Matsuo Takashi, Ushiroda Yoshihiko
Internal Medicine, Nobeoka city Medical Association Hospital, Nobeoka, Japan
Endocrinol Diabetes Metab Case Rep. 2015 Jul 28;2016:15-0121. doi: 10.1530/EDM-15-0121.
A 32-year-old woman presented with 3days of epigastric pain and was admitted to our hospital (day 3 of disease). We diagnosed acute pancreatitis based on epigastric abdominal pain, hyperamylasemia, and an inflammatory reaction of withdrawn blood, pancreatic enlargement, and so on. Her condition improved with treatment; however, on day 8, she had decreased level of consciousness. Laboratory results led to a diagnosis of fulminant type 1 diabetes mellitus (FT1DM) with concomitant diabetic ketoacidosis. Insulin therapy improved her blood glucose levels as well as her symptoms. Fatty liver with liver dysfunction was observed on day 14, which improved by day 24. Blood levels of free fatty acids (FFAs) increased rapidly from 440μEq/L (normal range: 140–850μEq/L) on day 4 to 2097μEq/L on days 7–8 (onset of FT1DM) and subsequently decreased to 246μEq/L at the onset of fatty liver. The rapid decrease in insulin at the onset of FT1DM likely freed fatty acids derived from triglycerides in peripheral adipocytes into the bloodstream. Insulin therapy rapidly transferred FFAs from the periphery to the liver. In addition, insulin promotes the de novo synthesis of triglycerides in the liver, using newly acquired FFAs as substrates. At the same time, inhibitory effects of insulin on VLDL secretion outside of the liver promote the accumulation of triglycerides in the liver, leading to fatty liver. We describe the process by which liver dysfunction and severe fatty liver occurs after the onset of FT1DM, from the perspective of disturbed fatty acid metabolism.
FT1DM is rare but should be considered in patients with pancreatitis and a decreased level of consciousness. Fatty liver should be considered in patients with FT1DM when liver dysfunction is observed. Insulin is involved in mechanisms that promote fatty liver formation. Pathophysiological changes in fatty acid metabolism may provide clues on lipid metabolism in the early phases of FT1DM.
一名32岁女性因上腹部疼痛3天入院（病程第3天）。根据上腹部疼痛、高淀粉酶血症以及抽血炎症反应、胰腺肿大等情况，我们诊断为急性胰腺炎。经治疗病情好转；然而，在第8天，她出现意识水平下降。实验室检查结果诊断为暴发性1型糖尿病（FT1DM）伴糖尿病酮症酸中毒。胰岛素治疗改善了她的血糖水平及症状。在第14天观察到脂肪肝伴肝功能障碍，到第24天有所改善。游离脂肪酸（FFA）血水平从第4天的440μEq/L（正常范围：140 - 850μEq/L）迅速升高至第7 - 8天（FT1DM发病时）的2097μEq/L，随后在脂肪肝发病时降至246μEq/L。FT1DM发病时胰岛素迅速减少，可能使外周脂肪细胞中甘油三酯衍生的脂肪酸释放到血液中。胰岛素治疗使FFA迅速从外周转移至肝脏。此外，胰岛素以新获取的FFA为底物促进肝脏中甘油三酯的从头合成。同时，胰岛素对肝脏外极低密度脂蛋白（VLDL）分泌的抑制作用促进肝脏中甘油三酯的蓄积，导致脂肪肝。我们从脂肪酸代谢紊乱的角度描述了FT1DM发病后肝功能障碍和严重脂肪肝的发生过程。
FT1DM罕见，但胰腺炎且意识水平下降的患者应考虑此病。FT1DM患者出现肝功能障碍时应考虑脂肪肝。胰岛素参与促进脂肪肝形成的机制。脂肪酸代谢的病理生理变化可能为FT1DM早期脂质代谢提供线索。
