Changes in the expression of hypothalamic lipid sensing genes in rat model of intrauterine growth retardation (IUGR)

Antonella Puglianiello, Daniela Germani, Sara Antignani, Gianpaolo Scalia Tomba, Stefano Cianfarani

Research output: Contribution to journalArticlepeer-review

Abstract

Intrauterine growth retardation (IUGR) has been linked to the development of type 2 diabetes in later life. The mechanisms underlying this phenomenon are unknown. Recent data suggest that some of the molecular defects underlying type 2 diabetes reside in the CNS. The enzyme carnitine palmitoyltransferase-1 (CPT1) regulates long-chain fatty acid (LCFA) entry into mitochondria, where LCFA undergo β-oxidation. Hypothalamic inhibition of CPT1 decreases food intake and suppresses endogenous glucose production. Our aim was to investigate the effects of uterine artery ligation, a procedure that mimics uteroplacental insufficiency, on the CNS expression of CPT1 and other key enzymes of LCFA metabolism. Bilateral uterine artery ligation was performed on d 19 of gestation in the pregnant rat; sham-operated pregnant rats served as controls. Hypothalamus, cerebellum, hippocampus, and cortex were dissected and analyzed at birth by real-time PCR. Nonesterified fatty acid (NEFA) serum levels were significantly higher in IUGR pups (p <0.0001). In IUGR rats, the hypothalamic expression of CPT1 isoform C (p = 0.005) and acetyl-CoA carboxylase (ACC) isoforms alpha (p <0.05) and beta (p = 0.005) were significantly decreased. The data presented here support the hypothesis that an abnormal intrauterine milieu can induce changes in hypothalamic lipid sensing.

Original languageEnglish
Pages (from-to)433-437
Number of pages5
JournalPediatric Research
Volume61
Issue number4
DOIs
Publication statusPublished - Apr 2007

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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