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Integrated Physiology—Insulin Secretion in Vivo

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Integrated Physiology—Insulin Secretion in Vivo INTEGRATED PHYSIOLOGY—INSULINCATEGORY SECRETION IN VIVO the elevated blood glucose and oral glucose challenge induced hyperglycemia in HFD+STZ rats. Interestingly, GLP-1 analogue but not sitagliptin signifi cantly reduced the body weight/fat mass and fasted plasma insulin. The major mechanism of action for GLP-1 analogue and DPPIV inhibitor in treatment of diabetes is to improve the pancreatic β-cell function and promotion of β-cell regeneration. Consistent to the observations in humans, the present study demonstrated the effi cacy differences on effect of pancreatic β-cell function and mass with GLP-1 analogue and DPPIV inhibitor. These results showed that we have established a sensitive model for the evaluation of novel drugs on pancreatic β-cell function and mass. 2847-PO Ketosis-Onset Type 2 Diabetes Had Better Islet β-Cell Function and More Serious Insulin Resistance LINGLING ZOU, HONGYUN LU, YINGJUAN ZENG, SHUNKUI LUO, YING SUN, HONG LIU, LIAO SUN, Guangzhou, China This case control study was aimed to investigate the clinical characteristics INTEGRATED PHYSIOLOGY—INSULIN SECRETION and β-cell function of ketosis-onset type 2 diabetes, and provide evidence for IN VIVO treatment selection. 122 cases of newly diagnosed type 2 diabetic patients were divided into two groups based on the presence of urine acetone bodies 2845-PO (51cases) or not (71cases). We collected their clinical and C-peptide (CP) data, WITHDRAWN calculated the area under the curve(AUC)during CP release test. Insulin resis- tance index (HOMA-IR) and β-cell function index (HOMA-β) were used to estimate insulin sensitivity and β-cell function.We found that compared with non-ketosis group, Fasting CP, 0.5hCP, 3hCP, AUC of ketosis group were sig- nifi cantly higher (P<0.05) [Fig.1].Insulin resistance in ketosis group was more obvious (HOMA-IR, ketosis vs. non-ketosis group: 3.04±0.19 vs. 2.58±0.10, P<0.05) and β-cell function injury was less slight than non-ketosis group (HOMA-β, ketosis vs. non-ketosis group: 35.89±4.62 vs. 25.16±2.71, P<0.05). Plasma triglyceride level in ketosis group was signifi cantly higher than non- ketosis group (2.34±0.23mmol/L vs.1.86±0.11mmol/L, P<0.05), and the percent- age complicated with fatty liver was also higher (ketosis vs. non-ketosis group 54.90% vs. 36.62%, P<0.01). In conclusion, compared with non-ketosis onset type 2 diabetic patients, ketosis-onset patients had better islet β-cell function and more serious insulin resistance which may be caused by liptoxicity. 2846-PO 2848-PO A Rat Model for Later Phase Diabetes—Effi cacy Assessments of WITHDRAWN DPPIV Inhibitor and GLP-1 Analogue HONG LI, ZHAOHONG WANG, WENLING YIN, JISONG CUI, Beijing, China The present study was aimed to establish a rat model that refl ects the later phase T2DM in humans, especially in patients with decreased pancreatic β-cell function and mass. Effects of a GLP-1 analogue and sitagliptin on the improvement of impaired β-cell function/mass and other diabetic parameters Obesity were assessed in this model. SD rats were divided into 4 groups: (1) healthy control (HC) fed by chow; (2) rats fed by high fat diet (HFD) followed a single PUBLISHED ONLY dose of Streptozotocin (STZ), designated as HFD+STZ then treated with Integrated Physiology/ vehicle; (3) HFD+STZ treated with GLP-1 analogue 1mg/kg; or (4) with sita- gliptin 450 mg/kg once daily for 14 days. Pancreatic β-cell function and mass were evaluated by hyperglycemia clamp and insulin/Ki67 immunohistochem- ical staining. OGTT, body weight & composition, food & water intake, blood glucose and plasma insulin levels were measured. By 2-steps hyperglycemia clamp, the maximal insulin secretion (ng/ml) in HC rats (group 1) was 3.5±0.9, which was decreased to 0.9±0.3 in group 2 rats. The impaired insulin secretion was recovered to 3.5±0.7 in the rats given GLP-1 analogue (group 3) and 2.2±0.1 in the rats given sitagliptin (group 4), respectively. Histology fi ndings confi rmed the functional evaluation. Additionally, both medicines signifi cantly decreased ADA-Funded Research For author disclosure information, see page 829. A723 INTEGRATEDCATEGORY PHYSIOLOGY—LIVER 2851-PO Research on Insulin Resistance and the Function of Islet α,β-Cells in Elderly Patients With Type 2 Diabetes Mellitus and the Reaction of DDP-IV Inhibitors Before and After Treatment REN MIN, CHEN SHU, ZHANG MIN, WANG JUNKANG, Chengdu, China Methods: Fasting plasma glucose( FPG) ,fasting serum insulin( FNS) , C- peptide and glucagon were measured in 30 elderly patients 2 DM (Group A) respectively. Homeostasis model assessment- insulin resistance index (HOMA- IR) and insulin sensitivity index ( ISI) were applied to assess the status of insulin resistance, HOM A-βwas