Loss of low-molecular-weight protein tyrosine phosphatase shows limited improvement in glucose tolerance but causes mild cardiac hypertrophy in mice

Author:

Jensen-Cody Sharon1,Coyne Erin S.1,Ding Xunshan1,Sebin Anu1,Vogel Jen1,Goldstein Jaclyn1,Rosahl Thomas W.2,Zhou Heather H.3,Jacobs Hugues4,Champy Marie-France4,About Ghina Bou4,Talukdar Saswata1,Zhou Yingjiang1

Affiliation:

1. Merck & Co., Inc., South San Francisco, California

2. Merck & Co., Inc., West Point, Pennsylvania

3. Merck & Co., Inc., Kenilworth, New Jersey

4. CELPHEDIA, PHENOMIN, Institut Clinique de la Souris, Université de Strasbourg, CNRS, INSERM, Illkirch, France

Abstract

Inhibition of LMPTP with a small-molecular inhibitor, Cmpd23, improves glucose tolerance in mice as reported earlier. However, genetic deficiency of the LMPTP gene, Acp, has limited effects on glucose metabolism but leads to mild cardiac hypertrophy in mice. The findings suggest the potential off-target effects of Cmpd23 and call for reevaluation of LMPTP as a therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism

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