BETA CELL FUNCTION ACHIEVED BY HEMI-PANCREATECTOMY WITH THE HYPERGLYCEMIC CLAMP

使用高血糖钳进行半胰腺切除术实现的 β 细胞功能

• 批准号: 7957968
• 负责人: RAUL A BASTARRACHEA
• 金额: $ 1.64万
• 依托单位: TEXAS BIOMEDICAL RESEARCH INSTITUTE
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-06-06 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7957968
• 关键词: Acute; Beta Cell; Cell physiology; Cells; Computer Retrieval of Information on Scientific Projects Database; Data; Female; Funding; Glycosylated hemoglobin A; Grant; Human; Hyperglycemia; Institution; Insulin; Islets of Langerhans; Names; Pancreatectomy; Papio; Primates; Research; Research Personnel; Resources; Source; Stress; United States National Institutes of Health; fasting glucose

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. To examine the effects and adaptive mechanisms (adaptation vs decompensation) of an acute increase in insulin secretory demand (achieved with hemipancreatectomy, HPx ) on the ¿-cell function, in insulin sensitive young female baboons without abnormalities in fasting glucose levels and normal HbA1c. Such increased insulin secretory demand will be created by the hyperglycaemic clamp before and after the HPx. The data obtained will be used as preliminary findings to apply for an RO1 named "Mechanisms of ¿-cell adaptation to stress in baboon and human pancreatic islets" we intend to send to NIH this coming February 1st, 2007.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资助， 因此可以出现在其他 CRISP 条目中 列出的机构是。 对于中心来说，它不一定是研究者的机构。 检查胰岛素分泌需求急剧增加（通过半胰切除术，HPx 实现）对 ¿ 的影响和适应机制（适应与失代偿） - 胰岛素敏感的年轻雌性狒狒的空腹血糖水平和 HbA1c 正常的情况下，胰岛素分泌需求的增加将由 HPx 之前和之后的高血糖钳制产生，所获得的数据将用作申请的初步结果。我们打算在 2007 年 2 月 1 日将一份名为“狒狒和人类胰岛细胞适应压力的机制”的 RO1 发送给 NIH。