RESUMO
BACKGROUND: Perinatal exposure to a poor nutritional environment predisposes the progeny to the development of metabolic disease at the adult age, both in experimental models and humans. Numerous adaptive responses to maternal protein restriction have been reported in metabolic tissues. However, the expression of glucose/fatty acid metabolism-related genes in adipose tissue and liver needs to be described. AIM: To evaluate the metabolic impact of perinatal malnutrition, we determined malnutrition-associated gene expression alterations in liver and adipose tissue. METHODS: In the present study, we evaluated the alterations in gene expression of glycolytic/Krebs cycle genes (Pyruvate dehydrogenase kinase 4 and citrate synthase), adipogenic and lipolytic genes and leptin in the adipose tissue of offspring rats at 30 d and 90 d of age exposed to maternal isocaloric low protein (LP) diet throughout gestation and lactation. We also evaluated, in the livers of the same animals, the same set of genes as well as the gene expression of the transcription factors peroxisome proliferator-activated receptor gamma coactivator 1, forkhead box protein O1 and hepatocyte nuclear factor 4 and of gluconeogenic genes. RESULTS: In the adipose tissue, we observed a transitory (i.e., at 30 d) downregulation of pyruvate dehydrogenase kinase 4, citrate synthase and carnitine palmitoyl transferase 1b gene expression. Such transcriptional changes did not persist in adult LP rats (90 d), but we observed a tendency towards a decreased gene expression of leptin (P = 0.052). The liver featured some gene expression alterations comparable to the adipose tissue, such as pyruvate dehydrogenase kinase 4 downregulation at 30 d and displayed other tissue-specific changes, including citrate synthase and fatty acid synthase upregulation, but pyruvate kinase downregulation at 30 d in the LP group and carnitine palmitoyl transferase 1b downregulation at 90 d. These gene alterations, together with previously described changes in gene expression in skeletal muscle, may account for the metabolic adaptations in response to maternal LP diet and highlight the occurrence of persistent transcriptional defects in key metabolic genes that may contribute to the development of metabolic alterations during the adult life as a consequence of perinatal malnutrition. CONCLUSION: We conclude that perinatal malnutrition relays long-lasting transcriptional alterations in metabolically active organs, i.e., liver and adipose tissue.