Sex-dimorphic acceleration of pericardial, subcutaneous, and plasma lipid increase in offspring of poorly nourished baboons

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Developmental programming by reduced maternal nutrition alters function in multiple offspring physiological systems, including lipid metabolism. We have shown that intrauterine growth restriction (IUGR) leads to offspring cardiovascular dysfunction with an accelerated aging phenotype in our nonhuman primate, baboon model. We hypothesized age-advanced pericardial fat and blood lipid changes. In pregnancy and lactation, pregnant baboons ate ad lib (control) or 70% ad lib diet (IUGR). We studied baboon offspring pericardial lipid deposition with magnetic resonance imaging at 5–6 years (human equivalent 20–24 years), skinfold thickness, and serum lipid profile at 8–9 years (human equivalent 32–36 years), comparing values with a normative life-course baboon cohort, 4–23 years. Increased pericardial fat deposition occurred in IUGR males but not females. Female but not male total cholesterol, low-density lipoprotein, and subcutaneous fat were increased with a trend of triglycerides increase. When comparing IUGR changes to values in normal older baboons, the increase in male apical pericardial fat was equivalent to advancing age by 6 years and the increase in female low-density lipoprotein to an increase of 3 years. We conclude that reduced maternal diet accelerates offspring lipid changes in a sex-dimorphic manner. The interaction between programming and accelerated lipogenesis warrants further investigation.

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We thank Dr Robert Lanford and the Southwest National Primate Center staff for their ongoing support of the baboon research program described in this article. We also acknowledge the technical support of Steven Rios, Sam Vega, Susan Jenkins, and McKenna Considine, as well as the administrative support of Karen Moore.


This work was supported by the National Institutes of Health 5P01HD021350 (to PWN), 5R24OD011183 (to PWN), 5K25DK089012 (to GDC) and 1R25EB016631 (to AHK). NIH grant OD P51 OD011133 was from the Office of Research Infrastructure Programs/Office of the Director. This work was supported in part by funding from the EU FP 7/HEALTH/GA No.: 279281: BrainAge–Impact of Prenatal Stress on BRAINAGEing as well as Julio C Palmaz Endowment for Excellence in Radiology Research Pilot Grant (to AHK).

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Correspondence to Anderson H Kuo.

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