FIGURE 5.

Glucose inhibits palmitate but not oleate oxidation in hypothalamic slices. A, basal and KCl-stimulated NPY secretion in MBH slices. B, palmitate oxidation in MBH slices and peripheral tissues. C, palmitate oxidation in MBH and cortical slices with or without etomoxir (200 μm). Palmitate oxidation in MBH (D) and cortical (E) slices in response to increasing concentrations of glucose are shown. F, glucose utilization in MBH and cortical slices. Western blot (G) and quantitation of Thr-172 phospho-AMPK levels (H) in response to glucose in MBH and cortical slices. Oleate oxidation (I) in response to glucose in MBH slices is shown. J, palmitate and oleate oxidation in MBH slices at 1 mm glucose treated or not with CpC (25 μm). K, oleate oxidation in MBH slices at 1 mm glucose ± etomoxir (200 μm). Results are shown as the means ± S.E. n = 4–5 per condition for Western blots, 5–6 per condition for glucose utilization, and 8–14 animals per condition for palmitate and oleate oxidation. Statistical analyses were performed with one-way ANOVA with Bonferroni post-tests except for oleate oxidation and quantitation of AMPK phosphorylation (unpaired Student's t test). *, **, and ***, p < 0.05, 0.01, and 0.001, respectively versus 0.5 and 1 mm glucose or vehicle. $$, p < 0.01 versus MBH.