FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2062302492> ?p ?o ?g. }

• W2062302492 endingPage "67" @default.
• W2062302492 startingPage "58" @default.
• W2062302492 abstract "The occurrence of type II diabetes is highly correlated with obesity, although the mechanisms linking the two conditions are incompletely understood. Leptin is a potent insulin sensitiser and, in leptin-deficient, insulin insensitive, Lepob/ob mice, leptin improves glucose tolerance, indicating that leptin resistance may link obesity to insulin insensitivity. Leptin resistance occurs in response to a high-fat diet (HFD) and both hyperleptinaemia and inflammation have been proposed as causative mechanisms. Scrutinising the role of hyperleptinaemia in this process, central hyperleptinaemia in Lepob/ob mice was induced by chronic i.c.v. infusion of leptin (4.2 μg/day) over 10 days. This treatment led to a dramatic decline in body weight and food intake, as well as an improvement in glucose tolerance. Transfer to HFD for 4 days markedly arrested the beneficial effects of leptin on these parameters. Because Lepob/ob mice are exquisitely sensitive to leptin, the possibility that leptin could reverse HFD-induced glucose intolerance in these animals was investigated. HFD led to increased body weight and glucose intolerance compared to a low-fat diet (LFD). Older and heavier Lepob/ob mice were used as body weight-matched controls. Mice in each group received either i.p. leptin (1.25 mg/kg) or vehicle, and glucose tolerance, food intake and the number of phosphorylated signal transducer and activator of transcription (pSTAT)3 immunoreactive cells in the arcuate nucleus (ARC) and ventromedial hypothalamus (VMH) were analysed. Leptin improved glucose tolerance (P = 0. 019) and reduced food intake in Lepob/ob mice on LFD (P ≤ 0.001) but was ineffective in mice on HFD. Furthermore, when leptin was administered centrally, the glucose tolerance of Lepob/ob mice on HFD was significantly impaired (P = 0.007). Although leptin induced the number of pSTAT3 immunoreactive cells in the ARC and VMH of Lepob/ob mice on LFD, HFD was associated with elevated pSTAT3 immunoreactivity in vehicle-treated Lepob/ob mice that was unaffected by leptin treatment, suggesting central leptin resistance. Negating central inflammation by co-administering a c-Jun n-terminal kinase (JNK) inhibitor reinstated the glucose-lowering effects of leptin. These findings demonstrate that Lepob/ob mice develop leptin resistance on a HFD independent of hyperleptinaemia and also indicate that the JNK inflammatory pathway plays a key role in the induction of diet-induced glucose intolerance." @default.
• W2062302492 created "2016-06-24" @default.
• W2062302492 creator A5022388174 @default.
• W2062302492 creator A5031648665 @default.
• W2062302492 creator A5047052311 @default.
• W2062302492 creator A5050157265 @default.
• W2062302492 creator A5054870682 @default.
• W2062302492 creator A5059372071 @default.
• W2062302492 date "2014-02-01" @default.
• W2062302492 modified "2023-09-26" @default.
• W2062302492 title "High-Fat Diet Induces Leptin Resistance in Leptin-Deficient Mice" @default.
• W2062302492 cites W1512875938 @default.
• W2062302492 cites W1580569338 @default.
• W2062302492 cites W1631449371 @default.
• W2062302492 cites W1900852307 @default.
• W2062302492 cites W1970142642 @default.
• W2062302492 cites W1974838371 @default.
• W2062302492 cites W1987594950 @default.
• W2062302492 cites W1995300425 @default.
• W2062302492 cites W1996713062 @default.
• W2062302492 cites W2003578093 @default.
• W2062302492 cites W2005519734 @default.
• W2062302492 cites W2006272024 @default.
• W2062302492 cites W2007114243 @default.
• W2062302492 cites W2009968514 @default.
• W2062302492 cites W2013583119 @default.
• W2062302492 cites W2014093920 @default.
• W2062302492 cites W2027810463 @default.
• W2062302492 cites W2033937869 @default.
