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Review
Glucagon like peptide-1 receptor agonists for the management of obesity and non-alcoholic fatty liver disease: a novel therapeutic option
  1. Gauri Dhir1,2,
  2. Kenneth Cusi1,2
  1. 1Division of Endocrinology, Diabetes and Metabolism, University of Florida, Gainesville, Florida, USA
  2. 2Division of Endocrinology, Diabetes and Metabolism, Malcom Randall VA Medical Center, Gainesville, Florida, USA
  1. Correspondence to Dr Kenneth Cusi, Department of Endocrinology, Diabetes and Metabolism Division University of Florida, Gainesville, Florida 32610, USA; kcusi{at}ufl.edu

Abstract

Obesity is a major risk factor for the development of type 2 diabetes mellitus (T2DM), and is associated with a cluster of metabolic factors that lead to poor cardiovascular outcomes. In non-alcoholic fatty liver disease (NAFLD), liver fat (triglyceride) accumulation closely mirrors adipose tissue dysfunction and insulin resistance in obesity and T2DM. It is now recognized as the most common chronic liver disease in Westernized societies, often progressing to more severe forms of the disease such as nonalcoholic steatohepatitis (NASH), or cirrhosis and hepatocellular carcinoma. However, NAFLD remains largely overlooked by healthcare providers although it affects about two-thirds of patients with obesity and it promotes the development of T2DM. NAFLD mirrors adipose tissue and systemic insulin resistance, the liver being a ’barometer' of metabolic health. Although pioglitazone is emerging as the treatment of choice for NASH in patients with insulin-resistance, or those with T2DM, many other options are being tested. Due to their overall safety and efficacy, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are becoming one of the cornerstones for the management of both obesity and T2DM, and emerging as an alternative for the treatment of NAFLD. In this review, we will briefly summarize the status of GLP-1RA for the treatment of obesity and NAFLD.

  • GLP-1
  • obesity
  • fatty liver
  • steatosis
  • NASH
  • type 2 diabetes mellitus

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Footnotes

  • Contributors GD performed the initial review of the available literature, created figure 1 and wrote the initial manuscript draft; KC reviewed the literature, mentored GD and worked on revising and submitting the final version of the manuscript.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; externally peer reviewed.

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