| Title: | Taurine supplementation in high-fat diet fed male mice attenuates endocrine pancreatic dysfunction in their male offspring |
| Author(s): | Freitas IN; Dos Reis Araujo T; Vettorazzi JF; Magalhaes EA; Carneiro EM; Bonfleur ML; Ribeiro RA; |
| Address: | "Universidade Federal do Rio de Janeiro, Campus UFRJ-Macae, Avenida Sao Jose do Barreto, 764, Macae, RJ, CEP 27965-045, Brazil. Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, Brazil. Centro de Ciencias Biologicas e da Saude, Universidade Estadual do Oeste do Parana (UNIOESTE), Cascavel, PR, Brazil. Universidade Federal do Rio de Janeiro, Campus UFRJ-Macae, Avenida Sao Jose do Barreto, 764, Macae, RJ, CEP 27965-045, Brazil. rosaneribeirobio@gmail.com" |
| DOI: | 10.1007/s00726-019-02712-7 |
| ISSN/ISBN: | 1438-2199 (Electronic) 0939-4451 (Linking) |
| Abstract: | "Obesity in fathers leads to DNA damage and epigenetic changes in sperm that may carry potential risk factors for metabolic diseases to the next generation. Taurine (TAU) supplementation has demonstrated benefits against testicular dysfunction and pancreatic islet impairments induced by obesity, but it is not known if these protective actions prevent the propagation of metabolic disruptions to the next generation; as such, we hypothesized that paternal obesity may increase the probability of endocrine pancreatic dysfunction in offspring, and that this could be prevented by TAU supplementation in male progenitors. To test this, male C57Bl/6 mice were fed on a control diet (CTL) or a high-fat diet (HFD) without or with 5% TAU in their drinking water (CTAU and HTAU) for 4 months. Subsequently, all groups of mice were mated with CTL females, and the F1 offspring were identified as: CTL-F1, CTAU-F1, HFD-F1, and HTAU-F1. HFD-fed mice were normoglycemic, but glucose intolerant and their islets hypersecreted insulin. However, at 90 days of age, HFD-F1 offspring displayed normal glucose homeostasis and adiposity, but reduced glucose-induced insulin release. HFD-F1 islets also exhibited beta- and alpha-cell hypotrophy, and lower delta-cell number per islet. Paternal TAU supplementation prevented the decrease in glucose-induced insulin secretion and normalized beta-cell size and delta-cell number, and increased alpha-cell size/islet in HTAU-F1 mice. In conclusion, HFD consumption by male founders decreases beta-cell secretion and islet-cell distribution in their offspring. TAU attenuates the deleterious effects of paternal obesity on insulin secretion and islet-cell morphology in F1 offspring" |
| Keywords: | "Animals Diet, High-Fat/*adverse effects *Dietary Supplements Endocrine System/*drug effects/physiopathology Glucose Intolerance/*drug therapy/etiology/pathology Homeostasis Insulin Secretion Islets of Langerhans/*drug effects/physiopathology Male Mice Mic;" |
| Notes: | "MedlineFreitas, Israelle Netto Dos Reis Araujo, Thiago Vettorazzi, Jean Franciesco Magalhaes, Emily Amorim Carneiro, Everardo Magalhaes Bonfleur, Maria Lucia Ribeiro, Rosane Aparecida eng E-26/203.632/2015/Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro/ Austria 2019/03/05 Amino Acids. 2019 Apr; 51(4):727-738. doi: 10.1007/s00726-019-02712-7. Epub 2019 Mar 4" |
