Triglyceride hydrolysis by the perfused rat hindlimb is enhanced with serotonin-induced nonnutritive flow (NNF) and may be due to the presence of nonnutritive route-associated connective tissue fat cells. Here, we assess whether NNF influences muscle uptake of 0.55 mM palmitate in the perfused hindlimb. Comparisons were made with insulin-mediated glucose uptake. NNF induced during 60 nM insulin infusion inhibited hindlimb oxygen uptake from 22.0 ± 0.5 to 9.7 ± 0.8 μmol·g-1·h-1 (P < 0.001), 1-methylxanthine metabolism (indicator of nutritive flow) from 5.8 ± 0.4 to 3.8 ± 0.4 nmol·min-1·g-1 (P = 0.004), glucose uptake from 29.2 ± 1.7 to 23.1 ± 1.8 μmol·g-1·h-1 (P = 0.005) and muscle 2-deoxy-glucose uptake from 82.1 ± 4.6 to 41.6 ± 6.7 μmol·g-1·h-1 (P < 0.001). Palmitate uptake, unaffected by insulin alone, was inhibited by NNF in extensor digitorum longus, white gastrocnemius, and tibialis anterior muscles; average inhibition was from 13.9 ± 1.2 to 6.9 ± 1.4 μmol·g-1·h-1 (P = 0.02). Thus NNF impairs both fatty acid and glucose uptake by muscle by restricting flow to myocytes but, as shown previously, favors triglyceride hydrolysis and uptake into nearby connective tissue fat cells. The findings have implications for lipid partitioning in limb muscles between myocytes and attendant adipocytes.
History
Publication title
American Journal of Physiology: Endocrinology and Metabolism