Ejaz 2016 Diabetes
Ejaz A, Martinez-Guino L, Goldfine AB, Ribas-Aulinas F, De Nigris V, RibΓ³ S, Gonzalez-Franquesa A, Garcia-Roves PM, Li E, Dreyfuss JM, Gall W, Kim JK, Bottiglieri T, Villarroya F, Gerszten RE, Patti ME, Lerin C (2016) Dietary betaine supplementation increases Fgf21 levels to improve glucose homeostasis and reduce hepatic lipid accumulation in mice. Diabetes 65:902-12. |
Ejaz A, Martinez-Guino L, Goldfine AB, Ribas-Aulinas F, De Nigris V, Ribo S, Gonzalez-Franquesa A, Garcia-Roves PM, Li E, Dreyfuss JM, Gall W, Kim JK, Bottiglieri T, Villarroya F, Gerszten RE, Patti ME, Lerin C (2016) Diabetes
Abstract: Identifying markers of human insulin resistance may permit development of new approaches for treatment and prevention of type 2 diabetes. To this end, we analyzed the fasting plasma metabolome in metabolically characterized human volunteers across a spectrum of insulin resistance. We demonstrate that plasma betaine levels are reduced in insulin-resistant humans and correlate closely with insulin sensitivity. Moreover, betaine administration to mice with diet-induced obesity prevents the development of impaired glucose homeostasis, reduces hepatic lipid accumulation, increases white adipose oxidative capacity, and enhances whole-body energy expenditure. In parallel with these beneficial metabolic effects, betaine supplementation robustly increased hepatic and circulating fibroblast growth factor (Fgf)21 levels. Betaine administration failed to improve glucose homeostasis and liver fat content in Fgf21(-/-) mice, demonstrating that Fgf21 is necessary for betaine's beneficial effects. Together, these data indicate that dietary betaine increases Fgf21 levels to improve metabolic health in mice and suggest that betaine supplementation merits further investigation as a supplement for treatment or prevention of type 2 diabetes in humans.
Β© 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
β’ O2k-Network Lab: ES Barcelona Garcia-Roves PM, ES Barcelona IDIBAPS Hospital Clinic, SE Stockholm Morein T
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Pathology: Diabetes
Organism: Mouse Tissue;cell: Fat Preparation: Homogenate
Coupling state: LEAK, OXPHOS
Pathway: NS, Other combinations, ROX
HRR: Oxygraph-2k
PBI-Shredder, 2016-06