Hepatic phosphate trapping, decreased ATP, and increased feeding after 2,5-anhydro-D-mannitol
Autor: | M. I. Friedman, H. Blum, Mary Osbakken, Nancy E. Rawson |
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Rok vydání: | 1994 |
Předmět: |
Male
medicine.medical_specialty Magnetic Resonance Spectroscopy Physiology Biology Phosphates Rats Sprague-Dawley Eating chemistry.chemical_compound Adenosine Triphosphate In vivo Physiology (medical) Internal medicine medicine Animals Mannitol Esters Phosphorus Fructose Metabolism Carbohydrate Phosphate Rats Uric Acid Endocrinology Liver chemistry Uric acid Chromatography Thin Layer Adenosine triphosphate medicine.drug |
Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 266:R112-R117 |
ISSN: | 1522-1490 0363-6119 |
DOI: | 10.1152/ajpregu.1994.266.1.r112 |
Popis: | The mechanism by which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits feeding behavior was investigated by studying its metabolism and biochemical effects in liver. Thin-layer chromatography of liver extracts from rats given 2,5-AM containing 14C-labeled 2,5-AM showed that the analogue is phosphorylated in vivo with a time course that parallels the eating response. In vivo 31P nuclear magnetic resonance spectroscopy of rat liver during intravenous infusion of 2,5-AM and high-resolution nuclear magnetic resonance analyses of liver extracts showed that 2,5-AM is rapidly phosphorylated in liver, trapping hepatic phosphate and decreasing ATP, inorganic phosphate, and phosphate diesters. These changes occurred in a time frame in which the feeding response is elicited in conscious animals given the same dose of 2,5-AM by the same route. During an interval in which 2,5-AM increased eating, it also increased urinary uric acid excretion, implicating enhanced adenosine degradation in the reduction in hepatic ATP. These results provide the first direct evidence that changes in a high-energy phosphate-carrying compound in liver may provide a signal to initiate eating behavior. |
Databáze: | OpenAIRE |
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