2011 ADA Posters 1261-2041.indd - Diabetes

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(t=5, t=10, t=15, t=30, t=60) and following cessation of stimulation (t=90 and t=120 minutes) to determine blood glucose and plasma insulin levels. To exclude that the effects on glucose metabolism were stress-induced we also measured plasma corticosterone levels. In the 200 μA stimulated animals, plasma insulin levels signifi cantly increased to 122% of base-line at onset of stimulation (t=5) compared to sham stimulated animals whereas blood glucose values showed a slight (4%) increase during the fi rst 15 min of stimulation. In contrast, stimulation at lower intensity (100 μA) did not affect either measure. Plasma corticosterone levels were not signifi cantly changed as compared to the sham and 100 μA conditions and thus can not explain changes in insulin secretion or the slight glucose rise. These data suggest a role for the NAc in the regulation of glucose metabolism and we hypothesize that the NAc controls the pancreas and thereby insulin secretion via the central nervous system. Supported by: ZonMW & 1633-P Synergism of Dopamine Agonist Plus GLP-1 Analog Therapy on Improvement of Glucose Intolerance in Syrian Hamsters MICHAEL EZROKHI, SHUQIN LUO, YELENA TRUBITSYNA, ANTHONY H. CIN- COTTA, Tiverton, RI Previous studies have demonstrated that timed daily treatment of bromocriptine, a dopamine D2 receptor agonist, to insulin resistant animals and humans improves postprandial insulin sensitivity. Such treatment reduces post-meal or post-glucose challenge levels of glucose while simultaneously markedly reducing hyperinsulinemia. GLP-1 analogs such as exendin-4, are known to enhance glucose – mediated insulin secretion and reduce glucagon secretion. Therefore, the possibility exists of a positive interaction between such a postprandial insulin sensitizing mechanism with such an enhanced postprandial insulin secretory response to improve glucose intolerance. To test such a postulate, glucose intolerant insulin resistant Syrian hamsters weighing 200 grams were treated with either vehicle (N=20) or bromocriptine (4 mg/kg; N=20) for 2 weeks and then each group was further subdivided into 2 groups and treated with either vehicle or exendin-4 (4 µg/ kg) just prior to being subjected to a glucose tolerance test (GTT) (3g/kg). Relative to the vehicle/vehicle (control), bromocriptine markedly reduced the insulin area under the curve (AUC) by 39% (from 1311 ± 177 to 796 ± 119 ng*min/ml) (P=0.03) while reducing the glucose AUC by 21% (from 42576 ± 3889 to 33752 ± 2763 mg*min/dl) (P
Integrated Physiology/ Obesity POSTERS 1637-P Delayed Insulin Secretory Responses Are Seen in Patients with Long Duration of Type 1 <strong>Diabetes</strong> and Residual Insulin* JENNIFER SHERR, LINDA RINK, KEVAN HEROLD, New Haven, CT Calculation of insulin secretory rates (ISR) can provide quantitative and qualitative information of insulin secretion during a mixed meal test (MMT). We previously reported that some patients with type 1 diabetes (T1D) have a delayed secretory response during a MMT compared to non-diabetic controls and that their decline in insulin secretion was less than patients with T1D who showed an early secretion profi le (i.e. @< 45min). To determine if there is a relationship between disease duration and ISRs, data derived from MMT were analyzed in 1) 20 subjects with T1D diagnosed < 1 year 2) 12 subjects with T1D 2-5 years duration, 3) 21 subjects with T1D >5 years, 4) 38 non-diabetic controls. All subjects with T1D 5 years subjects had undetectable c-peptide levels and were excluded from further analysis. Chronobiological Series Analyzer (CSA) software was used to calculate ISR by deconvolution of C-peptide using a two-compartment model for hormone clearance. Parameters used accounted for the subject’s age, sex, height, and diabetes status. Total ISR area under the curve (AUC) and time of peak insulin secretion was calculated for each subject. There was a decline in total insulin secretion with duration of T1D (p
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2011 ADA Posters 1261-2041.indd - Diabetes

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