Introduction The vast majority of brain insulin-like growth factor (IGF) studies have been done in rodent models. However, the fact that much of brain development that goes on during gestation (G) in primates occurs postnatally in laboratory rodents is a clear disadvantage in rodent models [1]. In addition, it is important to emphasize a point made by Rice and Barone that""""""""... both the visual and auditory systems of albino animals of all species are abnormal;therefore, albino rats or mice are a poor choice for assessment when the nervous system is of interest."""""""" [2]. This very important caveat makes it imperative that observations made in rats be confirmed in a primate model prior to assuming applicability to humans. The present application looks at the effects of 30% maternal (M) nutrient restriction (NR) on fetal brain development in a primate model, the baboon. The paradigm does not produce weight loss in the fetus;however as will be shown, it does produce dramatic reductions in many parameters in the developing brain. In addition, our 30% MNR paradigm reduces fetal blood urea nitrogen thus suggesting fetal NR and demonstrating that body weight is a very poor indicator of fetal NR. We have chosen to look at the frontal cortex since it is an area of the brain that has been shown in rodent models to be adversely affected by even relatively mild (isocaloric, two thirds less protein) nutrient restriction [3] and we wish to determine if a similar result will be seen in a primate model. In addition, we believe that NR effects in this area will be mirrored by detriments in other areas such as the cerebellum and accordingly, we will retain other brain areas for future studies. Investigations of this type cannot ethically be done in humans;this fact makes studies in a model with a brain that is similar to humans such as the baboon, all the more urgent. Without knowledge in this area, diagnostic procedures and therapies for deficits cannot be designed and strategies for pro-active interventions cannot be planned.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Program Projects (P01)
Project #
5P01HD021350-19
Application #
8129571
Study Section
Special Emphasis Panel (ZHD1)
Project Start
Project End
Budget Start
2010-08-01
Budget End
2011-07-31
Support Year
19
Fiscal Year
2010
Total Cost
$82,712
Indirect Cost
Name
University of Texas Health Science Center San Antonio
Department
Type
DUNS #
800772162
City
San Antonio
State
TX
Country
United States
Zip Code
78229
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Kuo, Anderson H; Li, Cun; Mattern, Vicki et al. (2018) Sex-dimorphic acceleration of pericardial, subcutaneous, and plasma lipid increase in offspring of poorly nourished baboons. Int J Obes (Lond) 42:1092-1096
Kuo, A H; Li, J; Li, C et al. (2017) Prenatal steroid administration leads to adult pericardial and hepatic steatosis in male baboons. Int J Obes (Lond) 41:1299-1302
Proffitt, J Michael; Glenn, Jeremy; Cesnik, Anthony J et al. (2017) Proteomics in non-human primates: utilizing RNA-Seq data to improve protein identification by mass spectrometry in vervet monkeys. BMC Genomics 18:877
Muralimanoharan, Sribalasubashini; Li, Cun; Nakayasu, Ernesto S et al. (2017) Sexual dimorphism in the fetal cardiac response to maternal nutrient restriction. J Mol Cell Cardiol 108:181-193
Li, Cun; Jenkins, Susan; Mattern, Vicki et al. (2017) Effect of moderate, 30 percent global maternal nutrient reduction on fetal and postnatal baboon phenotype. J Med Primatol 46:293-303

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