Matches in SemOpenAlex for { <https://semopenalex.org/work/W2147630553> ?p ?o ?g. }
- W2147630553 abstract "Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB), play a paramount role in the central regulation of energy balance. Despite the substantial body of genetic evidence implicating BDNF- or TrkB-deficiency in human obesity, the critical brain region(s) contributing to the endogenous role of BDNF/TrkB signaling in metabolic control remain unknown.We assessed the importance of intact hypothalamic or hindbrain TrkB signaling in central regulation of energy balance by generating Nkx2.1-Ntrk2-/- and Phox2b-Ntrk2+/- mice, respectively, and comparing metabolic parameters (body weight, adiposity, food intake, energy expenditure and glucose homeostasis) under high-fat diet or chow fed conditions.Our data show that when fed a high-fat diet, male and female Nkx2.1-Ntrk2-/- mice have significantly increased body weight and adiposity that is likely driven by reduced locomotor activity and core body temperature. When maintained on a chow diet, female Nkx2.1-Ntrk2-/- mice exhibit an increased body weight and adiposity phenotype more robust than in males, which is accompanied by hyperphagia that precedes the onset of a body weight difference. In addition, under both diet conditions, Nkx2.1-Ntrk2-/- mice show increased blood glucose, serum insulin and leptin levels. Mice with complete hindbrain TrkB-deficiency (Phox2b-Ntrk2-/-) are perinatal lethal, potentially indicating a vital role for TrkB in visceral motor neurons that control cardiovascular, respiratory, and digestive functions during development. Phox2b-Ntrk2+/- heterozygous mice are similar in body weight, adiposity and glucose homeostasis parameters compared to wild type littermate controls when maintained on a high-fat or chow diet. Interestingly, despite the absence of a body weight difference, Phox2b-Ntrk2+/- heterozygous mice exhibit pronounced hyperphagia.Taken together, our findings suggest that the hypothalamus is a key brain region involved in endogenous BDNF/TrkB signaling and central metabolic control and that endogenous hindbrain TrkB likely plays a role in modulating food intake and survival of mice. Our findings also show that female mice lacking TrkB in the hypothalamus have a more robust metabolic phenotype." @default.
- W2147630553 created "2016-06-24" @default.
- W2147630553 creator A5002901691 @default.
- W2147630553 creator A5018039619 @default.
- W2147630553 creator A5057808087 @default.
- W2147630553 creator A5067849248 @default.
- W2147630553 creator A5079833063 @default.
- W2147630553 date "2015-11-01" @default.
- W2147630553 modified "2023-10-17" @default.
- W2147630553 title "Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance" @default.
- W2147630553 cites W1495527708 @default.
- W2147630553 cites W1570458334 @default.
- W2147630553 cites W1571949671 @default.
- W2147630553 cites W1971002481 @default.
- W2147630553 cites W1979722180 @default.
- W2147630553 cites W1987920581 @default.
- W2147630553 cites W1990768779 @default.
- W2147630553 cites W1995307068 @default.
- W2147630553 cites W2002265484 @default.
- W2147630553 cites W2002473696 @default.
- W2147630553 cites W2010142606 @default.
- W2147630553 cites W2016392763 @default.
- W2147630553 cites W2017498568 @default.
- W2147630553 cites W2018358437 @default.
- W2147630553 cites W2019562188 @default.
- W2147630553 cites W2023271687 @default.
- W2147630553 cites W2025054473 @default.
- W2147630553 cites W2029303080 @default.
- W2147630553 cites W2033333756 @default.
- W2147630553 cites W2038122755 @default.
- W2147630553 cites W2039153962 @default.
- W2147630553 cites W2041328277 @default.
- W2147630553 cites W2055862169 @default.
- W2147630553 cites W2056105272 @default.
- W2147630553 cites W2059507131 @default.
- W2147630553 cites W2069312841 @default.
- W2147630553 cites W2071815304 @default.
- W2147630553 cites W2074348556 @default.
- W2147630553 cites W2082057007 @default.
- W2147630553 cites W2084188625 @default.
- W2147630553 cites W2085695384 @default.
- W2147630553 cites W2086505088 @default.
- W2147630553 cites W2086831139 @default.
- W2147630553 cites W2088864173 @default.
- W2147630553 cites W2089059131 @default.
- W2147630553 cites W2091316910 @default.
- W2147630553 cites W2096264487 @default.
- W2147630553 cites W2098533907 @default.
- W2147630553 cites W2102918395 @default.
- W2147630553 cites W2109309568 @default.
- W2147630553 cites W2109470426 @default.
- W2147630553 cites W2112451262 @default.
- W2147630553 cites W2115079887 @default.
- W2147630553 cites W2115681043 @default.
- W2147630553 cites W2118743996 @default.
- W2147630553 cites W2133819667 @default.
- W2147630553 cites W2133824155 @default.
- W2147630553 cites W2137031888 @default.
- W2147630553 cites W2142552497 @default.
- W2147630553 cites W2142638433 @default.
- W2147630553 cites W2146399707 @default.
- W2147630553 cites W2151172917 @default.
- W2147630553 cites W2151672471 @default.
- W2147630553 cites W2157226283 @default.
- W2147630553 cites W2161050830 @default.
- W2147630553 cites W2161649767 @default.
- W2147630553 doi "https://doi.org/10.1016/j.molmet.2015.08.002" @default.
- W2147630553 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4632115" @default.
- W2147630553 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26629410" @default.
- W2147630553 hasPublicationYear "2015" @default.
- W2147630553 type Work @default.
- W2147630553 sameAs 2147630553 @default.
- W2147630553 citedByCount "22" @default.
- W2147630553 countsByYear W21476305532016 @default.
- W2147630553 countsByYear W21476305532017 @default.
- W2147630553 countsByYear W21476305532018 @default.
- W2147630553 countsByYear W21476305532019 @default.
- W2147630553 countsByYear W21476305532020 @default.
- W2147630553 countsByYear W21476305532021 @default.
- W2147630553 countsByYear W21476305532023 @default.
- W2147630553 crossrefType "journal-article" @default.
- W2147630553 hasAuthorship W2147630553A5002901691 @default.
- W2147630553 hasAuthorship W2147630553A5018039619 @default.
- W2147630553 hasAuthorship W2147630553A5057808087 @default.
- W2147630553 hasAuthorship W2147630553A5067849248 @default.
- W2147630553 hasAuthorship W2147630553A5079833063 @default.
- W2147630553 hasBestOaLocation W21476305531 @default.
- W2147630553 hasConcept C126322002 @default.
- W2147630553 hasConcept C134018914 @default.
- W2147630553 hasConcept C160539049 @default.
- W2147630553 hasConcept C170493617 @default.
- W2147630553 hasConcept C2491326 @default.
- W2147630553 hasConcept C2777075493 @default.
- W2147630553 hasConcept C2777391703 @default.
- W2147630553 hasConcept C2778790584 @default.
- W2147630553 hasConcept C2780613262 @default.
- W2147630553 hasConcept C3018667095 @default.
- W2147630553 hasConcept C511355011 @default.
- W2147630553 hasConcept C529278444 @default.
- W2147630553 hasConcept C71924100 @default.