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Late Breaking Abstracts Late Breaking Abstracts June 2016 | Volume 65 | Suppl. 1A | www.diabetes.org/diabetes Late Breaking Abstracts LB1–LB88 Subject Index LB89–LB91 Abstract Author Index LB92–LB101 Abstract Author Disclosure Information LB102–LB117 scientificsessions.diabetes.org COMLatePLI catBREAIOKINGNS—Hy ABSTRACTSPOGLYCEMIA COMplIcatIONS—HYpoGLYceMIA 3-LB Hypothalamic Glucose Transport Kinetics in Experimentally Induced Hypoglycemia-associated Autonomic Failure (HAAF) in Humans 1-LB AMIR MOHEET, ELIZABETH R. SEAQUIST, PIERRE-GILLES HENRY, JAMES JOERS, The Role of NPY in Adrenal Function during Recurrent Hypogly- ANJALI KUMAR, DINESH DEELCHAND, MELISSA TERPSTRA, KRISTINE KUBISIAK, cemia LYNN EBERLY, GULIN OZ, Minneapolis, MN YUNBING MA, QIAN WANG, MATTHEW D. WHIM, New Orleans, LA The hypothalamus is thought to play a critical role in glucose sensing and The counter regulatory response (CRR) is a hormonal and neuroendo- regulating counterregulatory hormone response to hypoglycemia (HG). The crine mechanism essential in restoring blood glucose levels following POSTERS mechanisms responsible for the development of HAAF remain uncertain, Complications hypoglycemia. In type 1 diabetes, the CRR is often impaired and restora- but some suggest that increased glucose transport may contribute. Here we Acute and Chronic tion of euglycemia is critically dependent on epinephrine release from the tested the hypothesis that hypothalamic glucose transport will be upregu- adrenal glands. Following recurrent episodes of hypoglycemia, common lated in healthy volunteers preconditioned with recurrent HG to induce HAAF in the diabetic state, the ability to evoke epinephrine release becomes compared to preconditioning with euglycemia (EU). progressively worse. The reasons are not clear but could involve central In these experiments we employed a standard experimental model of HAAF or peripheral mechanisms (e.g., an adrenal impairment of epinephrine syn- in humans. For preconditioning, subjects underwent 2 hyperinsulinemic EU or thesis or release). HG clamp studies on day 1 and a 3rd on day 2. Hypothalamic glucose transport To examine this issue we quantified the adrenal expression of tyrosine kinetics were assessed on day 2 after the 3rd preconditioning clamp by measur- hydroxylase (TH; the rate limiting enzyme for catecholamine synthesis) in ing hypothalamic glucose concentrations using ¹H MRS at 3 tesla over a ~1 hour (i) control mice; (ii) mice exposed once to insulin-induced hypoglycemia period during which blood glucose was experimentally increased from 95 mg/dl (IIH, blood glucose < 60 mg/dL) and (iii) mice subjected to three episodes to one of 3 target hyperglycemic levels (200, 300 or 400 mg/dl). ¹H MR spectra of IIH. We first confirmed that the hypoglycemia-induced rise in urine epi- were collected from a 10 x 12 x 13 mm³ hypothalamic voxel. Metabolites were nephrine levels was blunted after recurrent IIH. Quantification of adrenal quantified using LCModel. Mathematical modeling was used to calculate maxi- TH-ir showed that single IIH resulted in an increase in TH expression, while mum transport rate/cerebral metabolic rate of glucose (Tmax/CMRglc). this effect was blunted after recurrent IIH. In contrast, the adrenal levels 11 subjects (9M/2F, age 30±8 yrs) completed the EU pre-conditioning studies, of neuropeptide Y (NPY), an adrenal co-transmitter that inhibits TH expres- of whom 7 subjects (6M/1F, age 27±3 yrs) also completed the HG pre-condition- sion via Y1 receptors (Wang et al, 2013), were increased after single and ing studies and had successful induction of HAAF. There was no significant dif- recurrent IIH. The levels of TH were quantified in NPY knockout mice and ference in Tmax/CMRglc in subjects exposed to recurrent HG with HAAF (1.749 were now elevated after both single and recurrent IIH. The removal of NPY ± 0.143) compared to control subjects exposed to EU (1.619 ± 0.098; p=0.45). also rescued the typical attenuation in epinephrine release after recurrent In conclusion, in healthy subjects exposure to recurrent HG with induction IIH. Electrophysiological and optogenetic studies revealed no differences of HAAF did not result in upregulation of hypothalamic glucose transport. in chromaffin cell secretory capacity in wild type mice after IIH challenges. Supported By: National Institutes of Health (2R01NS35192); National Center for No impairment was observed for hepatic glucose production after recur- Advancing Translational Sciences (UL1TR000114) rent IIH, indicating the CRR downstream of the adrenal was intact. These results suggest recurrent hypoglycemia-induced CRR failure involves a peripheral defect in adrenal signaling that is due to an activity- and neuro- 4-LB peptide Y-dependent inhibition of TH synthesis. Seven-Year