|UTHUS, ERIC - Former ARS Employee|
|JOHNSON, W - Former ARS Employee|
Submitted to: Annual Scientific Meeting NAASO, The Obesity Society
Publication Type: Abstract Only
Publication Acceptance Date: 9/9/2013
Publication Date: 11/11/2013
Citation: Claycombe, K.J., Roemmich, J.N., Uthus, E.O., Johnson, W.T. 2013. Maternal low protein diets decrease skeletal muscle growth, PGC-1alpha mRNA expression and mitochondrial oxidative respiration and increase obesity and insulin resistance in obesity prone Sprague-Dawley rats. Annual Scientific Meeting NAASO, The Obesity Society. www.obesityweek.com; 2013(S72).
Technical Abstract: Malnutrition during the fetal growth period followed by postnatal catch-up growth results in obesity and the development of type 2 diabetes (T2D). To determine whether a prenatal low protein diet followed by postnatal high fat diet increases propensity for obesity and T2D in offspring, obese-prone female Sprague-Dawley rats were fed 8% (low protein; LP) or 20% protein (normal protein; NP) diets 3 wks prior to mating. Dams were fed the same diet during pregnancy and lactation. Postnatally, male offspring were fed 10% (normal fat; NF) or 45% (high fat; HF) diets for 12 wks. Maternal LP and post natal HF diets resulted in offspring obesity and increased insulin resistance. Recent studies showed that reduction in peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1''' increases T2D risk due to decreased mitochondria biogenesis and oxidative metabolic function. No studies have tested whether maternal LP and postnatal HF diets influence muscle PGC-1''expression, mitochondria biogenesis, and mitochondrial oxidative respiratory functions. Current data showed that skeletal muscle PGC-1''mRNA'expression and mitochondrial oxygen consumption rate is decreased by maternal LP while postnatal HF diets had no effect. Mitochondria biogenesis, mRNA expression of mitochondrial biogenic factors including nuclear respiratory factor 1 (NRF1) and cytochrome c oxidase 1and 4 (COX-1 and 4) were unaffected by maternal LP and postnatal HF diets. Interestingly, skeletal muscle size was 12-17% smaller in the maternal LP group compared to NP group with corresponding decreases in insulin-like growth factor 1 and 2 (IGF-1 and 2) mRNA expression. Taken together these data suggest that maternal LP and postnatal HF diets increase risk for T2D by decreasing skeletal muscle growth, PGC-1''expression, and oxidative metabolic function.