FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2945808868> ?p ?o ?g. }

• W2945808868 endingPage "F217" @default.
• W2945808868 startingPage "F207" @default.
• W2945808868 abstract "Na + -glucose cotransporter (SGLT)1 mediates glucose reabsorption in late proximal tubules. SGLT1 also mediates macula densa (MD) sensing of an increase in luminal glucose, which increases nitric oxide (NO) synthase 1 (MD-NOS1)-mediated NO formation and potentially glomerular filtratrion rate (GFR). Here, the contribution of SGLT1 was tested by gene knockout (−/−) in type 1 diabetic Akita mice. A low-glucose diet was used to prevent intestinal malabsorption in Sglt1 −/− mice and minimize the contribution of intestinal SGLT1. Hyperglycemia was modestly reduced in Sglt1 −/− versus littermate wild-type Akita mice (480 vs. 550 mg/dl), associated with reduced diabetes-induced increases in GFR, kidney weight, glomerular size, and albuminuria. Blunted hyperfiltration was confirmed in streptozotocin-induced diabetic Sglt1 −/− mice, associated with similar hyperglycemia versus wild-type mice (350 vs. 385 mg/dl). Absence of SGLT1 attenuated upregulation of MD-NOS1 protein expression in diabetic Akita mice and in response to SGLT2 inhibition in nondiabetic mice. During SGLT2 inhibition in Akita mice, Sglt1 −/− mice had likewise reduced blood glucose (200 vs. 300 mg/dl), associated with lesser MD-NOS1 expression, GFR, kidney weight, glomerular size, and albuminuria. Absence of Sglt1 in Akita mice increased systolic blood pressure, associated with suppressed renal renin mRNA expression. This may reflect fluid retention due to blunted hyperfiltration. SGLT2 inhibition prevented the blood pressure increase in Sglt1 −/− Akita mice, possibly due to additive glucosuric/diuretic effects. The data indicate that SGLT1 contributes to diabetic hyperfiltration and limits diabetic hypertension. Potential mechanisms include its role in glucose-driven upregulation of MD-NOS1 expression. This pathway may increase GFR to maintain volume balance when enhanced MD glucose delivery indicates upstream saturation of SGLTs and thus hyperreabsorption." @default.
• W2945808868 created "2019-05-29" @default.
• W2945808868 creator A5009882078 @default.
• W2945808868 creator A5014319544 @default.
• W2945808868 creator A5020811053 @default.
• W2945808868 creator A5021651367 @default.
• W2945808868 creator A5039715058 @default.
• W2945808868 creator A5040810589 @default.
• W2945808868 creator A5042239404 @default.
• W2945808868 creator A5045686015 @default.
• W2945808868 creator A5064438527 @default.
• W2945808868 creator A5067491779 @default.
• W2945808868 creator A5074354992 @default.
• W2945808868 creator A5085734264 @default.
• W2945808868 date "2019-07-01" @default.
• W2945808868 modified "2023-10-17" @default.
• W2945808868 title "Knockout of Na⁺-glucose cotransporter SGLT1 mitigates diabetes-induced upregulation of nitric oxide synthase NOS1 in the macula densa and glomerular hyperfiltration" @default.
• W2945808868 cites W1540594287 @default.
• W2945808868 cites W1569391814 @default.
• W2945808868 cites W1965294836 @default.
• W2945808868 cites W1966187721 @default.
• W2945808868 cites W1990025047 @default.
• W2945808868 cites W2000806054 @default.
• W2945808868 cites W2004582643 @default.
• W2945808868 cites W2013448178 @default.
• W2945808868 cites W2027545319 @default.
• W2945808868 cites W2029954557 @default.
• W2945808868 cites W2060577101 @default.
• W2945808868 cites W2063116226 @default.
• W2945808868 cites W2108244474 @default.
• W2945808868 cites W2112710337 @default.
• W2945808868 cites W2113687888 @default.
• W2945808868 cites W2115385271 @default.
• W2945808868 cites W2128814368 @default.
• W2945808868 cites W2134415018 @default.
• W2945808868 cites W2139137948 @default.
• W2945808868 cites W2140379794 @default.
• W2945808868 cites W2141228342 @default.
• W2945808868 cites W2142065502 @default.
• W2945808868 cites W2144862658 @default.
• W2945808868 cites W2146609045 @default.
• W2945808868 cites W2150192337 @default.
• W2945808868 cites W2159258864 @default.
• W2945808868 cites W2160471487 @default.
• W2945808868 cites W2164080605 @default.
• W2945808868 cites W2164368208 @default.
• W2945808868 cites W2166826914 @default.
• W2945808868 cites W2241870771 @default.
• W2945808868 cites W2286283267 @default.
• W2945808868 cites W2309487596 @default.
• W2945808868 cites W2419476487 @default.
• W2945808868 cites W2424539745 @default.
• W2945808868 cites W2553261268 @default.
• W2945808868 cites W2584401577 @default.
• W2945808868 cites W2626446274 @default.
• W2945808868 cites W2748154087 @default.
• W2945808868 cites W2756191633 @default.
• W2945808868 cites W2810892857 @default.
• W2945808868 cites W2898733623 @default.
• W2945808868 cites W2922268276 @default.
• W2945808868 cites W2936122593 @default.
• W2945808868 doi "https://doi.org/10.1152/ajprenal.00120.2019" @default.
• W2945808868 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6692722" @default.
• W2945808868 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31091127" @default.
• W2945808868 hasPublicationYear "2019" @default.
• W2945808868 type Work @default.
• W2945808868 sameAs 2945808868 @default.
• W2945808868 citedByCount "36" @default.
• W2945808868 countsByYear W29458088682019 @default.
• W2945808868 countsByYear W29458088682020 @default.
• W2945808868 countsByYear W29458088682021 @default.
• W2945808868 countsByYear W29458088682022 @default.
• W2945808868 countsByYear W29458088682023 @default.
• W2945808868 crossrefType "journal-article" @default.
• W2945808868 hasAuthorship W2945808868A5009882078 @default.
• W2945808868 hasAuthorship W2945808868A5014319544 @default.
• W2945808868 hasAuthorship W2945808868A5020811053 @default.
• W2945808868 hasAuthorship W2945808868A5021651367 @default.
• W2945808868 hasAuthorship W2945808868A5039715058 @default.
• W2945808868 hasAuthorship W2945808868A5040810589 @default.
• W2945808868 hasAuthorship W2945808868A5042239404 @default.
• W2945808868 hasAuthorship W2945808868A5045686015 @default.
• W2945808868 hasAuthorship W2945808868A5064438527 @default.
• W2945808868 hasAuthorship W2945808868A5067491779 @default.
• W2945808868 hasAuthorship W2945808868A5074354992 @default.
• W2945808868 hasAuthorship W2945808868A5085734264 @default.
• W2945808868 hasBestOaLocation W29458088681 @default.
• W2945808868 hasConcept C126322002 @default.
• W2945808868 hasConcept C134018914 @default.
• W2945808868 hasConcept C185592680 @default.
• W2945808868 hasConcept C198710026 @default.
• W2945808868 hasConcept C2776174234 @default.
• W2945808868 hasConcept C2776179406 @default.
• W2945808868 hasConcept C2777622882 @default.
• W2945808868 hasConcept C2779922275 @default.
• W2945808868 hasConcept C2780091579 @default.
• W2945808868 hasConcept C2781236342 @default.
• W2945808868 hasConcept C519581460 @default.

• next