Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 Sep 11;9(1):80.
doi: 10.1186/1743-7075-9-80.

Early postnatal low-protein nutrition, metabolic programming and the autonomic nervous system in adult life

Affiliations

Early postnatal low-protein nutrition, metabolic programming and the autonomic nervous system in adult life

Júlio Cezar de Oliveira et al. Nutr Metab (Lond). .

Abstract

Protein restriction during lactation has been used as a rat model of metabolic programming to study the impact of perinatal malnutrition on adult metabolism. In contrast to protein restriction during fetal life, protein restriction during lactation did not appear to cause either obesity or the hallmarks of metabolic syndrome, such as hyperinsulinemia, when individuals reached adulthood. However, protein restriction provokes body underweight and hypoinsulinemia. This review is focused on the regulation of insulin secretion and the influence of the autonomic nervous system (ANS) in adult rats that were protein-malnourished during lactation. The data available on the topic suggest that the perinatal phase of lactation, when insulted by protein deficit, imprints the adult metabolism and thereby alters the glycemic control. Although hypoinsulinemia programs adult rats to maintain normoglycemia, pancreatic β-cells are less sensitive to secretion stimuli, such as glucose and cholinergic agents. These pancreatic dysfunctions may be attributed to an imbalance of ANS activity recorded in adult rats that experienced maternal protein restriction.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic model of metabolic programming resulting from a maternal low-protein diet during lactation, the “Thrifty phenotype hypothesis” and the development of metabolic disease in late life. ANS, Autonomic nervous system.

Similar articles

Cited by

References

    1. Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5–20. doi: 10.1093/bmb/60.1.5. - DOI - PubMed
    1. Hales CN, Barker DJ, Clark PM, Cox LJ, Fall C, Osmond C, Winter PD. Fetal and infant growth and impaired glucose tolerance at age 64. BMJ. 1991;303:1019–1022. doi: 10.1136/bmj.303.6809.1019. - DOI - PMC - PubMed
    1. Molendi-Coste O, Laborie C, Scarpa MC, Montel V, Vieau D, Breton C. Maternal perinatal undernutrition alters postnatal development of chromaffin cells in the male rat adrenal medulla. Neuroendocrinology. 2009;90:54–66. doi: 10.1159/000209222. - DOI - PubMed
    1. Sullivan EL, Grove KL. Metabolic imprinting in obesity. Forum Nutr. 2010;63:186–194. - PMC - PubMed
    1. de Oliveira JC, Scomparin DX, Andreazzi AE, Branco RC, Martins AG, Gravena C, Grassiolli S, Rinaldi W, Barbosa FB, Mathias PC. Metabolic imprinting by maternal protein malnourishment impairs vagal activity in adult rats. J Neuroendocrinol. 2011;23:148–157. doi: 10.1111/j.1365-2826.2010.02095.x. - DOI - PubMed

LinkOut - more resources