FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2000714609> ?p ?o ?g. }

• W2000714609 endingPage "e25231" @default.
• W2000714609 startingPage "e25231" @default.
• W2000714609 abstract "A link between circadian rhythm and metabolism has long been discussed. Circadian rhythm is controlled by positive and negative transcriptional and translational feedback loops composed of several clock genes. Among clock genes, the brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor output cycles kaput (CLOCK) play important roles in the regulation of the positive rhythmic transcription. In addition to control of circadian rhythm, we have previously shown that BMAL1 regulates adipogenesis. In metabolic syndrome patients, the function of BMAL1 is dysregulated in visceral adipose tissue. In addition, analysis of SNPs has revealed that BMAL1 is associated with susceptibility to hypertension and type II diabetes. Furthermore, the significant roles of BMAL1 in pancreatic β cells proliferation and maturation were recently reported. These results suggest that BMAL1 regulates energy homeostasis. Therefore, in this study, we examined whether loss of BMAL1 function is capable of inducing metabolic syndrome. Deficient of the Bmal1 gene in mice resulted in elevation of the respiratory quotient value, indicating that BMAL1 is involved in the utilization of fat as an energy source. Indeed, lack of Bmal1 reduced the capacity of fat storage in adipose tissue, resulting in an increase in the levels of circulating fatty acids, including triglycerides, free fatty acids, and cholesterol. Elevation of the circulating fatty acids level induced the formation of ectopic fat in the liver and skeletal muscle in Bmal1 -/- mice. Interestingly, ectopic fat formation was not observed in tissue-specific (liver or skeletal muscle) Bmal1 -/- mice even under high fat diet feeding condition. Therefore, we were led to conclude that BMAL1 is a crucial factor in the regulation of energy homeostasis, and disorders of the functions of BMAL1 lead to the development of metabolic syndrome." @default.
• W2000714609 created "2016-06-24" @default.
• W2000714609 creator A5011979842 @default.
• W2000714609 creator A5030057038 @default.
• W2000714609 creator A5034662800 @default.
• W2000714609 creator A5044065716 @default.
• W2000714609 creator A5058521307 @default.
• W2000714609 creator A5059704901 @default.
• W2000714609 creator A5062627222 @default.
• W2000714609 creator A5063714751 @default.
• W2000714609 creator A5064690118 @default.
• W2000714609 creator A5065723905 @default.
• W2000714609 creator A5074545551 @default.
• W2000714609 creator A5077718624 @default.
• W2000714609 creator A5078462813 @default.
• W2000714609 creator A5082213845 @default.
• W2000714609 date "2011-09-22" @default.
• W2000714609 modified "2023-10-17" @default.
• W2000714609 title "Deficient of a Clock Gene, Brain and Muscle Arnt-Like Protein-1 (BMAL1), Induces Dyslipidemia and Ectopic Fat Formation" @default.
• W2000714609 cites W1530371171 @default.
• W2000714609 cites W1579719960 @default.
• W2000714609 cites W1979385177 @default.
• W2000714609 cites W1981990410 @default.
• W2000714609 cites W1984313233 @default.
• W2000714609 cites W1986248731 @default.
• W2000714609 cites W1992494470 @default.
• W2000714609 cites W1994994441 @default.
• W2000714609 cites W2002576833 @default.
• W2000714609 cites W2003302378 @default.
• W2000714609 cites W2020273326 @default.
• W2000714609 cites W2029818029 @default.
• W2000714609 cites W2032158359 @default.
• W2000714609 cites W2041772085 @default.
• W2000714609 cites W2047902467 @default.
• W2000714609 cites W2050363846 @default.
• W2000714609 cites W2053785118 @default.
• W2000714609 cites W2063041018 @default.
• W2000714609 cites W2073293204 @default.
• W2000714609 cites W2074633912 @default.
• W2000714609 cites W2088342838 @default.
• W2000714609 cites W2088348233 @default.
• W2000714609 cites W2092570634 @default.
• W2000714609 cites W2095790754 @default.
• W2000714609 cites W2096295878 @default.
• W2000714609 cites W2103049241 @default.
• W2000714609 cites W2108988707 @default.
• W2000714609 cites W2111330221 @default.
• W2000714609 cites W2115505876 @default.
• W2000714609 cites W2115783712 @default.
• W2000714609 cites W2121847288 @default.
• W2000714609 cites W2123789196 @default.
• W2000714609 cites W2123927456 @default.
• W2000714609 cites W2132468746 @default.
• W2000714609 cites W2137842897 @default.
• W2000714609 cites W2139367639 @default.
• W2000714609 cites W2140373043 @default.
• W2000714609 cites W2147712103 @default.
• W2000714609 cites W2151146978 @default.
• W2000714609 cites W2156067562 @default.
• W2000714609 cites W2162650381 @default.
• W2000714609 cites W2167558268 @default.
• W2000714609 cites W2168526937 @default.
• W2000714609 cites W2185025112 @default.
• W2000714609 cites W2318146142 @default.
• W2000714609 cites W2422798254 @default.
• W2000714609 doi "https://doi.org/10.1371/journal.pone.0025231" @default.
• W2000714609 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3178629" @default.
• W2000714609 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21966465" @default.
• W2000714609 hasPublicationYear "2011" @default.
• W2000714609 type Work @default.
• W2000714609 sameAs 2000714609 @default.
• W2000714609 citedByCount "256" @default.
• W2000714609 countsByYear W20007146092012 @default.
• W2000714609 countsByYear W20007146092013 @default.
• W2000714609 countsByYear W20007146092014 @default.
• W2000714609 countsByYear W20007146092015 @default.
• W2000714609 countsByYear W20007146092016 @default.
• W2000714609 countsByYear W20007146092017 @default.
• W2000714609 countsByYear W20007146092018 @default.
• W2000714609 countsByYear W20007146092019 @default.
• W2000714609 countsByYear W20007146092020 @default.
• W2000714609 countsByYear W20007146092021 @default.
• W2000714609 countsByYear W20007146092022 @default.
• W2000714609 countsByYear W20007146092023 @default.
• W2000714609 crossrefType "journal-article" @default.
• W2000714609 hasAuthorship W2000714609A5011979842 @default.
• W2000714609 hasAuthorship W2000714609A5030057038 @default.
• W2000714609 hasAuthorship W2000714609A5034662800 @default.
• W2000714609 hasAuthorship W2000714609A5044065716 @default.
• W2000714609 hasAuthorship W2000714609A5058521307 @default.
• W2000714609 hasAuthorship W2000714609A5059704901 @default.
• W2000714609 hasAuthorship W2000714609A5062627222 @default.
• W2000714609 hasAuthorship W2000714609A5063714751 @default.
• W2000714609 hasAuthorship W2000714609A5064690118 @default.
• W2000714609 hasAuthorship W2000714609A5065723905 @default.
• W2000714609 hasAuthorship W2000714609A5074545551 @default.
• W2000714609 hasAuthorship W2000714609A5077718624 @default.
• W2000714609 hasAuthorship W2000714609A5078462813 @default.

• next