used to assess the basic function of islet βcells. Glucagon was used to assess the basic function of islet αcells. These values were compared with 30 healthy seniors (Group B),30 IGT 2849-PO (Impaired Glucose Tolerance) seniors (Group C),30 newly diagnosed patients A Cross-Discipline Survey Study: After the Wen Chuan Mega-Quake (Group D). Then give the treatment of DPP-IV inhibitors (sitagliptin 100mg qd) 3 Years the Infl uence of the Local Residents’ Stress on Pancreatic to patients in Group A for 3 months, observe the reaction of DPP-IV inhibitors Cell Function before and after treatment, include serum insulin,glucagon and C-peptide WANG JUN KANG, CHEN SHU, ZHANG XUE JUN, Chengdu, China levels. Results: The level of C-peptide and ISI and HOMA-βin Group A were Objective: To observe the infl uence of stress to mega-quakes on pancreatic lower than in other groups. But the level of glucagon was higher than in other cell function of the people in the 5.12 earthquake area after 3 years. Methods: groups. There were very signifi cant differences between T2DM group and The G1 group (1000) people lived in the Wenchuan area for over 3 years after other groups ( P< 0. 05) . In patients treated with DPP-IV inhibitors showed the earthquake. G2 group (1000) people lived in the temporary board rooms that the level of serum glucagon ascent and the level of C-peptide and ISI and in the Wen chuan area for over six months after the earthquake. G3 group HOMA-βdescent. Conclusion: Elderly patients 2DM have obvious insulin (800) was the residents of Chengdu city. Understanding stress condition by resistance and islet cells dysfunction and high-level glucagon. Hyperisuline- self-made meter.Fasting blood glucose (FPG), Fasting insulin (FIns), proinsulin, mia with low C- peptide level may exist in elderly patients with type 2 diabe- C-peptide, glucagon and glucocorticoid were measured. The insulin resistance tes mellitus. This study suggests that insulin resistance and islet cells dysfunc- was evaluated by HOMA-IR. The β-cell function was assessed by HOMA-β. tion may play a key role in glycometabolism disorder in elderly patient with Results: In the G1 group, 81 examples were diagnosed with diabetes mel- type 2 diabetes mellitus. DPP-IV inhibitors may play an important part in the litus, the morbidity is 10.12%; In the G2 group, 104 examples were diagnosed treatment of elderly patients 2DM. with diabetes mellitus, the morbidity is 10.40%. In the G3 group, 102 examples were diagnosed with diabetes mellitus, the morbidity is 10.20%. G2 group were higher than the prevalence rates of G3 group, (P<0.05). Risk factor INTEGRATED PHYSIOLOGY—LIVER analysis in the G3 Group found that obesity (OR 1.24) glucagon (OR2.13), glu- cocorticoid (OR 1.67), stress (OR1.32) were risk factors for insulin resistance 2852-PO (P<0.05). Age, (OR1.24) obesity (OR2.13), glucocorticoid (OR1.67), stress Multiple Nuclear Receptors Regulate Hepatic Gck Expression (OR1.32) were the islet secretion functions to reduce risk factors (P<0.05). through the Retinoic Acid Responsive Element in its Promoter Conclusions: The earthquake stress causes the island of Alpha cell secretion RUI LI, YANG LI, RUI ZHANG, GUOXUN CHEN, Knoxville, TN dysfunction, the Beta cell secretion decrease, the insulin resistance increases. The hepatic glucokinase (gene, Gck) plays a critical role in glucose homeo- Relieve stress and intervention may prevent diabetes and development. stasis. We have reported that retinoids synergize with insulin to induce Gck expression in primary rat hepatocytes. Here, we determine the retinoic acid 2850-PO responsive element (RARE) in the hepatic Gck promoter, and the transcription Restoration of the First-Phase Insulin Secretion and a Decline in Fat factors binding to it. A series of Gck promoter reporter gene constructs were Mass are Predictors for Achieving Long-Term Glycemic Control after made. Their responses to retinoic acid (RA) were analyzed using dual luciferase Early Intensive Insulin Therapy in Patients With Newly Diagnosed assay. Electrophoretic mobility shift (EMSA) and super-shift assays were used Type 2 Diabetes to analyze the protein binding activities in rat liver nuclear extract (NE). The JANG WON SON, HEE SUN KWON, SEONG SU LEE, SUNG RAE KIM, SOON JIB effects of these nuclear receptors on Gck expression were determined using YOO, Bucheon, Republic of Korea recombinant adenovirus-mediated over-expression in the absence or presence Recently, early intensive insulin therapy (IIT) was reported to improve β-cell of RA and insulin. We observed that RA and RA + insulin, not insulin, activated function and induce long-term remission in patients with newly diagnosed the reporter gene constructs containing 1 to 0.2 kb of the Gck promoter frag- type 2 diabetes. However, the possible mechanisms responsible for this ments in primary hepatocytes.
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