{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,7]],"date-time":"2025-11-07T19:03:35Z","timestamp":1762542215705},"reference-count":64,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2013,12,15]]},"abstract":"<jats:p>The impact of the GLP-1 receptor agonist lixisenatide on postprandial glucose disposition was examined in conscious dogs to identify mechanisms for its improvement of meal tolerance in humans and examine the tissue disposition of meal-derived carbohydrate. Catheterization for measurement of hepatic balance occurred \u224816 days before study. After being fasted overnight, dogs received a subcutaneous injection of 1.5 \u03bcg\/kg lixisenatide or vehicle (saline, control; n = 6\/group). Thirty minutes later, they received an oral meal feeding (93.4 kJ; 19% protein, 71% glucose polymers, and 10% lipid). Acetaminophen was included in the meal in four control and five lixisenatide dogs for assessment of gastric emptying. Observations continued for 510 min; absorption was incomplete in lixisenatide at that point. The plasma acetaminophen area under the curve (AUC) in lixisenatide was 65% of that in control ( P &lt; 0.05). Absorption of the meal began within 15 min in control but was delayed until \u224830\u201345 min in lixisenatide. Lixisenatide reduced ( P &lt; 0.05) the postprandial arterial glucose AUC \u224854% and insulin AUC \u224844%. Net hepatic glucose uptake did not differ significantly between groups. Nonhepatic glucose uptake tended to be reduced by lixisenatide (6,151 \u00b1 4,321 and 10,541 \u00b1 1,854 \u03bcmol\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7510 min<jats:sup>\u22121<\/jats:sup>in lixisenatide and control, respectively; P = 0.09), but adjusted (for glucose and insulin concentrations) values did not differ (18.9 \u00b1 3.8 and 19.6 \u00b1 7.9 l\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7pmol<jats:sup>\u22121<\/jats:sup>\u00b7l<jats:sup>\u22121<\/jats:sup>, lixisenatide and control, respectively; P = 0.94). Thus, lixisenatide delays gastric emptying, allowing more efficient disposal of the carbohydrate in the feeding without increasing liver glucose disposal. Lixisenatide could prove to be a valuable adjunct in treatment of postprandial hyperglycemia in impaired glucose tolerance or type 2 diabetes.<\/jats:p>","DOI":"10.1152\/ajpendo.00354.2013","type":"journal-article","created":{"date-parts":[[2013,10,23]],"date-time":"2013-10-23T07:33:31Z","timestamp":1382513611000},"page":"E1473-E1482","source":"Crossref","is-referenced-by-count":11,"title":["Effect of the glucagon-like peptide-1 receptor agonist lixisenatide on postprandial hepatic glucose metabolism in the conscious dog"],"prefix":"10.1152","volume":"305","author":[{"given":"Mary Courtney","family":"Moore","sequence":"first","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ulrich","family":"Werner","sequence":"additional","affiliation":[{"name":"Sanofi Deutschland, Frankfurt, 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