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

Nutrition & Metabolism, Sep 2017

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. 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. 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. 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. ChiCTR-IOR- 16008435 . Registered 8 May 2016.

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

Wang et al. Nutrition & Metabolism Effects of a liquid high-fat meal on postprandial lipid metabolism in type 2 diabetic patients with abdominal obesity Feng Wang 0 Huixia Lu 2 Fukang Liu 0 Huizhen Cai 0 1 Zhixiu Song 0 3 Fei Guo 2 Yulan Xie 2 Guofang Shu 2 Guiju Sun 0 0 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 1 School of Public Health, Ningxia Medical University , Yinchuan , China 2 Zhongda Hospital, Southeast University , Nanjing , China 3 Second Clinical Medical College, Nanjing University of Traditional Chinese Medicine , Nanjing , China 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. Type 2 diabetes; Abdominal obesity; Liquid high-fat meal; Lipid metabolism; PvuII polymorphisms Background It is generally known that individuals were in the state of not fasting during most of the time. Determination of blood lipids, however, is mostly based on the fasting condition. This mode of detection does not accurately reflect the level of lipids. In 1979, Zilversmit first proposed that postprandial lipemia was associated with an increased risk of atherosclerosis [ 1 ].This finding attracted growing attention in postprandial lipid metabolism and confirmed by others [ 2, 3 ]. At present, postprandial lipid disturbance have been seen in persons with obesity [ 4–6 ], impaired glucose tolerance [7], first degree relatives of type 2 diabetes families [ 8 ], and type 2 diabetes [ 9–13 ]. Type 2 diabetes is a global epidemic that poses an immense medical challenge to health-care systems. Abdominal obesity that accompanies type 2 diabetes is frequently associated with atherogenic dyslipidemia [ 14 ]. In addition, lipoprotein lipase (LPL) also plays a pivotal role in lipid homeostasis [ 15 ]. The PvuII polymorphisms are found in intron 6 of the LPL gene. This genetic polymorphisms might influence the risk of the appearance of coronary arterial disease [ 16 ]. However, the effects of PvuII polymorphisms of LPL on postprandial lipid profiles in response to a liquid high-fat meal have not been reported so far in type 2 diabetic patients with abdominal obesity. Therefore, the aims of this study were to evaluate the postprandial lipid responses 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 metabolism. Methods Subjects The study was conducted in 51 type 2 diabetic patients with abdominal obesity and 31 type 2 diabetic patients without abdominal obesity, recruited from the Nanjing Jiangpu People Hospital. A group of 39 (...truncated)


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Feng Wang, Huixia Lu, Fukang Liu, Huizhen Cai, Zhixiu Song, Fei Guo, Yulan Xie, Guofang Shu, Guiju Sun. Effects of a liquid high-fat meal on postprandial lipid metabolism in type 2 diabetic patients with abdominal obesity, Nutrition & Metabolism, 2017, pp. 54,