Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus C, Denmark; Danish Diabetes Academy, Odense University Hospital, Kløvervænget 10, Entrance 112, 3rd floor, 5000 Odense C, Denmark; Endocrine Research Unit, Mayo Clinic, 1216 2nd St SW, Rochester, MN 55902, USA.
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Nørrebrogade 44, 8000 Aarhus C, Denmark.
Metabolism. 2017 Oct;75:25-35. doi: 10.1016/j.metabol.2017.07.002. Epub 2017 Jul 19.
Type 2 diabetes is associated with excess postprandial lipemia due to accumulation of chylomicrons and VLDL particles. This is a risk factor for development of cardiovascular disease. However, whether the excess lipemia is associated with an impaired suppression of VLDL-TG secretion and/or reduced clearance into adipose tissue is unknown.
We measured the postprandial VLDL-TG secretion, clearance and adipose tissue storage to test the hypothesis that impaired postprandial suppression of VLDL-TG secretion, combined with impaired VLDL-TG storage in adipose tissue, is associated with excess postprandial lipemia.
We studied 11 men with type 2 diabetes and 10 weight-matched non-diabetic men using ex-vivo labeled VLDL-TG tracers during an oral high-fat mixed-meal tolerance test to measure postprandial VLDL-TG secretion, clearance and storage. In addition, adipose tissue biopsies were analyzed for LPL activity and cellular storage factors.
Men with type 2 diabetes had greater postprandial VLDL-TG concentration compared to non-diabetic men. However, postprandial VLDL-TG secretion rate was similar in the two groups with equal suppression of VLDL-TG secretion rate (≈50%) and clearance rate. In addition, postprandial VLDL-TG storage was similar in the two groups in both upper body and lower body subcutaneous adipose tissue.
Despite greater postprandial VLDL-TG concentration, men with type 2 diabetes have similar postprandial suppression of VLDL-TG secretion and a similar ability to store VLDL-TG in adipose tissue compared to non-diabetic men. This may indicate that abnormalities in postprandial VLDL-TG metabolism are a consequence of obesity/insulin resistance more than a result of type 2 diabetes per se.
2 型糖尿病与乳糜微粒和 VLDL 颗粒的积累有关,导致餐后脂质过多。这是心血管疾病发展的一个危险因素。然而,过量的脂质血症是否与 VLDL-TG 分泌抑制受损以及/或进入脂肪组织的清除减少有关尚不清楚。
我们测量了餐后 VLDL-TG 的分泌、清除和脂肪组织储存,以检验这样一个假设,即餐后 VLDL-TG 分泌抑制受损,加上脂肪组织中 VLDL-TG 储存受损,与餐后脂质过多有关。
我们使用口服高脂肪混合餐耐量试验中体外标记的 VLDL-TG 示踪剂,研究了 11 例 2 型糖尿病男性和 10 例体重匹配的非糖尿病男性,以测量餐后 VLDL-TG 的分泌、清除和储存。此外,还分析了脂肪组织活检中的 LPL 活性和细胞储存因子。
2 型糖尿病男性的餐后 VLDL-TG 浓度高于非糖尿病男性。然而,两组的餐后 VLDL-TG 分泌率相似,VLDL-TG 分泌率(≈50%)和清除率的抑制率也相似。此外,两组的餐后 VLDL-TG 储存量在上半身和下半身皮下脂肪组织中也相似。
尽管餐后 VLDL-TG 浓度较高,但与非糖尿病男性相比,2 型糖尿病男性的 VLDL-TG 分泌抑制和 VLDL-TG 在脂肪组织中的储存能力相似。这可能表明,餐后 VLDL-TG 代谢异常是肥胖/胰岛素抵抗的结果,而不是 2 型糖尿病本身的结果。