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In IUGR lambs ADR\u03b22 activation increased whole\u2010body glucose utilization rates and insulin sensitivity but had no effect on isolated islet or myocyte deficiencies.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>IUGR establishes risk for developing diabetes. In IUGR lambs we identified disparities in key aspects of glucose\u2010stimulated insulin secretion and insulin\u2010stimulated glucose oxidation, providing new insights into potential mechanisms for this risk.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated \u03b2 adrenergic receptor (ADR\u03b2) desensitization. Our objectives were to measure insulin\u2010sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADR\u03b22 agonist and ADR\u03b21\/\u03b23 antagonists for 1\u00a0month normalizes their glucose metabolism. Growth, glucose\u2010stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR\u2010AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole\u2010body GUR were not different from controls. Of importance, ADR\u03b22 stimulation with \u03b21\/\u03b23 inhibition increases both insulin sensitivity and whole\u2010body glucose utilization in IUGR lambs. In IUGR and IUGR\u2010AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and\n                      <jats:italic>ex vivo<\/jats:italic>\n                      skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR\u2010AR skeletal muscle than in controls but GLUT1 was greater in IUGR\u2010AR. ADR\u03b22, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR\u2010AR lambs heart rates were greater, which was independent of cardiac ADR\u03b21 activation. We conclude that targeted ADR\u03b22 stimulation improved whole\u2010body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch\u2010up growth in IUGR lambs as early as 1\u00a0month of age and are inherent to the islets and myocytes.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp278726","type":"journal-article","created":{"date-parts":[[2019,10,30]],"date-time":"2019-10-30T17:09:12Z","timestamp":1572455352000},"page":"5835-5858","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Postnatal \u03b22 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle"],"prefix":"10.1113","volume":"597","author":[{"given":"Dustin T.","family":"Yates","sequence":"first","affiliation":[{"name":"School of Animal and Comparative Biomedical Sciences University of Arizona Tucson AZ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leticia 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