Key result
Morbid obesity is linked to upregulated FATPs and ~156% higher systemic apoptosis markers.
Why the study?
Hepatocyte apoptosis is a key event in NASH, but the effect of obesity on free fatty acid levels, fatty acid transport proteins, and apoptosis activation in the liver was not fully understood.
Population
52 morbidly obese patients undergoing bariatric surgery
Comparison
Obese patients vs healthy controls
Design
Observational cross-sectional study
Authors
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May link fatty acid transport to apoptosis in obese NASH; hypothesis-generating and requires prospective validation before clinical adoption.
Observational (n=52)
Absolute Event Rate: 212.61% vs 83.12%
Increased free fatty acids and fatty acid transport proteins are associated with extrinsically and intrinsically induced apoptosis, liver damage, and fibrosis in morbidly obese patients with NASH.
Bechmann et al. (2009) conducted an observational in Non-alcoholic steatohepatitis (NASH) (n=52). Morbid obesity vs. Controls was evaluated on Systemic apoptosis (M30 levels, U/L). Morbid obesity was associated with upregulated fatty acid transport proteins and significantly elevated systemic apoptosis markers (M30: 212.61 vs 83.12 U/L) compared to controls.
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