• W2062302492 cites W2038018821 @default.
• W2062302492 cites W2041608075 @default.
• W2062302492 cites W2042535492 @default.
• W2062302492 cites W2045522606 @default.
• W2062302492 cites W2059764720 @default.
• W2062302492 cites W2060682066 @default.
• W2062302492 cites W2071839617 @default.
• W2062302492 cites W2088266150 @default.
• W2062302492 cites W2088666203 @default.
• W2062302492 cites W2111732109 @default.
• W2062302492 cites W2124756048 @default.
• W2062302492 cites W2137736712 @default.
• W2062302492 cites W2142851934 @default.
• W2062302492 cites W2144536242 @default.
• W2062302492 cites W2148083005 @default.
• W2062302492 cites W2154555913 @default.
• W2062302492 cites W2319361543 @default.
• W2062302492 cites W4256066274 @default.
• W2062302492 doi "https://doi.org/10.1111/jne.12131" @default.
• W2062302492 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24382295" @default.
• W2062302492 hasPublicationYear "2014" @default.
• W2062302492 type Work @default.
• W2062302492 sameAs 2062302492 @default.
• W2062302492 citedByCount "83" @default.
• W2062302492 countsByYear W20623024922014 @default.
• W2062302492 countsByYear W20623024922015 @default.
• W2062302492 countsByYear W20623024922016 @default.
• W2062302492 countsByYear W20623024922017 @default.
• W2062302492 countsByYear W20623024922018 @default.
• W2062302492 countsByYear W20623024922019 @default.
• W2062302492 countsByYear W20623024922020 @default.
• W2062302492 countsByYear W20623024922021 @default.
• W2062302492 countsByYear W20623024922022 @default.
• W2062302492 countsByYear W20623024922023 @default.
• W2062302492 crossrefType "journal-article" @default.
• W2062302492 hasAuthorship W2062302492A5022388174 @default.
• W2062302492 hasAuthorship W2062302492A5031648665 @default.
• W2062302492 hasAuthorship W2062302492A5047052311 @default.
• W2062302492 hasAuthorship W2062302492A5050157265 @default.
• W2062302492 hasAuthorship W2062302492A5054870682 @default.
• W2062302492 hasAuthorship W2062302492A5059372071 @default.
• W2062302492 hasConcept C126322002 @default.
• W2062302492 hasConcept C134018914 @default.
• W2062302492 hasConcept C14372207 @default.
• W2062302492 hasConcept C185592680 @default.
• W2062302492 hasConcept C2777391703 @default.
• W2062302492 hasConcept C2779306644 @default.
• W2062302492 hasConcept C2780613262 @default.
• W2062302492 hasConcept C511355011 @default.
• W2062302492 hasConcept C71924100 @default.
• W2062302492 hasConcept C75908981 @default.
• W2062302492 hasConcept C86803240 @default.
• W2062302492 hasConceptScore W2062302492C126322002 @default.
• W2062302492 hasConceptScore W2062302492C134018914 @default.
• W2062302492 hasConceptScore W2062302492C14372207 @default.
• W2062302492 hasConceptScore W2062302492C185592680 @default.
• W2062302492 hasConceptScore W2062302492C2777391703 @default.
• W2062302492 hasConceptScore W2062302492C2779306644 @default.
• W2062302492 hasConceptScore W2062302492C2780613262 @default.
• W2062302492 hasConceptScore W2062302492C511355011 @default.
• W2062302492 hasConceptScore W2062302492C71924100 @default.
• W2062302492 hasConceptScore W2062302492C75908981 @default.
• W2062302492 hasConceptScore W2062302492C86803240 @default.
• W2062302492 hasIssue "2" @default.
• W2062302492 hasLocation W20623024921 @default.
• W2062302492 hasLocation W20623024922 @default.
• W2062302492 hasOpenAccess W2062302492 @default.
• W2062302492 hasPrimaryLocation W20623024921 @default.
• W2062302492 hasRelatedWork W1985226700 @default.

• next