The use of intravenous oxonic acid to study the effects of fructose in sheep

Abstract

In monogastric animals, dietary fructose is rapidly phosphorylated in the liver to fructose-1-phosphate by fructokinase. This rapid unregulated phosphorylation depletes adenosine triphosphate (ATP) and consequently results in the generation of uric acid via the hypoxanthine pathway. In all mammals except primates, the uric acid is converted to allantoin via uricase. In humans, the resulting hyperuricaemia associated with high fructose intakes is linked to the development of insulin resistance, hypertension, fatty liver disease and hypertriglyceridaemia – collectively termed metabolic syndrome (Johnson et al., 2009). Suitable animal models other than primates with which to study the phenomenon are lacking.