Intrauterine growth-restricted Yucatan miniature pigs experience early catch-up growth, leading to greater adiposity and impaired lipid metabolism as young adults

Abstract

Early nutrition has critical influences on cardiovascular disease risk in adulthood. The study objectives were to evaluate the impact of low birth weight on fasting and postprandial lipid metabolism and endothelium function in Yucatan miniature pigs. Intrauterine growth-restricted (IUGR) piglets (n = 6; 3 days old, 0.73 ± 0.04 kg) were paired with normal-weight (NW) same-sex littermates (n = 6; 1.11 ± 0.05 kg) and fed milk replacer ad libitum for 4 weeks. Thereafter, all pigs were fed a standard diet ad libitum for 5 h/day with growth, intakes, and blood samples collected for 8 months. At 9 months old, pigs were surgically fitted with venous catheters and an oral fat tolerance test was performed. At 10 months old, pigs were killed and endothelium-dependent and -independent vasodilations of isolated coronary arteries were measured using wire-myographs. IUGR pigs demonstrated catch-up growth (P < 0.05) in body weight and abdominal circumference prior to sexual maturity (<7 months old) and had more (P < 0.05) subcutaneous fat at 10 months old compared with NW pigs. IUGR pigs had consistently higher fasting plasma triglyceride concentrations from 5 to 10 months old and higher liver triglyceride and total cholesterol concentrations at 10 months old (P < 0.05). The fat tolerance test revealed delayed postprandial triglyceride clearance in IUGR pigs, but no differences in plaque formation or vascular reactivity. To conclude, IUGR and early postnatal catch-up growth are associated with increased overall body fat deposition and altered triglyceride metabolism in adult Yucatan miniature swine.

Prenatal ethanol exposure induces susceptibility to premature ovarian insufficiency

“…In the present study, the body weight gain rate of female PEE offspring rats at PW6 was significantly higher, and then gradually slowed down; at PW12, the body weight was significantly reduced, but the ovarian index was increased. Several studies have confirmed that IUGR offspring caused by adverse environment during pregnancy will have catch-up growth in the early postnatal period-that is, a state in which growth is accelerated due to nutritional status or environmental improvement after birth and is associated with increased levels of IGF1 in vivo (Jensen et al 2015, Myrie et al 2017. In the present study, the IGF1 signalling pathway was converted from the activated state at PW6 to relative inhibition at PW12.…”

Prenatal Exposure to a Maternal High Fat Diet Increases Hepatic Cholesterol Accumulation in Intrauterine Growth Restricted Rats in Part Through MicroRNA-122 Inhibition of Cyp7a1

“…IUGR female baboons have increased LDL cholesterol and a trend for increased triglycerides in adulthood ( Kuo et al, 2018 ). Male and female IUGR Yucatan miniature pigs had increase serum and hepatic triglycerides in adulthood ( Myrie et al, 2017 ). IUGR rats had increased serum and hepatic triglycerides in early adulthood ( Chen et al, 2016 ).…”

In utero substrate restriction by placental insufficiency or maternal undernutrition decreases optical redox ratio in foetal perirenal fat

“…These adaptations may allow the allocation of critical energy resources to mechanisms that support the survival and sparing of heart [16–18] and brain [19, 20] growth; although there is still an impact on the development of these vital organs. Poor foetal substrate supply can result from placental insufficiency or maternal undernutrition at different stages of gestation [21–23]. IUGR often results in catch up growth in postnatal life and is related to enhanced fat deposition, leading to an increased risk of developing metabolic diseases in adult life such as obesity, type 2 diabetes and cardiovascular diseases [18, 21, 22].…”

“…Poor foetal substrate supply can result from placental insufficiency or maternal undernutrition at different stages of gestation [21–23]. IUGR often results in catch up growth in postnatal life and is related to enhanced fat deposition, leading to an increased risk of developing metabolic diseases in adult life such as obesity, type 2 diabetes and cardiovascular diseases [18, 21, 22].…”