.059) after adjustment for age, and 2.429 (95% CI 1.370-4.307) after ad- Guided Audio Tour: Islet Biology—Apoptosis (Posters: 2254-P to 2261-P), justment for age, sex, total cholesterol, systolic blood pressure and alcohol see page 15. drinking history. It was attenuated by inclusion of baseline fasting glucose level in the model. Subjects with the HTGW phenotype showed the highest & 2254-P risk of incident diabetes. This tool could be useful for identifying individuals Autophagy Induction Improves Function and Survival of Human at high risk of diabetes. Type 2 Diabetic β-Cells MARCO BUGLIANI, MASINI MATILDE, FAROOQ SYED, SANDRA MOSSUTO, 2252-P MARA SULEIMAN, LORELLA MARSELLI, UGO BOGGI, FRANCO FILIPPONI, DECIO Longevity of the Metabolic Impact of Laparoscopic Sleeve Gastrec- L. EIZIRIK, MIRIAM CNOP, PELLEGRINO MASIELLO, PIERO MARCHETTI, Pisa, Italy, tomy: Results in Morbidly Obese Indian Diabetic Patients at the End Brussels, Belgium of Seven Years Autophagy is the major mechanism involved in degradation and recycling JAYASHREE S. TODKAR, SHASHANK S. SHAH, Pune, India of intracellular components, and its alterations have been proposed to cause Laparoscopic sleeve gastrectomy (LSG) is a standard bariatric operation. β cell dysfunction. In the present study we explored the effects of autophagy It also shows a metabolic impact in terms of improvement in diabetes type 2 modulation in islets prepared from type 2 diabetic (T2D) and non-diabetic (T2DM) in morbidly obese patients. Sparse reports exist about the longivity (ND) human donors, studied under several different conditions. Islets were of its metabolic impact. This is the study to present the results of LSG in Indi- isolated from 5 T2D (age: 77±7yrs; gender: 3M/2F; BMI: 23.9±3.7 Kg/m2) and an obese patients with T2DM at the end of seven years. From 2006 till 2010, 10 non-diabetic (ND; age: 69±19 yrs; gender: 3M/7F; BMI: 23.6±2.9 Kg/m2) 124 patients of Indian origin with morbid obesity and T2DM have undergone organ donors. T2D and/or ND islets were then cultured for 1-5 days with 10 a LSG at our center by a single surgical team. The standard operation of LSG ng/ml rapamycin (autophagy inducer), or 5 mM 3-methyl-adenine (3MA) and and the multidisciplinary care with regular follow ups was provided to all of 1.0 nM concanamycin-A (ConcA) (autophagy blockers), either in the presence them. At the end of seven years we could collect information of 81 patients. or absence of metabolic (0.5 mM palmitate) or chemical (0.1 ug/ml brefeldin N =81. M:F: 29: 62. Age range 22 - 65 yrs. Duration of T2DM: 6 mths to 21 A) endoplasmic reticulum (ER) stressors. Compared to untreated T2D islets, yrs. BMI range: 35 - 68 kg/m2. On OHA only: 56. OHA + Insulin: 25. Average rapamycin exposed (24h) diabetic islets showed improved insulin secretion glycosylated Haemoglobin was 8.5%. At the end of seven years average BMI (glucose-induced insulin stimulation index from 1.6±0.8 to 2.1±1.1, p=0.05), loss was found to be 18 kg/m2. The average glycosylated hemoglobin was reduced amount of β cells with signs of apoptosis (from 6.6±1.7 to 2.0±0.8% 6.8%. The insulin usage (in redced doses) was needed in only 3 patients. by electron microscopy, p<0.05), and better insulin granules, mitochondria 68 patients out of 81 did not need any anti diabetic medication. 10 patients and ER ultrastructure. This was associated with signifi cant reduction of were on a single OHA. 76/81 had other medical comorbidities related to obe- PERK, CHOP and Bip gene expression (qRT-PCR). As expected, in ND islets sity and all showed an improvement even at the end of seven years. 