Freyja D. James

Transporter-mediated absorption is the primary route of entry and is required for passive absorption of intestinal glucose into the blood of conscious dogs.

Prior exercise enhances passive absorption of intraduodenal glucose.

Suppression of endogenous glucose production by mild hyperinsulinemia during exercise is determined predominantly by portal venous insulin.

Hepatic glucose autoregulation: responses to small, non-insulin-induced changes in arterial glucose.

Portal venous hyperinsulinemia does not stimulate gut glucose absorption in the conscious dog.

Portal vein caffeine infusion enhances net hepatic glucose uptake during a glucose load in conscious dogs.

Exercise-induced changes in insulin and glucagon are not required for enhanced hepatic glucose uptake after exercise but influence the fate of glucose within the liver.

5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside causes acute hepatic insulin resistance in vivo.

Portal venous 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside infusion overcomes hyperinsulinemic suppression of endogenous glucose output.

5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside renders glucose output by the liver of the dog insensitive to a pharmacological increment in insulin.

Energy state of the liver during short-term and exhaustive exercise in C57BL/6J mice.

The glucagon-like peptide-1 receptor regulates endogenous glucose production and muscle glucose uptake independent of its incretin action.

Endothelial nitric oxide synthase is central to skeletal muscle metabolic regulation and enzymatic signaling during exercise in vivo.

Glucagon-like peptide-1 receptor knockout mice are protected from high-fat diet-induced insulin resistance.

Diet-induced muscle insulin resistance is associated with extracellular matrix remodeling and interaction with integrin alpha2beta1 in mice.

Mesenchymal stem cell transplantation for the infarcted heart: a role in minimizing abnormalities in cardiac-specific energy metabolism.