Matches in SemOpenAlex for { <https://semopenalex.org/work/W2567111941> ?p ?o ?g. }
- W2567111941 endingPage "162" @default.
- W2567111941 startingPage "150" @default.
- W2567111941 abstract "Background Obese individuals present with an increased inflammatory tone as compared to healthy, normal-weight individuals, which is associated with insulin resistance. One factor hypothesized to contribute to increased inflammation in obese and diabetic states is elevated blood endotoxin levels, a condition known as metabolic endotoxemia. In non-obese and insulin sensitive individuals, circulating endotoxin concentrations fluctuate over the course of the day with elevations in the post-prandial state that return to baseline levels in the post-absorptive state. Evidence suggests that high-fat feeding alters these fluctuations causing endotoxin levels to remain high throughout the day. The effects of alterations in endotoxin levels on glucose metabolism are not clearly understood. Purpose/Procedures The goal of this study was to determine the effects of both short-term and long-term increases in endotoxin (lipopolysaccharide, LPS) of a low magnitude on the glucose tolerance and insulin signaling in a human primary cell line as well as the effects of short-term endotoxin treatments on glucose homeostasis in a C57/Bl6 mouse model. First, we tested the hypothesis that short-term low-dose endotoxin treatments would augment insulin signaling and glycogen synthesis while long-term treatments would be disruptive in the cell culture model. Second, we examined if these short-term low dose treatments of endotoxin would contribute to similar improvements in whole-body glucose homeostasis in a mouse model. Main findings Contrary to our initial hypothesis, short-term endotoxin treatment had no effect on insulin signaling or glycogen synthesis, however long-term treatment indeed decreased glycogen synthesis (P < .05). Interestingly, short-term endotoxin treatment resulted in significant improvements in glucose homeostasis in the mouse model (P < .01); which is believed to be at least partly attributed to an inhibitory action of LPS on liver glucose production. Conclusions This research shows that low-magnitude, short-term changes in LPS can have significant effects on whole body glucose metabolism and this likely occurs through its direct actions on the liver. Additional studies are necessary to understand the mechanisms responsible for altered glucose metabolism in response to low magnitude changes in LPS levels." @default.
- W2567111941 created "2017-01-06" @default.
- W2567111941 creator A5013925849 @default.
- W2567111941 creator A5020025550 @default.
- W2567111941 creator A5026763431 @default.
- W2567111941 creator A5027028201 @default.
- W2567111941 creator A5030753588 @default.
- W2567111941 creator A5055135481 @default.
- W2567111941 creator A5076239980 @default.
- W2567111941 creator A5077744463 @default.
- W2567111941 creator A5085901278 @default.
- W2567111941 date "2017-03-01" @default.
- W2567111941 modified "2023-10-15" @default.
- W2567111941 title "Acute low-dose endotoxin treatment results in improved whole-body glucose homeostasis in mice" @default.
- W2567111941 cites W1501595810 @default.
- W2567111941 cites W1517160664 @default.
- W2567111941 cites W17913752 @default.
- W2567111941 cites W1923666344 @default.
- W2567111941 cites W1931191788 @default.
- W2567111941 cites W1965247049 @default.
- W2567111941 cites W1972934337 @default.
- W2567111941 cites W1977609213 @default.
- W2567111941 cites W1979956590 @default.
- W2567111941 cites W1985333297 @default.
- W2567111941 cites W1988317251 @default.
- W2567111941 cites W1991401793 @default.
- W2567111941 cites W2018066581 @default.
- W2567111941 cites W2021839146 @default.
- W2567111941 cites W2023632053 @default.
- W2567111941 cites W2028370541 @default.
- W2567111941 cites W2035104292 @default.
- W2567111941 cites W2037218238 @default.
- W2567111941 cites W2045271318 @default.
- W2567111941 cites W2058163002 @default.
- W2567111941 cites W2060454917 @default.
- W2567111941 cites W2067184340 @default.
- W2567111941 cites W2083260532 @default.
- W2567111941 cites W2093788957 @default.
- W2567111941 cites W2096876054 @default.
- W2567111941 cites W2097669656 @default.
- W2567111941 cites W2118769195 @default.
- W2567111941 cites W2128184967 @default.
- W2567111941 cites W2129911161 @default.
- W2567111941 cites W2129917444 @default.
- W2567111941 cites W2131536322 @default.
- W2567111941 cites W2133010654 @default.
- W2567111941 cites W2134100055 @default.
- W2567111941 cites W2140040700 @default.
- W2567111941 cites W2159001939 @default.
- W2567111941 cites W2160645541 @default.
- W2567111941 cites W2162898271 @default.
- W2567111941 cites W2163660677 @default.
- W2567111941 cites W2171831692 @default.
- W2567111941 cites W2180398604 @default.
- W2567111941 cites W2194294353 @default.
- W2567111941 cites W2196267615 @default.
- W2567111941 cites W2201071160 @default.
- W2567111941 cites W2217060260 @default.
- W2567111941 cites W2396817814 @default.
- W2567111941 cites W2414714594 @default.
- W2567111941 cites W2419150001 @default.
- W2567111941 cites W4230408420 @default.
- W2567111941 cites W42487677 @default.
- W2567111941 cites W769942964 @default.
- W2567111941 doi "https://doi.org/10.1016/j.metabol.2016.12.008" @default.
- W2567111941 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5319723" @default.
- W2567111941 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28183447" @default.
- W2567111941 hasPublicationYear "2017" @default.
- W2567111941 type Work @default.
- W2567111941 sameAs 2567111941 @default.
- W2567111941 citedByCount "3" @default.
- W2567111941 countsByYear W25671119412019 @default.
- W2567111941 countsByYear W25671119412023 @default.
- W2567111941 crossrefType "journal-article" @default.
- W2567111941 hasAuthorship W2567111941A5013925849 @default.
- W2567111941 hasAuthorship W2567111941A5020025550 @default.
- W2567111941 hasAuthorship W2567111941A5026763431 @default.
- W2567111941 hasAuthorship W2567111941A5027028201 @default.
- W2567111941 hasAuthorship W2567111941A5030753588 @default.
- W2567111941 hasAuthorship W2567111941A5055135481 @default.
- W2567111941 hasAuthorship W2567111941A5076239980 @default.
- W2567111941 hasAuthorship W2567111941A5077744463 @default.
- W2567111941 hasAuthorship W2567111941A5085901278 @default.
- W2567111941 hasBestOaLocation W25671119412 @default.
- W2567111941 hasConcept C126322002 @default.
- W2567111941 hasConcept C134018914 @default.
- W2567111941 hasConcept C17093226 @default.
- W2567111941 hasConcept C192118531 @default.
- W2567111941 hasConcept C2776914184 @default.
- W2567111941 hasConcept C2777391703 @default.
- W2567111941 hasConcept C2777499176 @default.
- W2567111941 hasConcept C2778754761 @default.
- W2567111941 hasConcept C2779306644 @default.
- W2567111941 hasConcept C3018667095 @default.
- W2567111941 hasConcept C62231903 @default.
- W2567111941 hasConcept C63645605 @default.
- W2567111941 hasConcept C71924100 @default.
- W2567111941 hasConcept C86803240 @default.