Effects of a liquid high-fat meal on postprandial lipid metabolism in type 2 diabetic patients with abdominal obesity

Feng Wang; Huixia Lu; Fukang Liu; Huizhen Cai; Zhixiu Song; Fei Guo; Yulan Xie; Guofang Shu; Guiju Sun

doi:10.1186/s12986-017-0211-5

Effects of a liquid high-fat meal on postprandial lipid metabolism in type 2 diabetic patients with abdominal obesity

Nutr Metab (Lond). 2017 Aug 14:14:54. doi: 10.1186/s12986-017-0211-5. eCollection 2017.

Authors

Feng Wang¹, Huixia Lu², Fukang Liu¹, Huizhen Cai^{1

3}, Zhixiu Song^{1

4}, Fei Guo², Yulan Xie², Guofang Shu², Guiju Sun¹

Affiliations

¹ Key Laboratory of Environmental Medicine and Engineering of Ministry of Education, and Department of Nutrition and Food Hygiene, School of Public Health, Southeast University, Nanjing, China.
² Zhongda Hospital, Southeast University, Nanjing, China.
³ School of Public Health, Ningxia Medical University, Yinchuan, China.
⁴ Second Clinical Medical College, Nanjing University of Traditional Chinese Medicine, Nanjing, China.

Abstract

Background: Postprandial lipemia and lipoprotein lipase (LPL) activity play crucial roles in the pathogenesis of accelerated atherosclerosis. This study aimed to evaluate the postprandial lipid metabolism after the ingestion of a liquid high-fat meal in type 2 diabetic patients with abdominal obesity, and determine if the PvuII polymorphisms of LPL influence their postprandial lipid responses.

Methods: Serum glucose, insulin, triglycerides (TG), total cholesterol (TC) and high density lipoprotein cholesterol (HDL-C) were measured in fasting and postprandial state at 0.5, 1, 2, 4, 6 and 8 h after a liquid high-fat meal in 51 type 2 diabetic patients with abdominal obesity, 31 type 2 diabetic patients without abdominal obesity and 39 controls. Their PvuII polymorphisms of LPL were tested in fasting.

Results: Type 2 diabetic patients with abdominal obesity had significantly higher postprandial areas under the curve (AUC) of glucose [least square mean difference (LSMD) = 30.763, 95% confidence interval (CI) = 23.071-38.455, F = 37.346, P < 0.05] and TC (LSMD = 3.995, 95% CI = 1.043-6.947, F = 3.681, P < 0.05) than controls. Postprandial AUCs for insulin, homeostasis model assessment-insulin resistance (HOMA-IR) and TG were higher (LSMD = 86.987, 95% CI = 37.421-136.553, F = 16.739, P < 0.05; LSMD = 37.456, 95% CI = 16.312-58.600, F = 27.012, P < 0.05; LSMD = 4.684, 95% CI = 2.662-6.705, F = 26.158, P < 0.05), whereas HDL-C AUC was lower (LSMD = -1.652, 95% CI = -2.685 - -0.620, F = 8.190, P < 0.05) in type 2 diabetic subjects with abdominal obesity than those without abdominal obesity. In type 2 diabetic patients with abdominal obesity, postprandial TG AUC was lower in P-/- than in P+/- (LSMD = -4.393, 95% CI = -9.278 - -0.491, F = 4.476, P < 0.05) and P+/+ (LSMD = -7.180, 95% CI = -12.319 - -2.014, F = 4.476, P < 0.05) phenotypes. Postprandial AUCs for glucose, insulin, HOMA-IR, TC and HDL-C were not different according to PvuII phenotypes.

Conclusions: Abdominal obesity exacerbates the postprandial lipid responses in type 2 diabetic patients, which partly explains the excess atherogenic risk in these patients. In addition, the presence of P+ allele could contribute to a greater postprandial TG increase in type 2 diabetic patients with abdominal obesity.

Trial registration: ChiCTR-IOR-16008435. Registered 8 May 2016.

Keywords: Abdominal obesity; Lipid metabolism; Liquid high-fat meal; PvuII polymorphisms; Type 2 diabetes.