C-peptide potentiates the vasoconstrictor effect of neuropeptide Y in insulin-dependent diabetic patients.
C-peptide potentiates the vasoconstrictor effect of neuropeptide Y in insulin-dependent diabetic patients.
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C 肽增强神经肽 Y 对胰岛素依赖型糖尿病患者的血管收缩作用。
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发表时间：
1999
期刊：
影响因子：
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通讯作者：
J. Pernow
中科院分区：
文献类型：
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作者：
B. Johansson;J. Pernow
最近的研究结果表明，胰岛素原C肽改善肾脏和神经功能，以及微循环胰岛素依赖型糖尿病患者可能通过刺激Na-K +-ATP酶活性。此外，对近端大鼠肾小管细胞的体外研究表明，在血管收缩肽神经肽Y存在下，C肽对Na+，K+-ATP酶活性的影响增强。本研究的目的是检查神经肽Y对胰岛素依赖患者静息前臂血流的影响是否在C肽存在下改变。前臂血流量测量体积描记法在8个胰岛素依赖患者和6个健康对照组。在静脉输注C肽（5 pmol kg（-1）min（-1））之前和期间，将神经肽Y（20、200和2000 pmol min（-1））输注到肱动脉中。基础血流量为36.7 +/- 2.2 mL min（-1）L（-1）组织。在输注神经肽Y期间，其以剂量依赖性方式分别降低11 +/- 2、18 +/- 3和25 +/-3%。给予C肽使基础血流量增加25 +/-6%，达到46.3 +/- 3.5 mL min（-1）L（-1）组织（P < 0.01），前臂葡萄糖摄取增加76 +/- 34%（P < 0.05）。在C肽给药期间输注三种剂量的神经肽Y使前臂血流量分别减少14 +/- 4、22 +/- 3和42 +/-4%。在C肽输注前和输注期间，高剂量（2000 pmol min（-1））神经肽Y引起的血流量减少之间存在显著差异（43%，P < 0.001）。当数据计算为血管阻力的变化时，也获得了类似的差异。在健康对照组中，C肽不影响静息前臂血流或对神经肽Y的反应。总之，目前的数据表明，C肽增加静息前臂血流量和增强血管收缩神经肽Y的胰岛素依赖患者的影响。
Recent findings suggest that proinsulin C-peptide improves renal and nerve function as well as microcirculation in patients with insulin-dependent diabetes possibly by stimulating Na-K+-ATPase activity. Furthermore, in vitro studies on proximal rat renal tubule cells show that the effect of C-peptide on Na+, K+-ATPase activity is potentiated in the presence of the vasoconstrictor peptide neuropeptide Y. The aim of the present study was to examine whether the effects of neuropeptide Y on resting forearm blood flow in insulin-dependent patients is altered in the presence of C-peptide. Forearm blood flow was measured by a plethysmographic method in eight insulin-dependent patients and six healthy control subjects. Neuropeptide Y (20, 200 and 2000 pmol min(-1)) was infused into the brachial artery before and during an i.v. infusion of C-peptide (5 pmol kg(-1) min(-1)). Basal blood flow was 36.7 +/- 2.2 mL min(-1) L(-1) tissue. It decreased in a dose dependent manner by 11 +/- 2, 18 +/- 3 and 25 +/- 3%, respectively, during infusion of neuropeptide Y. Administration of C-peptide increased basal blood flow by 25 +/- 6%, to 46.3 +/- 3.5 mL min(-1) L(-1) tissue (P < 0.01) and forearm glucose uptake by 76 +/- 34% (P < 0.05). Infusion of the three doses of neuropeptide Y during administration of C-peptide decreased forearm blood flow by 14 +/- 4, 22 +/- 3 and 42 +/- 4%. There was a significant difference (43%, P < 0.001) between the reduction in blood flow evoked by the high dose (2000 pmol min(-1)) of neuropeptide Y before and during C-peptide infusion. Similar differences were also obtained when data were calculated as changes in vascular resistance. C-peptide did not affect resting forearm blood flow or the response to neuropeptide Y in healthy controls. In conclusion, the present data demonstrate that C-peptide increases resting forearm blood flow and augments the vasoconstrictor effects of neuropeptide Y in insulin-dependent patients.