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首页> 外文期刊>American Journal of Medicine and Medical Sciences >What Induces Diabetic Ketoacidosis or Lactic Acidosis in Diabetic Alcoholic Patients Complicated with Chronic Calcific Pancreatitis?
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What Induces Diabetic Ketoacidosis or Lactic Acidosis in Diabetic Alcoholic Patients Complicated with Chronic Calcific Pancreatitis?

机译：是什么导致糖尿病性酒精中毒并发慢性钙化性胰腺炎的糖尿病酮症酸中毒或乳酸酸中毒？

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Diabetic ketoacidosis (DKA) and lactic acidosis (LA) are severe metabolic acidosis which develop in diabetic alcoholic patients. The insulin deficiency and elevation of glucagon leads to increased hepatic glucose output, and induces the release of free fatty acids (FFA) from adipose tissue, which are associated with the development of DKA. The insulin deficiency also plays a critical role in LA because pyruvate dehydrogenase complex (PDHc) requires insulin for activation, and increased FFA decreases PDH activity. Chronic calcific pancreatitis (CCP)-induced diabetes has been reported to be not prone to develop DKA because CCP leads to depletion of both insulin ( -cells) and glucagon-producing cells ( -cells) in pancreas. Further, to our knowledge, the development of LA in patients with CCP-induced diabetes has not ever been reported. We experienced alcoholic DKA and LA patients complicated with CCP-induced diabetes. The insulin deficiency is the critical factor for the development of both DKA and LA. FFA release from adipose tissue may be an important factor to determine the development of DKA. The absence of DKA in patient with LA may be due to extremely small volume of visceral adipose tissue. Although FFA is associated with the development of LA, a decreased activity of PDHc by insulin deficiency may be the most critical factor for the development of LA. Less insulin may be required to treat or prevent LA compared with DKA.
机译：糖尿病性酮症酸中毒（DKA）和乳酸性酸中毒（LA）是在糖尿病性酒精中毒患者中发生的严重代谢性酸中毒。胰岛素缺乏和胰高血糖素升高导致肝脏葡萄糖输出增加，并诱导脂肪组织中游离脂肪酸（FFA）的释放，这与DKA的发展有关。胰岛素缺乏症在LA中也起着关键作用，因为丙酮酸脱氢酶复合物（PDHc）需要胰岛素来激活，而增加的FFA会降低PDH活性。慢性钙化性胰腺炎（CCP）诱导的糖尿病据报道不易发展为DKA，因为CCP会导致胰腺中的胰岛素（-细胞）和胰高血糖素产生细胞（-细胞）消耗。此外，据我们所知，从未报道过在CCP诱发的糖尿病患者中LA的发展。我们经历了酒精性DKA和LA患者并发CCP诱发的糖尿病。胰岛素缺乏是DKA和LA发展的关键因素。从脂肪组织释放的FFA可能是决定DKA发生的重要因素。 LA患者缺乏DKA可能是由于内脏脂肪组织的体积非常小。尽管FFA与LA的发展有关，但胰岛素缺乏导致PDHc活性降低可能是LA发展的最关键因素。与DKA相比，治疗或预防LA所需的胰岛素更少。

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