Taurine supplementation improves liver glucose control in normal protein and malnourished mice fed a high-fat diet
Article first published online: 26 DEC 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 57, Issue 3, pages 423–434, March 2013
How to Cite
Batista, T. M., Ribeiro, R. A., da Silva, P. M. R., Camargo, R. L., Lollo, P. C. B., Boschero, A. C. and Carneiro, E. M. (2013), Taurine supplementation improves liver glucose control in normal protein and malnourished mice fed a high-fat diet. Mol. Nutr. Food Res., 57: 423–434. doi: 10.1002/mnfr.201200345
- Issue published online: 12 MAR 2013
- Article first published online: 26 DEC 2012
- Manuscript Accepted: 23 OCT 2012
- Manuscript Revised: 11 OCT 2012
- Manuscript Received: 2 JUN 2012
- Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
- Conselho Nacional para o Desenvolvimento Científico e Tecnológico (CNPq)
- Instituto Nacional de Ciência e Tecnologia (INCT)
- Glucose homeostasis;
- Insulin resistance;
- Protein malnutrition;
- Taurine supplementation
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).
Methods and 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.
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.