|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print May 15, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00037.2002
Submitted on January 22, 2002
Accepted on May 13, 2002
1 Nutrition, CNRS-UMR 7059, Paris, France
2 Biochimie, Hopital Robert-Debre, Reims, France
3 Biochimie, Centre de recherche Merck-Lipha, Chilly-Mazarin, France
* To whom correspondence should be addressed. E-mail: ebertin{at}chu-reims.fr.
Fetal malnutrition is now proposed as a risk factor of later obesity and type 2 diabetes. We previously analysed the long term impact of reduced protein and/or energy intake strictly limited to the last week of pregnancy in Wistar rats. Three protocols of gestational malnutrition were used : low protein isocaloric diet (5% instead of 15%) with pair-feeding to the mothers receiving the control diet; restricted diet (50% of control diet); low-protein restricted diet (50% of low protein diet). Only isolated protein restriction induced a long term ß-cell mass decrease. In the present study, we have used the same protocols of food restriction to analyse their short term impact (on 21.5 day of pregnancy) on ß-cell mass development. A 50% ß-cell mass decrease was present in the three restricted groups, but low protein diet, either associated or not to energy restriction, increased fetal ß-cell insulin content. Among all the parameters analysed to further explain our results, we found that the fetal plasma level of taurine was lowered by low protein diet, and was the main predictor of the fetal plasma insulin level (r = 0.63, p<0.01). In conclusion, rat fetuses exposed to protein and/or energy restriction during the third part of pregnancy have a similar dramatic decrease in ß-cell mass, and their ability to recover ß-cell mass development retardation depends on the type of malnutrition used. Moreover, our results support the hypothesis that taurine might play an important role on fetal ß-cell mass function.
This article has been cited by other articles:
![]() |
M. V. Chakravarthy, Y. Zhu, M. B. Wice, T. Coleman, K. L. Pappan, C. A. Marshall, M. L. McDaniel, and C. F. Semenkovich Decreased Fetal Size Is Associated With {beta}-Cell Hyperfunction in Early Life and Failure With Age Diabetes, October 1, 2008; 57(10): 2698 - 2707. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Fernandez, M. A. Martin, S. Fajardo, D. Bailbe, M. N. Gangnerau, B. Portha, F. Escriva, P. Serradas, and C. Alvarez Undernutrition does not alter the activation of beta-cell neogenesis and replication in adult rats after partial pancreatectomy Am J Physiol Endocrinol Metab, November 1, 2006; 291(5): E913 - E921. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. C. Mcmillen and J. S. Robinson Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming Physiol Rev, April 1, 2005; 85(2): 571 - 633. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Martin, E. Fernandez, A. M. Pascual-Leone, F. Escriva, and C. Alvarez Protein calorie restriction has opposite effects on glucose metabolism and insulin gene expression in fetal and adult rat endocrine pancreas Am J Physiol Endocrinol Metab, April 1, 2004; 286(4): E542 - E550. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |