FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2113257598> ?p ?o ?g. }

• W2113257598 endingPage "1576" @default.
• W2113257598 startingPage "1566" @default.
• W2113257598 abstract "OBJECTIVE The nitric oxide/cGMP/cGMP-dependent protein kinase type I (cGKI) signaling pathway regulates cell functions that play a pivotal role in the pathogenesis of type 2 diabetes. However, the impact of a dysfunction of this pathway for glucose metabolism in vivo is unknown. RESEARCH DESIGN AND METHODS The expression of cGKI in tissues relevant to insulin action was analyzed by immunohistochemistry. The metabolic consequences of a genetic deletion of cGKI were studied in mice that express cGKI selectively in smooth muscle but not in other cell types (cGKI-SM mice). RESULTS In wild-type mice, cGKI protein was detected in hepatic stellate cells, but not in hepatocytes, skeletal muscle, fat cells, or pancreatic β-cells. Compared with control animals, cGKI-SM mice had higher energy expenditure in the light phase associated with lower body weight and fat mass and increased insulin sensitivity. Mutant mice also showed higher fasting glucose levels, whereas insulin levels and intraperitoneal glucose tolerance test results were similar to those in control animals. Interleukin (IL)-6 signaling was strongly activated in the liver of cGKI-SM mice as demonstrated by increased levels of IL-6, phospho-signal transducer and activator of transcription 3 (Tyr 705), suppressor of cytokine signaling-3, and serum amyloid A2. Insulin-stimulated tyrosine phosphorylation of the insulin receptor in the liver was impaired in cGKI-SM mice. The fraction of Mac-2–positive macrophages in the liver was significantly higher in cGKI-SM mice than in control mice. In contrast with cGKI-SM mice, conditional knockout mice lacking cGKI only in the nervous system were normal with respect to body weight, energy expenditure, fasting glucose, IL-6, and insulin action in the liver. CONCLUSIONS Genetic deletion of cGKI in non-neuronal cells results in a complex metabolic phenotype, including liver inflammation and fasting hyperglycemia. Loss of cGKI in hepatic stellate cells may affect liver metabolism via a paracrine mechanism that involves enhanced macrophage infiltration and IL-6 signaling." @default.
• W2113257598 created "2016-06-24" @default.
• W2113257598 creator A5013089574 @default.
• W2113257598 creator A5013276052 @default.
• W2113257598 creator A5015192785 @default.
• W2113257598 creator A5016573915 @default.
• W2113257598 creator A5033072669 @default.
• W2113257598 creator A5036652363 @default.
• W2113257598 creator A5038987369 @default.
• W2113257598 creator A5056393712 @default.
• W2113257598 creator A5063920431 @default.
• W2113257598 creator A5076128208 @default.
• W2113257598 creator A5079582665 @default.
• W2113257598 creator A5084404405 @default.
• W2113257598 date "2011-04-23" @default.
• W2113257598 modified "2023-10-16" @default.
• W2113257598 title "Genetic Ablation of cGMP-Dependent Protein Kinase Type I Causes Liver Inflammation and Fasting Hyperglycemia" @default.
• W2113257598 cites W1505538037 @default.
• W2113257598 cites W1686249319 @default.
• W2113257598 cites W1888639125 @default.
• W2113257598 cites W1973416470 @default.
• W2113257598 cites W1980548122 @default.
• W2113257598 cites W1985221989 @default.
• W2113257598 cites W1993418845 @default.
• W2113257598 cites W1998493448 @default.
• W2113257598 cites W2000326910 @default.
• W2113257598 cites W2003659422 @default.
• W2113257598 cites W2006617466 @default.
• W2113257598 cites W2010415102 @default.
• W2113257598 cites W2011255130 @default.
• W2113257598 cites W2020798985 @default.
• W2113257598 cites W2021581260 @default.
• W2113257598 cites W2022864747 @default.
• W2113257598 cites W2025223906 @default.
• W2113257598 cites W2028035581 @default.
• W2113257598 cites W2044705572 @default.
• W2113257598 cites W2056501772 @default.
• W2113257598 cites W2064119981 @default.
• W2113257598 cites W2068117750 @default.
• W2113257598 cites W2069711307 @default.
• W2113257598 cites W2069825098 @default.
• W2113257598 cites W2077523101 @default.
• W2113257598 cites W2079503496 @default.
• W2113257598 cites W2080999576 @default.
• W2113257598 cites W2081068397 @default.
• W2113257598 cites W2081153263 @default.
• W2113257598 cites W2086682722 @default.
• W2113257598 cites W2097447032 @default.
• W2113257598 cites W2102683312 @default.
• W2113257598 cites W2111288662 @default.
• W2113257598 cites W2112688747 @default.
• W2113257598 cites W2115993532 @default.
• W2113257598 cites W2118103351 @default.
• W2113257598 cites W2121486402 @default.
• W2113257598 cites W2122573546 @default.
• W2113257598 cites W2130078845 @default.
• W2113257598 cites W2131947494 @default.
• W2113257598 cites W2139415978 @default.
• W2113257598 cites W2140793658 @default.
• W2113257598 cites W2143305307 @default.
• W2113257598 cites W2144805282 @default.
• W2113257598 cites W2155824086 @default.
• W2113257598 cites W2158370326 @default.
• W2113257598 cites W2312553081 @default.
• W2113257598 cites W4249150518 @default.
• W2113257598 doi "https://doi.org/10.2337/db10-0760" @default.
• W2113257598 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3292332" @default.
• W2113257598 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21464444" @default.
• W2113257598 hasPublicationYear "2011" @default.
• W2113257598 type Work @default.
• W2113257598 sameAs 2113257598 @default.
• W2113257598 citedByCount "32" @default.
• W2113257598 countsByYear W21132575982013 @default.
• W2113257598 countsByYear W21132575982014 @default.
• W2113257598 countsByYear W21132575982015 @default.
• W2113257598 countsByYear W21132575982016 @default.
• W2113257598 countsByYear W21132575982017 @default.
• W2113257598 countsByYear W21132575982018 @default.
• W2113257598 countsByYear W21132575982019 @default.
• W2113257598 countsByYear W21132575982020 @default.
• W2113257598 crossrefType "journal-article" @default.
• W2113257598 hasAuthorship W2113257598A5013089574 @default.
• W2113257598 hasAuthorship W2113257598A5013276052 @default.
• W2113257598 hasAuthorship W2113257598A5015192785 @default.
• W2113257598 hasAuthorship W2113257598A5016573915 @default.
• W2113257598 hasAuthorship W2113257598A5033072669 @default.
• W2113257598 hasAuthorship W2113257598A5036652363 @default.
• W2113257598 hasAuthorship W2113257598A5038987369 @default.
• W2113257598 hasAuthorship W2113257598A5056393712 @default.
• W2113257598 hasAuthorship W2113257598A5063920431 @default.
• W2113257598 hasAuthorship W2113257598A5076128208 @default.
• W2113257598 hasAuthorship W2113257598A5079582665 @default.
• W2113257598 hasAuthorship W2113257598A5084404405 @default.
• W2113257598 hasBestOaLocation W21132575981 @default.
• W2113257598 hasConcept C112446052 @default.
• W2113257598 hasConcept C126322002 @default.
• W2113257598 hasConcept C134018914 @default.
• W2113257598 hasConcept C171958077 @default.

• next