Hepatic fat content is a determinant of postprandial triglyceride levels in type 2 diabetes mellitus patients with normal fasting triglyceride

被引:6
|
作者
Nimitphong, Hatalkarn [1 ]
Phongkitkarun, Sith [2 ]
Rattarasarn, Chatchalit [1 ]
Kongsooksai, Atthana [1 ]
Chanprasertyothin, Suwannee [3 ]
Bunnag, Pong-Amorn [1 ]
Puavilai, Gobchai [1 ]
机构
[1] Mahidol Univ, Dept Med, Div Endocrinol & Metab, Bangkok 10700, Thailand
[2] Mahidol Univ, Dept Radiol, Bangkok 10700, Thailand
[3] Mahidol Univ, Ramathibodi Hosp, Res Ctr, Bangkok 10700, Thailand
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2008年 / 57卷 / 05期
关键词
D O I
10.1016/j.metabol.2007.12.008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 A(1c), 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 (0.815, P < .0001) and log.HFC (beta=.249, P = .035) predicted AUC of postprandial TG in regression model (adjusted R 2 = 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. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:644 / 649
页数:6
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