Abstract
BackgroundBetatrophin 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.MethodsThis study was designed to examine the association between plasma betatrophin level and C-peptide in 749 T2D and non-diabetics.ResultsBetatrophin 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].ConclusionIncreased 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.
Highlights
Betatrophin has been suggested as an inducer of β-cell proliferation in mice in addition to its function in regulating triglyceride
Using a large sample cohort we have recently showed that betatrophin level was increased in Type 2 Diabetes (T2D), it was not affecting fasting blood glucose (FBG) or insulin production in T2D subjects [30]
No association was observed between betatrophin and FBG, insulin or C-peptide in T2D subjects (Table 2)
Summary
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), 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. Yi et al has shown that betatrophin, a liver and adipose tissue derived hormone, was able to induce β-cell proliferation in insulin resistant mouse model [11]. This finding caused huge excitement in the field of beta-cell regeneration as a potential alternative treatment for diabetes [10, 19]. Gusarova et al showed that β-cells lacking both copies of betatrophin were producing insulin normally under insulin resistance conditions [22]
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