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首页> 外文期刊>American Journal of Physiology >Portal vein hypoglycemia is essential for full induction of hypoglycemia-associated autonomic failure with slow-onset hypoglycemia.
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Portal vein hypoglycemia is essential for full induction of hypoglycemia-associated autonomic failure with slow-onset hypoglycemia.

机译：门静脉低血糖对于充分诱发与慢发作低血糖相关的与低血糖相关的自主神经衰竭至关重要。

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Antecedent hypoglycemia leads to impaired counterregulation and hypoglycemic unawareness. To ascertain whether antecedent portal vein hypoglycemia impairs portal vein glucose sensing, thereby inducing counterregulatory failure, we compared the effects of antecedent hypoglycemia, with and without normalization of portal vein glycemia, upon the counterregulatory response to subsequent hypoglycemia. Male Wistar rats were chronically cannulated in the carotid artery (sampling), jugular vein (glucose and insulin infusion), and mesenteric vein (glucose infusion). On day 1, the following three distinct antecedent protocols were employed: 1) HYPO-HYPO: systemic hypoglycemia (2.52 +/- 0.11 mM); 2) HYPO-EUG: systemic hypoglycemia (2.70 +/- 0.03 mM) with normalization of portal vein glycemia (portal vein glucose = 5.86 +/- 0.10 mM); and 3) EUG-EUG: systemic euglycemia (6.33 +/- 0.31 mM). On day 2, all groups underwent a hyperinsulinemic-hypoglycemic clamp in which the fall in glycemia was controlled so as to reach the nadir (2.34 +/- 0.04 mM) by minute 75. Counterregulatory hormone responses were measured at basal (-30 and 0) and during hypoglycemia (60-105 min). Compared with EUG-EUG, antecedent hypoglycemia (HYPO-HYPO) significantly blunted the peak epinephrine (10.44 +/- 1.35 vs. 15.75 +/- 1.33 nM: P = 0.01) and glucagon (341 +/- 16 vs. 597 +/- 82 pg/ml: P = 0.03) responses to next-day hypoglycemia. Normalization of portal glycemia during systemic hypoglycemia on day 1 (HYPO-EUG) prevented blunting of the peak epinephrine (15.59 +/- 1.43 vs. 15.75 +/- 1.33 nM: P = 0.94) and glucagon (523 +/- 169 vs. 597 +/- 82 pg/ml: P = 0.66) responses to day 2 hypoglycemia. Consistent with hormonal responses, the glucose infusion rate during day 2 hypoglycemia was substantially elevated in HYPO-HYPO (74 +/- 12 vs. 49 +/- 4 micromol x kg(-1) x min(-1); P = 0.03) but not HYPO-EUG (39 +/- 7 vs. 49 +/- 4 micromol x kg(-1) x min(-1): P = 0.36). Antecedent hypoglycemia local to the portal vein is required for the full induction ofhypoglycemia-associated counterregulatory failure with slow-onset hypoglycemia.
机译：先前的低血糖症会导致调节异常和低血糖意识不足。为了确定前门静脉血糖过低是否会削弱门静脉葡萄糖的感应，从而诱发反调节失败，我们比较了在没有门静脉血糖正常化的情况下，在对随后的低血糖的反调节反应中，前低血糖的影响。雄性Wistar大鼠在颈动脉（采样），颈静脉（葡萄糖和胰岛素输注）和肠系膜静脉（葡萄糖输注）中进行慢性插管。在第1天，采用以下三种不同的先行方案：1）HYPO-HYPO：全身性低血糖（2.52 +/- 0.11 mM）; 2）HYPO-EUG：全身性低血糖（2.70 +/- 0.03 mM），门静脉血糖正常化（门静脉葡萄糖= 5.86 +/- 0.10 mM）; 3）EUG-EUG：全身性正常血糖（6.33 +/- 0.31 mM）。在第2天，所有组均进行高胰岛素-低血糖钳夹，其中血糖的下降受到控制，以至第75分钟达到最低点（2.34 +/- 0.04 mM）。在基础（-30和0时）处测量逆调节激素反应。 ）和低血糖期间（60-105分钟）。与EUG-EUG相比，先前的低血糖（HYPO-HYPO）使肾上腺素峰值（10.44 +/- 1.35 vs. 15.75 +/- 1.33 nM：P = 0.01）和胰高血糖素（341 +/- 16 vs. 597 + /）显着减弱。 -82 pg / ml：对第二天的低血糖反应。第1天（HYPO-EUG）全身性低血糖期间门静脉血糖的正常化可防止肾上腺素峰值（15.59 +/- 1.43 vs. 15.75 +/- 1.33 nM：P = 0.94）和胰高血糖素（523 +/- 169 vs. 597 +/- 82 pg / ml：P = 0.66）对第2天低血糖的反应。与荷尔蒙反应一致，HYPO-HYPO在第2天低血糖期间的葡萄糖输注速率显着升高（74 +/- 12 vs. 49 +/- 4 micromol x kg（-1）x min（-1）; P = 0.03 ）而不是HYPO-EUG（39 +/- 7 vs. 49 +/- 4 micromol x kg（-1）x min（-1）：P = 0.36）。要充分诱发与慢发作性低血糖相关的低血糖相关的反调节失败，需要门静脉局部的前期低血糖。

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