hyperglycemia
Mice with complete deletion of insulin receptor substrate 2 (IRS2) develop hyperglycemia, impaired hepatic insulin signaling, and elevated gluconeogenesis, whereas mice deficient for protein tyrosine phosphatase (PTP)1B display an opposing hepatic phenotype characterized by increased sensitivity to insulin.
Mice with complete deletion of <span class="gene" id="20028942-1-31-59">insulin receptor substrate 2</span> (<span class="gene" id="20028942-1-61-65">IRS2</span>) develop <span class="disease" id="20028942-1-75-88">hyperglycemia</span>, impaired hepatic insulin signaling, and elevated gluconeogenesis, whereas mice deficient for protein tyrosine phosphatase (PTP)1B display an opposing hepatic phenotype characterized by increased sensitivity to insulin.