Glucagon like peptide-1 analogue, Liraglutide, improves liver fibrosis markers in obese women with polycystic ovary syndrome and non-alcoholic fatty liver disease

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 532-553-Hyperandrogenic Disorders
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-541
Hassan Kahal*1, George Abouda2, Alan S Rigby1, Anne Marie Coady3, Eric S Kilpatrick3 and Stephen Lawrence Atkin4
1Hull York Medical School, Hull, United Kingdom, 2Hull and East Yorkshire Hospitals NHS Trust, Hull, United Kingdom, 3Hull and East Yorkshire NHS Trust, Hull, United Kingdom, 4Hull York Medical School, E Yorkshire, United Kingdom
Introduction: Non-alcoholic fatty liver disease (NAFLD) has been linked to polycystic ovary syndrome (PCOS) and carries an increased risk of liver cirrhosis and mortality. Hyaluronic acid (HA), and procollagen type 3 amino terminal peptide (PIIINP) are independent predictors of liver cirrhosis. Glucagon like peptide-1 (GLP-1) analogues cause weight loss and have been found to reduce hepatic steatosis in pre-clinical trials.

Objective: To assess if six months treatment with GLP-1 analogue, liraglutide, improves markers of liver fibrosis.

Design: A case-control study comparing women with PCOS to age and weight matched controls. PCOS was diagnosed according to the Rotterdam criteria. All participants underwent liver function tests and liver ultrasound scan to assess for fatty infiltration. Serum markers for liver fibrosis, PIIINP and HA, were measured at baseline and after six months of treatment with Liraglutide 1.8mg od. Data were summarised by the mean and standard deviation and analysed using the independent or dependent t-test.

Results: Twenty one obese women with PCOS and 19 controls were recruited, age (32.8±7.2 vs. 33.5±6.7years) and weight (100.9±16.7 vs. 99.3±14.7kg), respectively.

At baseline, the PCOS group had higher testosterone 1.2±0.3 vs. 0.9±0.3nmol/L (P=0.01), HOMA-IR 2.5±1.7 vs. 1.7±1.0 (P=0.08), urinary isoprostane 16.0±4.4 vs. 11.8±7.1ng/ml (P=0.04), fatty infiltration suggestive of NAFLD seven (35%) vs. none, aspartate aminotransferase (AST) 22.4 ±5.2 vs.18.8 ±3.4u/L (P=0.04), and PIIINP 4.4 ±0.8 vs. 3.5±0.8 ug/ml (P=0.01), compared to controls. NAFLD clinical score (BARD), alanine aminotransferase and HA did not significantly differ between the two groups.  

Twenty five (62%) participants completed the study (13 PCOS, 12 controls).  Following treatment, weight was reduced by 3.7±4.8kg (P=0.016) and 4.6±3.5kg (P=0.001); triglycerides by 0.4±0.5mmol/L (P=0.007) and 0.3±0.5mmol/L (P=0.057); and PIIINP by 0.8±0.8ug/ml (P=0.005) and 0.6±0.8 ug/ml (P=0.02) in the PCOS and control groups, respectively.

Conclusions: Treatment with the GLP-1 analogue, liraglutide, and/or associated weight loss significantly reduced the levels of liver fibrosis marker PIIINP in obese women with PCOS and controls. Liraglutide may be a potential treatment for women with PCOS, obesity and NAFLD.

Nothing to Disclose: HK, GA, ASR, AMC, ESK, SLA

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