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

K E Metcalfe; R I Godwin; S M Cookson; K G Kauter

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.

Original language	English
Pages	189-189
Publication status	Published - 31 Dec 2009
Event	RAAN 2009: Recent Advances in Animal Nutrition - Australia - University of New England, Armidale, Australia Duration: 12 Jul 2009 → 15 Jul 2009

Conference

Conference	RAAN 2009: Recent Advances in Animal Nutrition - Australia
City	Armidale, Australia
Period	12/07/09 → 15/07/09

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Medical Biochemistry: Carbohydrates

Access to Document

https://hdl.handle.net/1959.11/5157

Handle.net

Persistent link

Cite this

@conference{dd5d95125f754dacaf16c0d655ef4702,

title = "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.",

keywords = "Medical Biochemistry: Carbohydrates",

author = "Metcalfe, \{K E\} and Godwin, \{R I\} and Cookson, \{S M\} and Kauter, \{K G\}",

year = "2009",

month = dec,

day = "31",

language = "English",

pages = "189--189",

note = "RAAN 2009: Recent Advances in Animal Nutrition - Australia ; Conference date: 12-07-2009 Through 15-07-2009",

}

TY - CONF

T1 - The use of intravenous oxonic acid to study the effects of fructose in sheep

AU - Metcalfe, K E

AU - Godwin, R I

AU - Cookson, S M

AU - Kauter, K G

PY - 2009/12/31

Y1 - 2009/12/31

N2 - 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.

AB - 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.

KW - Medical Biochemistry: Carbohydrates

UR - http://www.conferencecompany.com.au/animalnutrition/RAAN_Full_Program.pdf

UR - http://www.conferencecompany.com.au/animalnutrition/

M3 - Abstract

SP - 189

EP - 189

T2 - RAAN 2009: Recent Advances in Animal Nutrition - Australia

Y2 - 12 July 2009 through 15 July 2009

ER -