Fig. 5.

CNS NPY signaling via the Y1 receptor induces hepatic stearoyl-CoA desaturase-1 (SCD-1) gene expression. A and B: representative immunoblots of key lipid metabolic markers involved in VLDL assembly and secretion are shown. Protein extracts prepared from livers of 4-h-fasted lean rats (n = 5–7/group) isolated 60 or 120 min after icv injection of NPY (1 nmol) or Veh (A) or Y1 receptor agonist ([F7, P34]-NPY, 1 nmol) or Veh (B) were immunoblotted to detect levels of phosphorylated acetyl-CoA carboxylase (ACC; Ser⁷⁹), ACC, fatty acid synthase (FAS), apolipoprotein B-48 (apoB-48), and microsomal TG transfer protein (MTP). Western blots were analyzed by densitometry (normalized to Veh control) for icv NPY treatment at 60 (open bars) and 120 min (black bars) postinjection (A) and icv Y1 receptor agonist treatment at 60 (open bars) and 120 min (gray bars) postinjection (B). Densitometry results were corrected relative to those of the protein loading control GAPDH, actin, or heat shock protein 70 (HSP70). C and D: RNA were isolated from livers of 4-h-fasted rats that were obtained 60 or 120 min after treatment with icv NPY (black bars) or Veh (open bars) (C) or ICV Y1 receptor agonist (gray bars) or Veh (open bars) (D) and were assessed by quantitative RT-PCR for changes in SCD-1 mRNA levels. SCD-1 mRNA levels, normalized to the reference RNA ribosomal protein L13a (RPL13a), are shown. For comparative analysis, RNA ratios were normalized to the Veh control. Data are means ± SE and were analyzed by Student's t-test (unpaired, 2-tailed). *Significant difference (P < 0.05) between icv treatment and Veh.