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@ARTICLE{Maida:129107,
author = {A. Maida and A. Zota and K. A. Sjøberg and J.
Schumacher$^*$ and T. Sijmonsma$^*$ and A. Pfenninger and M.
M. Christensen and T. Gantert$^*$ and J. Fuhrmeister$^*$ and
U. Rothermel$^*$ and D. Schmoll and M. Heikenwälder$^*$ and
J. L. Iovanna and K. Stemmer and B. Kiens and S. Herzig and
A. J. Rose$^*$},
title = {{A} liver stress-endocrine nexus promotes metabolic
integrity during dietary protein dilution.},
journal = {The journal of clinical investigation},
volume = {126},
number = {9},
issn = {1558-8238},
address = {Ann Arbor, Mich.},
publisher = {ASCJ},
reportid = {DKFZ-2017-05112},
pages = {3263 - 3278},
year = {2016},
abstract = {Dietary protein intake is linked to an increased incidence
of type 2 diabetes (T2D). Although dietary protein dilution
(DPD) can slow the progression of some aging-related
disorders, whether this strategy affects the development and
risk for obesity-associated metabolic disease such as T2D is
unclear. Here, we determined that DPD in mice and humans
increases serum markers of metabolic health. In lean mice,
DPD promoted metabolic inefficiency by increasing
carbohydrate and fat oxidation. In nutritional and polygenic
murine models of obesity, DPD prevented and curtailed the
development of impaired glucose homeostasis independently of
obesity and food intake. DPD-mediated metabolic inefficiency
and improvement of glucose homeostasis were independent of
uncoupling protein 1 (UCP1), but required expression of
liver-derived fibroblast growth factor 21 (FGF21) in both
lean and obese mice. FGF21 expression and secretion as well
as the associated metabolic remodeling induced by DPD also
required induction of liver-integrated stress
response-driven nuclear protein 1 (NUPR1). Insufficiency of
select nonessential amino acids (NEAAs) was necessary and
adequate for NUPR1 and subsequent FGF21 induction and
secretion in hepatocytes in vitro and in vivo. Taken
together, these data indicate that DPD promotes improved
glucose homeostasis through an NEAA insufficiency-induced
liver NUPR1/FGF21 axis.},
keywords = {Basic Helix-Loop-Helix Transcription Factors (NLM
Chemicals) / DNA-Binding Proteins (NLM Chemicals) / Dietary
Proteins (NLM Chemicals) / Neoplasm Proteins (NLM Chemicals)
/ Nupr1 protein, mouse (NLM Chemicals) / P8 protein, human
(NLM Chemicals) / UCP1 protein, human (NLM Chemicals) / Ucp1
protein, mouse (NLM Chemicals) / Uncoupling Protein 1 (NLM
Chemicals) / fibroblast growth factor 21 (NLM Chemicals) /
Fibroblast Growth Factors (NLM Chemicals) / Glucose (NLM
Chemicals)},
cin = {F180 / G130 / A170 / A171},
ddc = {610},
cid = {I:(DE-He78)F180-20160331 / I:(DE-He78)G130-20160331 /
I:(DE-He78)A170-20160331 / I:(DE-He78)A171-20160331},
pnm = {323 - Metabolic Dysfunction as Risk Factor (POF3-323)},
pid = {G:(DE-HGF)POF3-323},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:27548521},
pmc = {pmc:PMC5004939},
doi = {10.1172/JCI85946},
url = {https://inrepo02.dkfz.de/record/129107},
}