Key result
Prader-Willi syndrome linked to ~38% lower ANGPTL8 levels than common obesity, tracking hepatic steatosis severity.
Why the study?
The relationship of circulating ANGPTL8 with obesity and liver function in Prader-Willi syndrome was unknown.
Are circulating ANGPTL8 levels altered in obese patients with Prader-Willi syndrome compared to common obesity, and is it associated with liver steatosis?
Cross-Sectional (n=40)
No
Are circulating ANGPTL8 levels altered in obese patients with Prader-Willi syndrome compared to common obesity, and is it associated with liver steatosis?
Absolute Event Rate: 0.58% vs 0.93%
p-value: p=0.007
Circulating ANGPTL8 levels are lower in Prader-Willi syndrome compared to common obesity and are inversely associated with liver steatosis severity.
ANGPTL8 may mark steatosis severity in obesity; leaves open its genetic regulation and biomarker role in PWS.
ANGPTL8 is a liver-derived protein related to insulin-sensitivity. Its relationship with obesity and liver function in Prader-Willi syndrome (PWS) is unknown. The present study investigated circulating ANGPTL8 in PWS and controls with common obesity, assessing its association to liver steatosis. For this purpose, 20 obese PWS and 20 controls matched for body mass index (BMI), sex and age underwent analysis of ANGPTL8 levels, glucose and lipid metabolism. Liver function tests and degree of liver steatosis by ultrasonography (US), fat-free mass (FFM) and fat mass (FM) by dual-energy x-ray absorptiometry (DEXA) were also assessed. In comparison to controls, obese PWS showed lower values of FFM (p < 0.0001) and higher FM (p = 0.01), while harbouring higher HDL cholesterol, lower triglycerides and OGTT-derived insulin levels, as well as a lower prevalence and severity of liver steatosis. With respect to obese controls, ANGPTL8 levels were significantly lower in PWS (p = 0.007) and overall correlated with transaminase levels and the severity of liver steatosis, as well as FFM (p < 0.05 for all). By a stepwise multivariable regression analysis, ANGPTL8 levels were independently predicted by PWS status (p = 0.01) and liver steatosis (p < 0.05). In conclusion, ANGPTL8 levels are lower in PWS than obese controls and are inversely associated with the severity of liver steatosis. Further studies should investigate the potential genetic basis for this observation.
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Mele et al. (2017) conducted a cross-sectional in Prader-Willi syndrome with obesity (n=40). Prader-Willi Syndrome vs. Common obesity (BMI-matched controls) was evaluated on Circulating ANGPTL8 levels (ng/mL) (p=0.007). Prader-Willi syndrome was associated with significantly lower circulating ANGPTL8 levels compared to common obesity (0.58 vs 0.93 ng/mL, p=0.007), which inversely correlated with the severity of liver steatosis.
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