Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2014) 35 P476 | DOI: 10.1530/endoabs.35.P476

ECE2014 Poster Presentations Diabetes therapy (40 abstracts)

Could favorable effects of liraglutide on steato-hepatitis be independent of weight loss in type 2 diabetes? A case report

Cyril Garcia , Lyse Bordier , Olivier Dupuy & Hervé Mayaudon


Hôpital D’Instruction des Armées Begin, Saint-Mande, France.


Introduction: Some data suggest a favorable effect of glucagon-like peptide 1 (GLP1) on steato-hepatitis (SH) in type 2 diabetes. We report here a case of improvement of SH in a patient treated by liraglutide.

Patients and methods: A 31-year-old woman presented type 2 diabetes. Her weight was 80 kg for 1.58 m (BMI=32 kg/m2). A treatment by liraglutide was initiated at 1.2 mg/day, percutaneously. A regular follow-up was performed with the recording of weight, HbA1c, iron and lipid status. Liver function was assessed regularly by liver enzymes dosage and fibromax score establishment.

Results: Before liraglutide initiation HbA1c was 8.6%, ASAT 45 UI/l, ALAT 58 UI/l, and GGT 174 UI/l. After only 3 months HbA1c dropped to 6.5%, ASAT 42, ALAT 52, and GGT 92 UI/l, as the weight was still 79.4 kg. At 1 year the results were: HbA1c 6.7%, ASAT 17 UI/l, ALAT 18 UI/l and GGT 26 UI/l. Triglycerides level decreased from 2.63 to 0.8 mmol/l. The FIBROMAX score indicated initially an important SH, which greatly improved at one year (Steatotest=1 vs 3, Nashtest=1 vs 2, and Actitest=0 vs 1–2), while her weight was 74 kg.

Discussion: This observation suggests a beneficial role of liraglutide on SH in this patient. Proving that this could be independent of weight loss is difficult, as the patient had lost 6 kg in 1 year. However at 3 months Nash-test decreased to 1 as her weight remained stable. A beneficial effect of GLP1 analogs on SH independently of weight loss has been suggested in mouse. This effect could be due to an action of the GLP1 analog on hepatocytes, which usually express GLP-1 receptors, leading to fat export and increase of β oxidation. A prospective study including more patients is currently in process in our department, in order to assess this hypothesis.

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