ARS | Publication request: Low dietary protein intake during pregnancy differentially affects mitochondrial copy number in stromal vascular cells from subcutaneous versus visceral adipose tissue in the offspring

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: November 14, 2011
Publication Date: March 29, 2012
Citation: Johnson, W.T., Uthus, E.O., Claycombe, K.J. 2012. Low dietary protein intake during pregnancy differentially affects mitochondrial copy number in stromal vascular cells from subcutaneous versus visceral adipose tissue in the offspring. Federation of American Societies for Experimental Biology Conference. 26:128.3.

Technical Abstract: The present study examined the influence of protein intake during pregnancy on mitochondrial metabolism in stromal vascular cells from subcutaneous (SVSu) and visceral (SVVi) adipose tissue of offspring fed a high fat diet. Obese-prone Sprague-Dawley rats were fed diets containing either 8% or 20% protein throughout pregnancy and lactation. Male weanling offspring were fed diets with 20% protein and and either 10% fat (NF) or 45% fat (HF) for 12 wks. The mitochondrial copy number showed a 5X increase in SVCu in offspring fed HE whose dams were fed normal protein compared to a 1.5X increase in offspring in offspring fed HE but whose dams were fed low protein. Neither pre- nor postnatal diets influenced mitochondrial number in SVVi. This finding suggests that prenatal protein intake and postnatal fat intake may differentially affect mitochondrial metabolism in SVSu versus SVVi. Although dietary treatments did not affect cellular respiration as measured with a Seahorse XF24 Analyzer with 5 mM glucose and 1mM pyruvate using cultured cells, SVSu exhibited lower maximum O2 consumption and lower reserve respiratory capacity than SVVi. Lower reserve capacity suggests that SVSu in offspring may not be able to sufficiently respond metabolically to HE diets and adapt by increasing mitochondrial biogenesis. Low prenatal protein intake during pregnancy may impair this adaptation in the offspring.