title: Taurine supplementation improves liver glucose control in normal protein and malnourished mice fed a high-fat diet.
abstract: METHODS
  Poor nutrition during the perinatal period is associated with an increased risk for metabolic syndrome in adulthood. Taurine (TAU) regulates β-cell function and glucose homeo-stasis. Here, we assessed the effects of TAU supplementation upon adiposity and glucose control in malnourished mice fed a high-fat diet (HFD).
  
  
  RESULTS
  Weaned male C57BL/6J mice were fed a control (14% protein - C) or a protein-restricted (6% protein - R) diet for 6 weeks. Afterwards, mice received or not an HFD for 8 weeks (CH and RH). Half of the HFDmice were supplemented with 5% TAU after weaning (CHT and RHT). Protein restriction led to typical malnutrition features. HFD increased body weight, adiposity, and led to hyperleptinemia, hyperphagia, glucose intolerance, and higher liver glucose output in RH and CH groups. Fasted R mice showed higher plasma adiponectin levels and increased phosphorylation of the AMP-activated protein kinase (p-AMPK) in the liver. These parameters were reduced in RH mice and increased p-AMPK persisted in RHT. TAU prevented obesity and improved glucose tolerance only in CHT, but liver glucose control was ameliorated in both supplemented groups. Better CHT liver glucose control was linked to increased Akt (thymoma viral proto-oncogene/protein kinase B) phosphorylation.
  
  
  CONCLUSIONS
  Malnourished mice fed an HFD developed obesity, glucose intolerance, and increased liver glucose output. TAU preserved only normal liver glucose control in RHT mice, an effect associated with increased liver p-AMPK content.
authors.affiliation: Departamento de Biologia Estrutural e Funcional, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil. thiagombatista84@gmail.com
authors.forename: Thiago M
authors.initials: TM
authors.lastname: Batista
authors.forename: Rosane A
authors.initials: RA
authors.lastname: Ribeiro
authors.forename: Priscilla M R
authors.initials: PM
authors.lastname: da Silva
authors.forename: Rafael L
authors.initials: RL
authors.lastname: Camargo
authors.forename: Pablo C B
authors.initials: PC
authors.lastname: Lollo
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Boschero
authors.forename: Everardo M
authors.initials: EM
authors.lastname: Carneiro
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D052242:Adiponectin / Q000097:blood; D050154:Adiposity / Q000187:drug effects; D000596:Amino Acids / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D059305:Diet, High-Fat / Q000009:adverse effects*; D019587:Dietary Supplements; D018149:Glucose Intolerance; D020738:Leptin / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D044342:Malnutrition / Q000178:diet therapy / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D013654:Taurine / Q000494:pharmacology*
chemical_list: D052242:Adiponectin; D000596:Amino Acids; D001786:Blood Glucose; D020738:Leptin; D013654:Taurine; D051057:Proto-Oncogene Proteins c-akt; D055372:AMP-Activated Protein Kinases