Altered tissue mineralization, increased hepatic lipid and inhibited autophagy in intrauterine growth retardation piglets

Mineral homeostasis is often disrupted in intrauterine growth retardation (IUGR) infants. Most studies focus on calcium or phosphorus metabolism of IUGR infants via determining serum mineral concentrations instead of tissues. This study was conducted to investigate the effects of IUGR on the mineralization and physiological functions of tissue in a piglet model. Six normal birth weight (NBW) and six IUGR neonatal piglets were slaughtered at 35 days. Mineral concentrations in blood and selected tissues (liver, kidney, lungs, heart, and longissimus dorsi muscle (LDM)), hepatic lipid, mRNA expressions of magnesium (Mg) metabolism, and autophagy were analysed. Results showed that IUGR pigs showed significantly lower phosphorus (P) in LDM, and lower Mg in the liver and LDM, and higher Mg in lungs than NBW pigs. There were no significant differences in concentrations of selenium (Se), calcium (Ca), copper (Cu), aluminium (Al), and lithium (Li) in selected tissues. IUGR pigs had similar mRNA expression of TRPM7 and MagT1 to NBW pigs, but significantly lower expressions of HNF1B and Mrs2 in the liver than NBW pigs. Hepatic triglyceride was significantly increased, and MAP1LC3B expression was significantly decreased in IUGR pigs compared with those of NBW pigs. These result suggested that IUGR pigs had tissue mineralization disturbance, especially for Mg, and liver dysfunction (increased hepatic lipid and inhibited autophagy). Hepatic Mg deficiency might result from increased Mg efflux via reducing HNF1B expression.