Key result
Serum betatrophin levels were significantly higher in lean, glucose-tolerant women with PCOS compared to healthy controls (median 322.3 vs 199.9 ng/L; p=0.005).
Why the study?
Are serum betatrophin levels elevated in lean, glucose-tolerant women with PCOS compared to healthy controls?
Case-Control
Are serum betatrophin levels elevated in lean, glucose-tolerant women with PCOS compared to healthy controls?
Absolute Event Rate: 322.3% vs 199.9%
p-value: p=0.005
Serum betatrophin levels are significantly elevated in lean, glucose-tolerant women with PCOS, potentially reflecting a compensatory mechanism against metabolic syndrome-related risk factors.
Elevated betatrophin may mark early metabolic stress in lean PCOS; hypothesis-generating and should not yet change practice.
) women diagnosed with PCOS using the Rotterdam criteria, and 60 age- and BMI-matched healthy controls without any features of clinical or biochemical hyperandrogenism. Before recruitment, glucose tolerance was evaluated in all of the subjects using the 2-h 75 g oral glucose-tolerance test, and only those exhibiting normal glucose tolerance were enrolled. Serum betatrophin levels were significantly higher in women with PCOS (median 322.3; range 44.7-1989.3 ng/L) compared to the controls (median 199.9; range 6.2-1912.9 ng/L; p = .005). In the control group, no significant correlation was evident between betatrophin levels and clinical or biochemical parameters. In the PCOS group, betatrophin levels were positively correlated with prolactin levels (r = .286, p = .046) and negatively correlated with BMI (r = -.283, p = .049), waist/hip ratio (r = -.324, p = .023), and low-density lipoprotein cholesterol levels (r = -.385, p = .006). Impact statement What is already known on this subject: Several studies have suggested that primary alteration in beta-cell function is a pathophysiological feature of PCOS, and insulin resistance is the most significant predictor of beta-cell dysfunction independent of obesity. Betatrophin is a circulating protein that is primarily expressed in the liver in humans. Early experimental investigations demonstrated that overexpression of betatrophin significantly promoted pancreatic beta-cell proliferation, insulin production and improved glucose tolerance. Few studies have investigated the association between PCOS and betatrophin. However, in contrast to our study, the authors included overweight/obese patients and glucose tolerance was not evaluated before recruitment. What the results of this study add: Our results showed that serum betatrophin levels were significantly higher in lean glucose-tolerant PCOS women than in age- and BMI-matched healthy controls. What are the implications of these findings for clinical practice and/or further research: Elevated betatrophin levels in PCOS women, in the absence of obesity and glucose intolerance, may reflect a compensatory mechanism in order to counteract metabolic syndrome-related risk factors.
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Erol et al. (2017) conducted a case-control in Polycystic ovary syndrome (PCOS). Polycystic ovary syndrome vs. Age- and BMI-matched healthy controls was evaluated on Serum betatrophin levels (ng/L) (p=0.005). Serum betatrophin levels were significantly higher in lean, glucose-tolerant women with PCOS compared to healthy controls (median 322.3 vs 199.9 ng/L; p=0.005).
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