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J. Biochem, 1988, Vol. 104, No. 5 847-850
© 1988 Japanese Biochemical Society

research-article

Hepatic Accumulation of Pyrophosphate during Acetate Metabolism1

Toru Yamada2, Toru Inoue, Toshirou Nishida, Eisuke Furuya and Kunio Tagawa2

Department of Physiological Chemistry, Medical School, Osaka University, Kita-ku, Osaka Osaka 530

3 To whom correspondence should be addressed

Accumulation of pyrophosphate induced by acetate administration was investigated in rat liver in situ and in perfused rat liver. Intraperitoneal injection of acetate into rats increased the pyrophosphate concentration in the liver to about 2 µmol/g liver, which was 200 times that in control liver. Perfusion of liver with acetate alone did not result in accumulation of pyrophosphate. However, the further addition of a Ca2+-mobilizing hormone, such as noradrenaline or angiotensin II, together with glucagon to the perfusion medium containing 1 mM acetate caused accumulation of pyrophosphate to a similar level to that observed in vivo. Acetate, glucagon and a Ca2+-mobilizing hormone were all required for accumulation of pyrophosphate in perfused liver. Omission of Ca2+ from the perfusion medium or addition of a Ca2+-antagonist reduced the accumulation significantly. The two kinds of hormones, glucagon and an {alpha}-agonist, either singly or in combination, did not affect the rate of acetate utilization. These results show that liver cells accumulate a large amount of pyrophosphate during acetate metabolism at high intracellular levels of Ca2+ that can be realized by the synergistic actions of the two kinds of hormones.

1 This study was supported in part by Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan

2 Present address: Laboratory of Biochemistry and Toxicology, Sumitomo Chemical Co., Kasugadenaka, Konohana-ku, Osaka 554.


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