Effects of Taurine Supplementation on Hepatic Markers of Inflammation and Lipid Metabolism in Mothers and Offspring in the Setting of Maternal Obesity

Abstract

Maternal obesity is associated with obesity and metabolic disorders in offspring. However, intervention strategies to reverse or ameliorate the effects of maternal obesity on offspring health are limited. Following maternal undernutrition, taurine supplementation can improve outcomes in offspring, possibly via effects on glucose homeostasis and insulin secretion. The effects of taurine in mediating inflammatory processes as a protective mechanism has not been investigated. Further, the efficacy of taurine supplementation in the setting of maternal obesity is not known. Using a model of maternal obesity, we examined the effects of maternal taurine supplementation on outcomes related to inflammation and lipid metabolism in mothers and neonates. Time-mated Wistar rats were randomised to either: 1) control : control diet during pregnancy and lactation (CON); 2) CON supplemented with 1.5% taurine in drinking water (CT); 3) maternal obesogenic diet (high fat, high fructose) during pregnancy and lactation (MO); or 4) MO supplemented with taurine (MOT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analysed. A MO diet resulted in maternal hyperinsulinemia and hyperleptinemia and increased plasma glucose, glutamate and TNF-α concentrations. Taurine normalised maternal plasma TNF-α and glutamate concentrations in MOT animals. Both MO and MOT mothers displayed evidence of fatty liver accompanied by alterations in key markers of hepatic lipid metabolism. MO neonates displayed a pro-inflammatory hepatic profile which was partially rescued in MOT offspring. Conversely, a pro-inflammatory phenotype was observed in MOT mothers suggesting a possible maternal trade-off to protect the neonate. Despite protective effects of taurine in MOT offspring, neonatal mortality was increased in CT neonates, indicating possible adverse effects of taurine in the setting of normal pregnancy. These data suggest that maternal taurine supplementation may ameliorate the adverse effects observed in offspring following a maternal obesogenic diet but these effects are dependent upon prior maternal nutritional background.

Maternal taurine supplementation attenuates maternal fructose-induced metabolic and inflammatory dysregulation and partially reverses adverse metabolic programming in offspring

“…These beneficial effects on glucose metabolism persist into adult life [23]. We have also shown recently that maternal taurine supplementation can modify maternal and offspring markers related to hepatic inflammation and lipid metabolism in the setting of maternal obesity [24].…”

“…Details on the protocol utilized for fructose and taurine supplementation have been published previously by our group [8,24]. Virgin Wistar rats were time mated at 100 days of age using an estrous cycle monitor (EC-40; Fine Science Tools, San Francisco, USA, USA), and mating was confirmed by the presence of spermatozoa following a vaginal lavage.…”

Taurine supplementation preserves hypothalamic leptin action in normal and protein-restricted mice fed on a high-fat diet

“…Solon et al (2012) reported that intracerebroventricular administration of Tau increased JAK2/STAT3 pathway activation. This amino acid also shows anti-inflammatory properties by decreasing cytokine levels in the brain and peripheral tissues (Lin et al 2013;Li et al 2013;Su et al 2014). In addition, hypothalamic pAkt/ Akt protein content was higher in CHT mice (Camargo et al 2013).…”

Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk

“…The outcome of maternal diet-induced obesity in animal models has been reviewed elsewhere (42) and will only be briefly reviewed here. In rodents, maternal HF diet during pregnancy and lactation induces obesity and hepatic steatosis in the offspring, irrespective of postnatal diet (43) and induces insulin and leptin resistance (44), hypertension (45), and hepatic inflammation in offspring (46). Sex-specific obesity risk and metabolic dysfunction have also been shown and have become a focus for some studies (47).…”