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Publication
Exogenous GDF11, but not GDF8, reduces body weight and improves glucose
homeostasis in mice.
Authors Walker RG, Barrandon O, Poggioli T, Dagdeviren S, Carroll SH, Mills MJ, Mendello
KR, Gomez Y, Loffredo FS, Pancoast JR, Macias-Trevino C, Marts C, LeClair KB,
Noh HL, Kim T, Banks AS, Kim JK, Cohen DE, Wagers AJ, Melton DA, Lee RT
Submitted By Submitted Externally on 12/3/2021
Status Published
Journal Scientific reports
Year 2020
Date Published 3/1/2020
Volume : Pages 10 : 4561
PubMed Reference 32165710
Abstract Insulin resistance is associated with aging in mice and humans. We have
previously shown that administration of recombinant GDF11 (rGDF11) to aged mice
alters aging phenotypes in the brain, skeletal muscle, and heart. While the
closely related protein GDF8 has a role in metabolism, limited data are
available on the potential metabolic effects of GDF11 or GDF8 in aging. To
determine the metabolic effects of these two ligands, we administered rGDF11 or
rGDF8 protein to young or aged mice fed a standard chow diet, short-term
high-fat diet (HFD), or long-term HFD. Under nearly all of these diet
conditions, administration of exogenous rGDF11 reduced body weight by 3-17% and
significantly improved glucose tolerance in aged mice fed a chow (~30% vs.
saline) or HF (~50% vs. saline) diet and young mice fed a HFD (~30%). On the
other hand, exogenous rGDF8 showed signifcantly lesser effect or no effect at
all on glucose tolerance compared to rGDF11, consistent with data demonstrating
that GFD11 is a more potent signaling ligand than GDF8. Collectively, our
results show that administration of exogenous rGDF11, but not rGDF8, can reduce
diet-induced weight gain and improve metabolic homeostasis.




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