RRC ID 65966
Author Matsumoto Y, Ishii M, Hasegawa S, Sekimizu K.
Title Enterococcus faecalis YM0831 suppresses sucrose-induced hyperglycemia in a silkworm model and in humans.
Journal Commun Biol
Abstract Hyperglycemia caused by excessive intake of sucrose leads to lifestyle-related diseases such as diabetes. Administration of a lactic acid bacterial strain to mice suppresses sucrose-induced hyperglycemia, but evidence for a similar effect in humans is lacking. Here we show that Enterococcus faecalis YM0831, identified using an in vivo screening system with silkworms, suppressed sucrose-induced hyperglycemia in humans. E. faecalis YM0831 also suppressed glucose-induced hyperglycemia in silkworms. E. faecalis YM0831 inhibited glucose uptake by the human intestinal epithelial cell line Caco-2. A transposon insertion mutant of E. faecalis YM0831, which showed decreased inhibitory activity against glucose uptake by Caco-2 cells, also exhibited decreased inhibitory activity against both sucrose-induced and glucose-induced hyperglycemia in silkworms. In human clinical trials, oral ingestion of E. faecalis YM0831 suppressed the increase in blood glucose in a sucrose tolerance test. These findings suggest that E. faecalis YM0831 inhibits intestinal glucose transport and suppresses sucrose-induced hyperglycemia in humans.
Volume 2
Pages 157
Published 2019-1-1
DOI 10.1038/s42003-019-0407-5
PII 407
PMID 31069266
PMC PMC6497652
MeSH Animals Biological Transport Bombyx / drug effects Bombyx / metabolism Bombyx / microbiology* Caco-2 Cells DNA Transposable Elements Disease Models, Animal Enterococcus faecalis / genetics Enterococcus faecalis / metabolism* Glucose / metabolism Glucose / pharmacology* Hemolymph / metabolism Hemolymph / microbiology Humans Hyperglycemia / chemically induced Hyperglycemia / microbiology Hyperglycemia / prevention & control* Intestinal Mucosa / metabolism Intestinal Mucosa / microbiology Mutagenesis, Insertional Sucrose / metabolism Sucrose / pharmacology* Symbiosis / physiology
IF 4.165