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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #333693
Title: Nutrition, genetic programming and immunometabolism

Author
item Larson, Kate
item DEKREY, EMILIE - University Of North Dakota
item Roemmich, James

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 4/25/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Diets with high saturated fat increase inflammation, insulin resistance, and obesity resulting in greater risk of as type 2 diabetes mellitus and other chronic diseases. However, it is not yet known whether the maternal diet influences offspring inflammatory responses to alter offspring metabolic disease risks. Previously, we demonstrated that a maternal low (8%) protein (LP) diet followed by a 45% high fat (HF) diet fed to the rat offspring resulted in offspring obesity and insulin resistance induced by epigenetic and metabolic gene expression mechanisms in white and brown adipose tissue, skeletal muscle, and placental tissue. In white adipose tissue, we demonstrated that offspring obesity and type 2 diabetes risk was associated with: 1. greater subcutaneous adipose tissue growth via increased DNA methylation of Igf2 gene; 2. decreased oxidative respiration via increased Sirt3 and decreased active form of succinate dehydrogenase (SDH) enzyme in skeletal muscle; 3. decreased beige adipocyte numbers, PR domain containing 16 (PRDM16), fibroblast growth factor 21 (FGF21), and CD137 mRNA expression and; 4. increased protein expression of an inhibitor of FGF21 transcription (histone methyltransferase, G9a). We have also found that a maternal LP diet decreased placental weight and iNKT cells while increasing TNFa producing macrophages. These results suggest that a maternal LP and postnatal HF diets results in placental inflammatory, offspring obesity, and insulin resistance due to epigenetic alterations in metabolic tissue functions.