The Effect of Dietary Protein Imbalance during Pregnancy on the Growth, Metabolism and Circulatory Metabolome of Neonatal and Weaned Juvenile Porcine Offspring

Abstract

Protein imbalance during pregnancy affects women in underdeveloped and developing countries and is associated with compromised offspring growth and an increased risk of metabolic diseases in later life. We studied in a porcine model the glucose and urea metabolism, and circulatory hormone and metabolite profile of offspring exposed during gestation, to maternal isoenergetic low–high (LP-HC), high–low (HP-LC) or adequate (AP) protein–carbohydrate ratio diets. At birth, LP-HC were lighter and the plasma acetylcarnitine to free carnitine ratios at 1 day of life was lower compared to AP offspring. Plasma urea concentrations were lower in 1 day old LP-HC offspring than HP-LC. In the juvenile period, increased insulin concentrations were observed in LP-HC and HP-LC offspring compared to AP, as was body weight from HP-LC compared to LP-HC. Plasma triglyceride concentrations were lower in 80 than 1 day old HP-LC offspring, and glucagon concentrations lower in 80 than 1 day old AP and HP-LC offspring. Plasma urea and the ratio of glucagon to insulin were lower in all 80 than 1 day old offspring. Aminoacyl-tRNA, arginine and phenylalanine, tyrosine and tryptophan metabolism, histidine and beta-alanine metabolism differed between 1 and 80 day old AP and HP-LC offspring. Maternal protein imbalance throughout pregnancy did not result in significant consequences in offspring metabolism compared to AP, indicating enormous plasticity by the placenta and developing offspring.

Determination of the Effects of Duodenal Infusion Soy Protein Hydrolysate on Hepatic Glucose and Lipid Metabolism in Pigs Through Multi-Omics Analysis

“…ACSL6 converts long-chain fatty acids to acyl-CoAs ( 30 ). Previous studies showed that HP intake increased the concentration of lysine and methionine, which increased l -carnitine production in the liver in pigs ( 31 , 32 ). l -carnitine can transport acyl-CoA into the mitochondrial matrix to promote fatty acid β-oxidation, which can be biosynthesized by l -lysine and l -methionine as substrates in the body ( 33 ), suggesting that SPH infusion accelerates fatty acid β-oxidation in the liver.…”