Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects

Mohamed Abu-Farha, Jehad Abubaker, Fiona Noronha, Irina Al-Khairi, Preethi Cherian, Monira Alarouj, Abdullah Bennakhi, Naser Elkum

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Background: 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. Methods: This study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics. Results: 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]. Conclusion: 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.

Original languageEnglish
Article number112
JournalCardiovascular Diabetology
Volume14
Issue number1
DOIs
Publication statusPublished - 20 Aug 2015

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C-Peptide
Type 2 Diabetes Mellitus
Insulin
Logistic Models
Helper-Inducer T-Lymphocytes
Insulin Resistance
Triglycerides
Age Groups
Odds Ratio
Cell Proliferation
Confidence Intervals

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine

Cite this

Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects. / Abu-Farha, Mohamed; Abubaker, Jehad; Noronha, Fiona; Al-Khairi, Irina; Cherian, Preethi; Alarouj, Monira; Bennakhi, Abdullah; Elkum, Naser.

In: Cardiovascular Diabetology, Vol. 14, No. 1, 112, 20.08.2015.

Research output: Contribution to journalArticle

Abu-Farha, M, Abubaker, J, Noronha, F, Al-Khairi, I, Cherian, P, Alarouj, M, Bennakhi, A & Elkum, N 2015, 'Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects', Cardiovascular Diabetology, vol. 14, no. 1, 112. https://doi.org/10.1186/s12933-015-0277-1
Abu-Farha, Mohamed ; Abubaker, Jehad ; Noronha, Fiona ; Al-Khairi, Irina ; Cherian, Preethi ; Alarouj, Monira ; Bennakhi, Abdullah ; Elkum, Naser. / Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects. In: Cardiovascular Diabetology. 2015 ; Vol. 14, No. 1.
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abstract = "Background: 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. Methods: This study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics. Results: 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]. Conclusion: 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.",
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T1 - Lack of associations between betatrophin/ANGPTL8 level and C-peptide in type 2 diabetic subjects

AU - Abu-Farha, Mohamed

AU - Abubaker, Jehad

AU - Noronha, Fiona

AU - Al-Khairi, Irina

AU - Cherian, Preethi

AU - Alarouj, Monira

AU - Bennakhi, Abdullah

AU - Elkum, Naser

PY - 2015/8/20

Y1 - 2015/8/20

N2 - Background: 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. Methods: This study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics. Results: 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]. Conclusion: 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.

AB - Background: 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. Methods: This study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics. Results: 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]. Conclusion: 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.

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