Kataboler Carnitinstoffwechsel. Reaktionsprodukte der Carnitin-Decarboxylase und der Carnitin-Dehydrogenase in vivo

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Abstract
Rats and mice were given large oral or subcutaneous doses of (-)-L-, (+)-D- and DL-carnitine (5 mg/g body weight). The carnitine metabolites, .beta.-methylcholine and acetonyltrimethylammonium, were isolated from the urine by special methods and determined as their characteristic derivatives (2,4-dinitrophenylhydrazone and butyric ester) by TLC or photometry. .beta.-Methylcholine, the product of carnitine decarboxylase, was not excreted even when animals were heavily dosed with both carnitine isomers, with or without starvation. After the administration of (+)-D- and DL-carnitine, both species excreted acetonyltrimethylammonium, which is already known as the spontaneous decarboxylation product of dehydrocarnitine (product of carnitine dehydrogenase) in bacteria. Injection of 0.71 mmol (+)-D-carnitine resulted in the excretion of 5.0 .mu.mol (average) acetonyltrimethylammonium/mouse during the 48 h post injection. Under the same conditions, rats produced up to 40 .mu.mol acetonyltrimethylammonium. The ratio of excreted acetonyltrimethylammonium to injected (+)-D-carnitine depended on the method of administration and the dose. Production of the pharmacologically active (+)-acetyl-L-.beta.-methylcholine is not to be expected, following high exogenous doses of (-)-L-carnitine or (-)acetyl-L-carnitine. The chief metabolites are trimethylamine, trimethylamine oxide and .gamma.-butyrobetaine, and both the (-)-L-carnitine pool and exogenous (-)-L-carnitine are dehydrogenated or decarboxylated only a very small extent, if at all. When DL-carnitine is used therapeutically, the formation of acetonyltrimethylammonium must be taken into account.

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