Incretin mimetics as a novel therapeutic option for hepatic steatosis

Maarten E. Tushuizen, Mathijs C. Bunck, Petra J. Pouwels, Jan Hein T van Waesberghe, Michaela Diamant, Robert J. Heine

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background: Fat accumulation in the liver or non-alcoholic fatty liver disease (NAFLD) is regarded as a key pathogenic factor and component of the metabolic syndrome. It was reported that administration of the incretin mimetic exenatide reversed hepatic steatosis in an obese mouse model. We had the opportunity to study the effect of additional exenatide administration on liver fat content in a patient with type 2 diabetes. Case report: A 59-year-old male with poorly controlled type 2 diabetes was treated with exenatide in addition to metformin monotherapy. Following 44 weeks of exenatide therapy, mean the liver fat measured by liver spectroscopy declined from 15.8% to 4.3%. This dramatic decrease in liver fat was accompanied by significant beneficial changes in several cardiovascular disease risk factors and improvement of all liver enzymes, in particular alanine aminotransferase, the most important marker of liver steatosis. Conclusion: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population.

Original languageEnglish
Pages (from-to)1015-1017
Number of pages3
JournalLiver International
Volume26
Issue number8
DOIs
Publication statusPublished - 1 Oct 2006

Cite this

Tushuizen, Maarten E. ; Bunck, Mathijs C. ; Pouwels, Petra J. ; van Waesberghe, Jan Hein T ; Diamant, Michaela ; Heine, Robert J. / Incretin mimetics as a novel therapeutic option for hepatic steatosis. In: Liver International. 2006 ; Vol. 26, No. 8. pp. 1015-1017.
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abstract = "Background: Fat accumulation in the liver or non-alcoholic fatty liver disease (NAFLD) is regarded as a key pathogenic factor and component of the metabolic syndrome. It was reported that administration of the incretin mimetic exenatide reversed hepatic steatosis in an obese mouse model. We had the opportunity to study the effect of additional exenatide administration on liver fat content in a patient with type 2 diabetes. Case report: A 59-year-old male with poorly controlled type 2 diabetes was treated with exenatide in addition to metformin monotherapy. Following 44 weeks of exenatide therapy, mean the liver fat measured by liver spectroscopy declined from 15.8{\%} to 4.3{\%}. This dramatic decrease in liver fat was accompanied by significant beneficial changes in several cardiovascular disease risk factors and improvement of all liver enzymes, in particular alanine aminotransferase, the most important marker of liver steatosis. Conclusion: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population.",
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Incretin mimetics as a novel therapeutic option for hepatic steatosis. / Tushuizen, Maarten E.; Bunck, Mathijs C.; Pouwels, Petra J.; van Waesberghe, Jan Hein T; Diamant, Michaela; Heine, Robert J.

In: Liver International, Vol. 26, No. 8, 01.10.2006, p. 1015-1017.

Research output: Contribution to journalArticleAcademicpeer-review

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AU - Pouwels, Petra J.

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AU - Diamant, Michaela

AU - Heine, Robert J.

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N2 - Background: Fat accumulation in the liver or non-alcoholic fatty liver disease (NAFLD) is regarded as a key pathogenic factor and component of the metabolic syndrome. It was reported that administration of the incretin mimetic exenatide reversed hepatic steatosis in an obese mouse model. We had the opportunity to study the effect of additional exenatide administration on liver fat content in a patient with type 2 diabetes. Case report: A 59-year-old male with poorly controlled type 2 diabetes was treated with exenatide in addition to metformin monotherapy. Following 44 weeks of exenatide therapy, mean the liver fat measured by liver spectroscopy declined from 15.8% to 4.3%. This dramatic decrease in liver fat was accompanied by significant beneficial changes in several cardiovascular disease risk factors and improvement of all liver enzymes, in particular alanine aminotransferase, the most important marker of liver steatosis. Conclusion: This case report suggests that the incretin mimetic exenatide decreases hepatic fat accumulation and may play a role in the future treatment of NAFLD, and the associated insulin resistance and cardiovascular risk factors in an ever-growing high-risk population.

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