Outcome Data from a Computer-guided Inpatient Glu- Supported By: National Institutes of Health (DK080441, DK098134) cose Management System ROBERT J. TANENBERG, SANDRA HARDEE, CAITLIN ROTHERMEL, Greenville, NC, Vashon, WA 2-LB Inpatient hyperglycemia (HG) and hypoglycemia (HO) independently predict Fasting-induced Activation of Sympathetic Plasticity Limits morbidity and mortality. Blood glucose (BG) management via protocol-driven Hypoglycemia insulin (I) administration improves patient outcomes. Algorithmically based MANQI WANG, MATTHEW D. WHIM, New Orleans, LA computerized systems optimize the timing of BG checks and I dosing. A rise in epinephrine secretion from adrenal chromaffin cells is a key A retrospective observational study (1/2009-12/2015) evaluated the impact event in the sympathetic nervous system response to fasting and contrib- of EndoTool® (ET) computer-guided BG management system in intensive care utes to the counter-regulatory response (CRR) that opposes hypoglycemia. units at a 900-bed tertiary care teaching hospital. Patients assigned to ET How this sympathetic response is regulated during fasting is not clear. To had an indication for IV I infusion, including uncontrolled diabetes, stress HG, address this question we studied sympatho-adrenal activity in mice that and/or post-operative BG levels >140 mg/dL. We evaluated time to achieve were fed ad lib or fasted for 1 day. Fasting increased urine epinephrine but BG control in patients with HG and HO incidence. did not alter the blood glucose level, indicating that the CRR could main- Data were available for all treated patients; over 7 years, 492,078 readings tain euglycemia during fasting. Neuropeptide Y (NPY) which is co-released were obtained from 16,850 patients. ET brought HG patients’ BG to 180 mg/ with the catecholamines from neuroendocrine chromaffin cells appears to ≤ dL within 1.5-2.3 h. Minimal HO was observed, with only 0.93% of values regulate this sympatho-adrenal response because fasting did not increase <70 mg/dL and 0.03% <40mg/dL. HO showed year-on-year decreases (Figure); urine epinephrine levels in NPY knockout (NPY k/o) mice and the mice were ANOVA analysis of the percentage of BG values <70 mg/dL found a significant hypoglycemic. I.p. injection of epinephrine in fasted NPY k/o mice restored reduction in frequency, from 1.04% in 2009 to 0.05% in 2015 (P<0.0001). This euglycemia. To determine how the loss of NPY prevented epinephrine study confirms that computerized IV I administration improves inpatient BG release we assessed transmission at the preganglionic chromaffin cell → control while minimizing HO. synapse. Using acute adrenal slices, synaptic transmission was quantified by measuring evoked excitatory postsynaptic currents (EPSCs) in chromaf- Figure. Percentage of Patient Glucose Values <70 mg/dL with EndoTool: 2009 fin cells. Fasting increased the amplitude of the evoked EPSC monitored to 2015. in chromaffin cells from wild type (wt) mice. In contrast, the amplitude of the evoked EPSC was decreased in the fasted NPY k/o animals compared to fed littermates. Fasting also led to a decrease in the paired-pulse ratio (PPR) in wt animals, but to an increase in NPY k/o mice, suggesting the involvement of a presynaptic component. Furthermore, pharmacological inhibition of Y5 receptors blocked the fasting-induced increase in synaptic plasticity and epinephrine release in wt mice, resulting in hypoglycemia. We conclude that an NPY-dependent modulation of the preganglionic → chromaffin cell synapse promotes the release of epinephrine that is required to maintain euglycemia during fasting. Supported By: National Institutes of Health (DK080441, DK098134) ADA-Supported Research For author disclosure information, see page LB102. LB1 COMPLIcatIONS—MACROVASCULAR—ATHEROSCLEROTIC CARDIOVASCULAR DISEASE AND HUMAN DIABETES COMplIcatIONS—MacroVascUlar— cant reduction in the risk of AMI (HR 0.80, 95% CI 0.65-0.99, P=0.04), CVA (HR AtherosclerotIC CardIOVascUlar DIsease AND 0.82, 95% CI 0.74-0.91, P=0.0001), overall mortality (HR 0.48, 95% CI 0.41-0.57, HUMAN DIabetes P<0.0001, and the composite outcome (HR 0.82, 95% CI 0.74-0.91, P=0.0002). In this analysis from a large U.S. integrated health system, GLP-1RA exposure was found to be associated with a reduction in the risk of cardiovascular events 5-LB observed and overall mortality among patients with T2D, after adjusting for POSTERS Advanced Glycation End Products, Oxidation Products, and Devel- potential confounders. These results support the use of GLP-1RAs in the man- Complications opment of Atherosclerosis in the Veterans Affairs Diabetes Trial Acute and Chronic agement of T2D. Conclusions regarding overall safety should be balanced by (VADT) results from prospectively designed cardiovascular
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