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Publication
UCP1 is an essential mediator of the effects of methionine restriction on energy
balance but not insulin sensitivity.
Authors Wanders D, Burk DH, Cortez CC, Van NT, Stone KP, Baker M, Mendoza T, Mynatt RL,
Gettys TW
Submitted By Desiree Wanders on 8/5/2015
Status Published
Journal FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Year 2015
Date Published 6/1/2015
Volume : Pages 29 : 2603 - 2615
PubMed Reference 25742717
Abstract Dietary methionine restriction (MR) by 80% increases energy expenditure (EE),
reduces adiposity, and improves insulin sensitivity. We propose that the
MR-induced increase in EE limits fat deposition by increasing sympathetic
nervous system-dependent remodeling of white adipose tissue and increasing
uncoupling protein 1 (UCP1) expression in both white and brown adipose tissue.
In independent assessments of the role of UCP1 as a mediator of MR's effects on
EE and insulin sensitivity, EE did not differ between wild-type (WT) and
Ucp1(-/-) mice on the control diet, but MR increased EE by 31% and reduced
adiposity by 25% in WT mice. In contrast, MR failed to increase EE or reduce
adiposity in Ucp1(-/-) mice. However, MR was able to increase overall insulin
sensitivity by 2.2-fold in both genotypes. Housing temperatures used to minimize
(28°C) or increase (23°C) sympathetic nervous system activity revealed
temperature-independent effects of the diet on EE. Metabolomics analysis showed
that genotypic and dietary effects on white adipose tissue remodeling resulted
in profound increases in fatty acid metabolism within this tissue. These
findings establish that UCP1 is required for the MR-induced increase in EE but
not insulin sensitivity and suggest that diet-induced improvements in insulin
sensitivity are not strictly derived from dietary effects on energy balance.




Strains




Genes
SymbolDescription
Ucp1uncoupling protein 1, mitochondrial

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