title: Maternal taurine supplementation in the late pregnant rat stimulates postnatal growth and induces obesity and insulin resistance in adult offspring.
abstract: An adequate supply of taurine during fetal life is important for normal beta-cell development and insulin action. An altered availability of taurine may programme glucose metabolism in utero and result in type 2 diabetes in adult age. We examined whether maternal taurine supplementation in late pregnant rats affects postnatal growth, adult body composition, insulin sensitivity and endogenous insulin secretion in intrauterine growth restricted (IUGR) and normal offspring. Uterine artery ligation or sham operations were performed on gestational day (GD) 19. Taurine supplementation was given to half of the dams from GD 18 until term, resulting in four groups of offspring: sham (n = 22), sham/taurine (n = 22), IUGR (n = 22) and IUGR/taurine (n = 24). The offspring were studied at 12 weeks of age. In offspring with normal birth weight, fetal taurine supplementation markedly stimulated postnatal growth. In sham/taurine females, fat depots, plasma free fatty acid and leptin concentrations were increased, and insulin sensitivity was reduced. Insulin sensitivity was unaltered in IUGR and IUGR/taurine offspring. However, whereas IUGR offspring showed little catch-up growth, 50% of IUGR/taurine animals displayed complete catch-up at 12 weeks of age, and these animals had increased fat depots and reduced insulin sensitivity. In conclusion, taurine supplementation in late gestation resulted in accelerated postnatal growth, which was associated with adult obesity and insulin resistance in both IUGR and normal offspring. This effect was particularly evident in females. These data suggest that fetal taurine availability is an important determinant for postnatal growth, insulin sensitivity and fat accumulation.
authors.affiliation: Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, Sweden. karin.hultman@neuro.gu.se
authors.forename: Karin
authors.initials: K
authors.lastname: Hultman
authors.forename: Camilla
authors.initials: C
authors.lastname: Alexanderson
authors.forename: Louise
authors.initials: L
authors.lastname: Mannerås
authors.forename: Mats
authors.initials: M
authors.lastname: Sandberg
authors.forename: Agneta
authors.initials: A
authors.lastname: Holmäng
authors.forename: Thomas
authors.initials: T
authors.lastname: Jansson
mesh_terms: D000273:Adipose Tissue / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001823:Body Composition; D001835:Body Weight; D005260:Female; D005865:Gestational Age; D015309:Glucose Clamp Technique; D006943:Hyperglycemia / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism / Q000502:physiology; D039382:Maternal Nutritional Physiological Phenomena / Q000187:drug effects; D009765:Obesity / Q000503:physiopathology / Q000517:prevention & control*; D010927:Placental Insufficiency / Q000188:drug therapy* / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000494:pharmacology*
chemical_list: D020738:Leptin; D013654:Taurine; D007334:Insulin-Like Growth Factor I