21/81 palmitate exposure (5 days) induced a 4-5 fold increase of β cell apoptosis showed some weight gain (average 5 kg) at the end of 7 years but could re- (from 0.4±0.2 to 2.0±0.8%, p<0.01); this deleterious action was completely tain their metabolic improvements as compared to the baseline. LSG seems prevented by rapamycin (0.3±0.3%) and signifi cantly exacerbated by 3-MA to be a good surgical and metabolic tool to improve the diabetic status in (7.0±1.1%) and ConcA (3.1±1.1%). Substantially similar results were observed morbidly obese Indian T2DM patients even at the end of seven years. with brefeldin treatment (24h). Both palmitate and brefeldin induced PERK, CHOP and Bip gene expression, which was signifi cantly, although partially, 2253-P prevented by rapamycin. This study emphasizes the importance of autophagy Serum Adiponectin Determines Circulating Vitamin D Concentra- in human β cell function and survival, likely in association with ER activity. tion Independently of Other Adipokines Modulation of autophagy could be instrumental to β cell protection. RAM P. NARAYANAN, LUKE D. BOYLE, SARAH NG, AMANDEEP KAHLON, AN- DREW CROSS, CHERLYN DING, CHEN BING, CONOR MAGEE, HASAN Z. MALIK, & 2255-P STEPHEN W. FENWICK, JOHN P.H. WILDING, Warrington, United Kingdom, Liver- Heat Shock Factor 1 Protects Beta Cells against Glucolipotoxicity- pool, United Kingdom induced Endoplasmic Reticulum Stress and Apoptosis Circulating vitamin D concentrations have been linked to adiponectin and INDRI PURWANA, JEAN BUTEAU, Edmonton, AB, Canada leptin, but not studied in the context of other adipokines. Our study aimed Excess exposure to glucose and fatty acid causes endoplasmic reticulum to assess the effects of adipokines on serum vitamin D levels in a predomi- (ER) stress, protein misfolding, and apoptosis, a condition termed “glucolipo- nantly obese middle aged Caucasian cohort in north west England. toxicity”. Heat Shock Factor 1 (HSF1) is a transcription factor that regulates We recruited 53 patients (11 male), the majority (79.2%) of whom were cell response to diverse stressors via the induction of the molecular chaper- due to undergo bariatric surgery. The remainder underwent elective laparo- ones heat shock proteins 70 and 90 (HSP70 and HSP90). Upon stress, HSF1 scopic cholecystectomy. Mean age was 48 years (95% CI 45.3 - 50.9). The binds to the heat shock response element (HSE) to initiate the transcription majority were obese (BMI>30: 88.6%; BMI>40: 77.3%). of HSPs, whose role is to keep proteins from being misfolded thereby al- Fasting serum samples were obtained from patients on the morning of leviating ER stress. the day of surgery. Serum total 25 hydroxyvitamin D (D2+D3), fasting insulin, We herein sought to test the hypothesis that HSF1 would protect beta- calcium, parathyroid hormone (PTH) were measured along with serum leptin, cells against glucolipotoxicity and to identify the posttranslational modifi ca- adiponectin, resistin, ASP and C reactive protein (hs-CRP). Body weight was tions involved in its activation. measured using TANITA scales. Thus, INS1 cells and human islets were treated with or without 25 mM POSTERS Details of measured proteins expressed as (Mean, SD, 95% CI, units): vi- glucose and 0.4 mM palmitate to induce glucolipotoxicity. Glucolipotoxicity Islet Biology/ Insulin Secretion tamin D (60, 28, 16-149, nmol/L); leptin (21, 8.5, 18.7-23.4, ng/ml); resistin caused ER stress as indicated by a rise in CHOP protein levels. This was (0.2, 0.01, 0.19-0.2, ng/ml); adiponectin (59.6, 61.3, 42-76, ng/ml); ASP (19.2, accompanied by an increase in HSE-luciferase promoter activity and the con- 7, 17.3-21, nm/L). sistent up-regulation of both chaperones hsp70 and hsp90. These effects of For author disclosure information, see page A810.
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