title: Maternal taurine supplementation attenuates maternal fructose-induced metabolic and inflammatory dysregulation and partially reverses adverse metabolic programming in offspring.
abstract: Excessive fructose consumption is associated with insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD), and high fructose intake during pregnancy can lead to compromised fetal development in the rat. Evidence suggests that the amino acid taurine can ameliorate fructose-induced IR and NAFLD in nonpregnant animals. This study investigated the efficacy of taurine supplementation on maternal fructose-induced metabolic dysfunction and neonatal health. Time-mated Wistar rats were randomized to four groups during pregnancy and lactation: (a) control diet (CON), (b) CON supplemented with 1.5% taurine in drinking water (CT), (c) CON supplemented with fructose solution (F) and (d) F supplemented with taurine (FT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analyzed. Maternal hyperinsulinemia, increased homeostasis model assessment of IR indices and elevated proinflammatory cytokines were observed in F group and normalized in FT group. Maternal fructose-induced hepatic steatosis accompanied with increased liver weight was ameliorated with taurine supplementation. Maternal hepatic sterol regulatory element-binding protein-1c and fatty acid synthase expression was significantly increased in the F group compared to the CON, CT and FT groups. Neonatal hepatic phosphoenolpyruvate carboxykinase expression was increased in male F neonates compared to the CON, CT and FT groups and was increased in female F and FT neonates compared to CON and CT. Interleukin-1β expression was decreased in male CT and FT neonates compared to other male groups. Hepatic tumour necrosis factor receptor-1 was lower in the male FT group than the F group. These results demonstrate that maternal taurine supplementation can partially reverse fructose-induced maternal metabolic dysfunction and may ameliorate adverse developmental programming effects in offspring in a sex-specific manner.
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand.
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand.
authors.forename: C M
authors.initials: CM
authors.lastname: Reynolds
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand; Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
authors.forename: D M
authors.initials: DM
authors.lastname: Sloboda
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand.
authors.forename: C
authors.initials: C
authors.lastname: Gray
authors.affiliation: Liggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Auckland, New Zealand. Electronic address: m.vickers@auckland.ac.nz.
authors.forename: M H
authors.initials: MH
authors.lastname: Vickers
mesh_terms: D000818:Animals; D016207:Cytokines / Q000097:blood; D019587:Dietary Supplements; D064429:Fatty Acid Synthases / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D005260:Female; D047109:Fetal Development; D005632:Fructose / Q000009:adverse effects*; D018507:Gene Expression Regulation, Developmental; D007333:Insulin Resistance; D007774:Lactation / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000151:congenital / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D065626:Non-alcoholic Fatty Liver Disease / Q000209:etiology / Q000517:prevention & control; D009929:Organ Size; D011247:Pregnancy; D011897:Random Allocation; D017208:Rats, Wistar; D012727:Sex Characteristics; D051780:Sterol Regulatory Element Binding Protein 1 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D013654:Taurine / Q000627:therapeutic use*
chemical_list: D016207:Cytokines; C497389:Srebf1 protein, rat; D051780:Sterol Regulatory Element Binding Protein 1; D013654:Taurine; D005632:Fructose; D064429:Fatty Acid Synthases
keywords: Animal models; Developmental programming; Fatty liver disease; Fructose; Inflammation; Maternal nutrition; Taurine