Nimitphong Hataikarn, Phongkitkarun Sith, Rattarasarn Chatchalit, Kongsooksai Atthana, Chanprasertyothin Suwannee, Bunnag Pong-Amorn, Puavilai Gobchai
Division of Endocrinology & Metabolism, Department of Medicine, Mahidol University, Bangkok, Thailand.
Metabolism. 2008 May;57(5):644-9. doi: 10.1016/j.metabol.2007.12.008.
Postprandial hypertriglyceridemia is common in type 2 diabetes mellitus (T2D). Significant numbers of T2D patients who have normal fasting triglyceride (TG) have postprandial hypertriglyceridemia. The role of regional adipose tissue and adiponectin on postprandial TG responses in this group of T2D patients is unclear. This study aimed to examine the contribution of regional adipose tissue and adiponectin to the variation of postprandial TG responses in T2D patients who have normal fasting TG levels. Thirty-one Thai T2D patients who had fasting TG<1.7 mmol/L were studied. All were treated with diet control or sulphonylurea and/or metformin. None was treated with lipid-lowering agents. Mixed-meal test was performed after overnight fast. Plasma glucose, insulin, and TG were measured before and 1, 2, 3, and 4 hours after the test. Adiponectin was measured in fasting state. Visceral as well as superficial and deep subcutaneous abdominal adipose tissues were determined by magnetic resonance imaging, and hepatic fat content (HFC) was determined by magnetic resonance spectroscopy. Univariate and multivariate regression analyses of postprandial TG and regional adipose tissue and metabolic parameters were performed. The TG levels before and 1, 2, 3, and 4 hours after the mixed meal were 1.32+/-0.40 (SD), 1.40+/-0.41, 1.59+/-0.40, 1.77+/-0.57, and 1.80+/-0.66 mmol/L, respectively (P<.0001). The area under the curve (AUC) of postprandial TG was positively and significantly correlated with fasting TG (r=0.84, P<.0001) and log.HFC (r=0.456, P=.033) and was inclined to be correlated with log.deep subcutaneous adipose tissue (r=0.38, P=.05) and sex (r=0.326, P=.073). The AUC of postprandial TG was not correlated with age, body mass index, waist circumference, log.superficial subcutaneous adipose tissue, log.visceral adipose tissue, hemoglobin A1c, fasting glucose, AUC.glucose, log.fasting insulin, log.AUC.insulin, log.homeostasis model assessment%B, log.homeostasis model assessment of insulin resistance, and adiponectin. Only fasting TG (beta=.815, P<.0001) and log.HFC (beta=.249, P=.035) predicted AUC of postprandial TG in regression model (adjusted R2=0.84, P<.0001). In conclusion, in T2D patients with normal fasting TG, the increase of postprandial TG levels is directly determined by fasting TG level and the amount of hepatic fat.
餐后高甘油三酯血症在2型糖尿病（T2D）中很常见。大量空腹甘油三酯（TG）正常的T2D患者存在餐后高甘油三酯血症。在这组T2D患者中，局部脂肪组织和脂联素对餐后TG反应的作用尚不清楚。本研究旨在探讨局部脂肪组织和脂联素对空腹TG水平正常的T2D患者餐后TG反应变化的影响。研究了31名空腹TG<1.7 mmol/L的泰国T2D患者。所有患者均接受饮食控制或磺脲类药物和/或二甲双胍治疗。无人接受降脂药物治疗。过夜禁食后进行混合餐试验。在试验前以及试验后1、2、3和4小时测量血浆葡萄糖、胰岛素和TG。在空腹状态下测量脂联素。通过磁共振成像确定内脏以及腹部浅表和深部皮下脂肪组织，并通过磁共振波谱测定肝脏脂肪含量（HFC）。对餐后TG与局部脂肪组织和代谢参数进行单变量和多变量回归分析。混合餐后0、1、2、3和4小时的TG水平分别为1.32±0.40（标准差）、1.40±0.41、1.59±0.40、1.77±0.57和1.80±0.66 mmol/L（P<0.0001）。餐后TG曲线下面积（AUC）与空腹TG（r=0.84，P<0.0001）和log.HFC（r=0.456，P=0.033）呈正相关且显著相关，并且倾向于与log.深部皮下脂肪组织（r=0.38，P=0.05）和性别（r=0.326，P=0.073）相关。餐后TG的AUC与年龄、体重指数、腰围、log.浅表皮下脂肪组织、log.内脏脂肪组织、糖化血红蛋白、空腹血糖、AUC.葡萄糖、log.空腹胰岛素、log.AUC.胰岛素、log.稳态模型评估%B、胰岛素抵抗稳态模型评估以及脂联素均无相关性。在回归模型中，只有空腹TG（β=0.815，P<0.0001）和log.HFC（β=0.249，P=0.035）可预测餐后TG的AUC（调整后R2=0.84，P<0.0001）。总之，在空腹TG正常的T2D患者中，餐后TG水平的升高直接由空腹TG水平和肝脏脂肪量决定。
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