非酒精性脂肪肝病（NAFLD）和2型糖尿病（T2DM）常常并存，并与彼此的不良结局有关。为了描绘出NAFLD和T2DM患者之间代谢异常的差异，来自同济大学医学院的曲伸教授及其团队进行了一项研究，该研究发现伴有T2DM和NAFLD患者和仅有T2DM患者之间有葡萄糖代谢有差异。
该研究中，患者被分为两组：挑选26例伴有NAFLD的T2DM患者（通过磁共振波谱诊断）和26例性别、年龄和BMI匹配的仅有T2DM的患者。对患者进行75g口服葡萄糖耐量试验，测量他们基线和服用葡萄糖后30min、60min、120min的血清胰岛素和血清C肽水平。
该研究结果表明，伴有T2DM和NAFLD患者和仅有T2DM患者血糖水平相似。与仅有T2DM患者相比，在伴有T2DM和NAFLD患者中观察到更明显的β细胞分泌亢进。与仅有T2DM的患者相比，伴有T2DM和NAFLD患者的早时相和晚时相C肽水平显著增加（△C肽0-30min P＜0.05；AUCC-p/PG30-120min比P＜0.01；C肽30-120min AUC P＜0.01）。OGTT期间，在伴有T2DM和NAFLD患者和仅有T2DM的患者之间，肝源性胰岛素抵抗和额外的肝源性胰岛素抵抗没有统计学差异。在伴有T2DM和NAFLD患者中，肝脏胰岛素敏感性单独导致OGTT的早时相（0-30min），然而，在仅有T2DM患者中，晚时相胰岛素分泌显著缺乏单独导致30-120min的葡萄糖状态。在具有同一水平胰岛素抵抗和高血糖的患者中间，伴有T2DM和NAFLD患者比仅有T2DM患者有更高的血清胰岛素水平。高胰岛素血症主要是由β细胞分泌亢进引起。
该研究论证了在伴有T2DM和NAFLD患者和仅有T2DM患者中不同形式严重胰岛素抵抗的病理生理学差异。
Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) usually coexist and are associated with the adverse outcomes of the other. The aim of our study was to figure out the metabolic abnormalities difference between the two groups of patients.
The patients were divided into two groups: 26 T2DM patients with NAFLD (diagnosed by magnetic resonance spectroscopy) and 26 gender age and BMI matched patients with T2DM only were selected. The patients took a 75-g oral glucose tolerance test which measured their serum insulin and serum C-peptide level at baseline(0 min) and 30min 60min 120min after the glucose were taken.
The patients with T2DM and NAFLD or T2DM only had similar level of blood glucose levels more obvious β-cell hypersecretion was observed in the patients with T2DM and NAFLD compared with those patients with T2DM only. Fasting early phase and late phase C-peptide levels were significantly increased in the patients with T2DM and NAFLD compared to the patients with T2DM only (ΔC-peptide 0-30min P< 0.05 AUCC-p / PG 30-120min ratio P< 0.01 and AUC C-peptide 30-120 min P< 0.01). Hepatic origin and extra hepatic origin insulin resistances during OGTT has no significant difference between T2DM and NAFLD patients and the patients with T2DM only. Hepatic insulin sensitivity independently contributed to the early phase (0-30 min) of the OGTT in patients with T2DM and NAFLD whereas a significant deficit in late insulin secretion independently contributed to 30-120min glucose status in the patients with T2DM only. For the patients who have same level of insulin resistances and hyperglycemia among them patients with T2DM and NAFLD have higher serum insulin level than the patients with T2DM only. Hyperinsulinemia is caused mainly by β-cell hypersecretion. This demonstrates the pathophysiological difference of different forms of severe insulin resistance in the patients with T2DM and NAFLD and patients with T2DM only.
