Turnover and fate of plasma free fatty acids in briefly‐fasted lymphoma‐bearing mice

Body fat loss during tumor growth may be due to increased mobilization of adipose triglycerides. Earlier work from this laboratory suggested that (i) lymphoma‐bearing AKR mice have a circulating lipid mobilizing factor (LMF) which caused body fat loss during cancer growth; that (ii) fatty acids (FA) mobilized in these tumor‐bearing (TB) mice were not oxidized to CO 2 as in starved mice that lose their body fat; and that (iii) instead, the mobilized FA were sequestered by the lymphoma. We tested these hypotheses by injecting [1‐ 14 C]palmitate‐albumin into lymphoma‐bearing and control mice. We measured turnover of plasma FFA for 24 hr and predicted the cumulative conversion of tracer into breath 14 CO 2 (at 85 min) in the TB mice. Plasma FFA were mobilized more slowly in briefly fasted tumor‐bearing mice than in controls with the same plasma FFA pool sizes. The fractional catabolic rate (FCR) (min −1 ) of plasma FFA turnover in both groups decreased during the night when the mice ate: postabsorptive controls, 1.07(±5.6%); fed controls, 0.25 (±13%); postabsorptive TB, 0.53 (±4.6%); fed TB, 0.29 (±7.3%). Virtually all of the plasma FFA irreversible disposal in TB mice was accounted for as breath 14 CO 2 (30 to 40% I.D.), not as tumor lipids (1.1±0.22% I.D.). Thus, FFA oxidation to CO 2 is the major fate of plasma FFA turnover in TB mice, and sequestration of FFA (palmitate) by tumor cells is a quantitatively minor process. The putative circulating LMF did not cause increased FFA mobilization in these lymphoma‐bearing mice in the post‐absorptive state.