Der tumorbedingte Gewichtsverlust ist regelmäβig mit hohen Lipolyse- und Fettoxidationsraten assoziiert. Um Einflüsse des Gewichtsverlustes selbst von der tumorabhängigen Regulation des Fettstoffwechsels zu differenzieren, wurden gewichtsstabile Tumorpatienten in gutem Ernährungszustand (Idealgewicht 109 ± 4% ( ± SEM), Body Mass Index 25,1 ± 0,9 kg/m2) untersucht. Lipolyseparameter (Glyzerin-, Fettsäurekonzentration) und die kalorimetrisch bestimmte Fettoxidationsrate wurden vor und während eines euglykämischen Insulin-Clamp-Protokolls (0,2 mU Insulin/kg/min) bei fünf Patienten mit gastrointestinalen Tumoren erfaβ. Bei hoher basaler Lipolyse- (Glyzerinkonzentration 112 ± 20 μmol/l, freie Fettsäuren 0,72 ± 0,13 mmol/l) und Fettoxidationsrate ( > 60% des Energieverbrauches) war die Insulinkonzentration niedrig normal (5,9 ± 0,5mU/l). Insulin hemmte Lipolyse und Fettoxidation und stimulierte die Kohlehydratoxidation. Gewichtsstabile Tumorpatienten zeigen nüchtern eine hohe Lipolyseund Fettoxidationsrate; die insulinabhängige Regulation des Fettstoffwechsels ist jedoch intakt, wie wir es bereits für gewichtsreduzierte Tumorpatienten zeigen konnten.

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