Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects.
Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects.
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DOI：
10.1186/s12933-015-0277-1
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发表时间：
2015-08-20
影响因子：
9.3
通讯作者：
Elkum N
中科院分区：
文献类型：
--
作者：
Abu-Farha M;Abubaker J;Noronha F;Al-Khairi I;Cherian P;Alarouj M;Bennakhi A;Elkum N
除了调节甘油三酯的功能外，贝托芬还被认为是小鼠β细胞增殖的诱导剂。最近的数据显示，β-托啡肽在2型糖尿病(T2D)中增加，但其诱导胰岛素产生的能力受到质疑。我们假设T2D中增加的β-托啡肽不会影响β细胞胰岛素的产生。为了验证这一假设，我们调查了贝托芬和人类C-肽水平之间的关系，C-肽水平是衡量β细胞内源性胰岛素产生的指标。本研究旨在研究749例T2D患者和非糖尿病患者血浆β-托啡肽水平与C-肽的关系。与非糖尿病患者相比，T2D患者的β-托啡肽和C-肽水平更高。在非糖尿病患者中，β-托啡肽与C-肽有很强的相关性(r=0.28，p=0.0001)。在T2D受试者中，未观察到贝托芬与C-肽之间的关联(r=0.07，p=0.3366)。根据β-托啡肽水平将肥胖和非肥胖受试者分为三组，发现肥胖组和非肥胖组中β-托啡肽水平较高的受试者的C-肽水平显著高于非糖尿病受试者，P-趋势系数为0.0046。另一方面，在所有年龄段的非糖尿病受试者中，C-肽水平显著高于非糖尿病受试者，但在T2D受试者中并不显著。对年龄、BMI、性别、种族和C肽水平进行调整后的多因素Logistic回归模型显示，贝托芬水平最高的三分位数的受试者患T2D的几率更高[奇比(OR)=77.3，95%可信区间(CI)4.0-13.3]。肥胖者的β-托啡肽水平升高与C-肽水平升高相关，这可能是由于胰岛素抵抗增加所致。另一方面，在T2D受试者中，β-托啡肽水平的升高与C-肽之间没有相关性。总而言之，T2D受试者的β-托啡肽增加并不会导致C-肽水平所指示的任何胰岛素产生的增加。
Betatrophin has been suggested as an inducer of β-cell proliferation in mice in addition to its function in regulating triglyceride. Recent data showed that betatrophin was increased in Type 2 Diabetes (T2D), however, its ability to induce insulin production has been questioned. We hypothesized that the increased betatrophin in T2D is not affecting insulin production from β-cells. To test this hypothesis, we investigated the association between betatrophin and C-peptide level in humans, which acts as a measure of endogenous insulin production from β-cells. This study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics. Betatrophin and C-peptide levels were higher in T2D subjects compared with non-diabetics subjects. Betatrophin showed strong correlation with C-peptide in non-diabetics subjects (r = 0.28, p = < 0.0001). No association between betatrophin and C-peptide were observed in T2D subjects (r = 0.07, p = 0.3366). Dividing obese and non-obese subjects into tertiles according to betatrophin level showed significantly higher C-peptide levels at higher tertiles of betatrophin in obese non-diabetics subjects P-trend = 0.0046. On the other hand, C-peptide level was significantly higher in subject with higher betatrophin level in non-diabetics subjects across all age groups but not in T2D subjects. Multiple logistic regression models adjusted for age, BMI, gender, ethnicity as well as C-peptide level showed that subjects in the highest tertiles of betatrophin had higher odds of having T2D [odd ratio (OR) = 7.3, 95 % confidence interval (CI) 4.0–13.3]. Increased betatrophin level in obese subjects is correlated with an increase in C-peptide level; which is possibly caused by the increased insulin resistance. On the other hand, no correlation is observed between increased betatrophin level and C-peptide in T2D subjects. In conclusion, the increased betatrophin in T2D subject does not cause any increase in insulin production as indicated by C-peptide level.