Organ-specific role of the lipogenic transcription factor ChREBP for metabolic adaptation in response to cold exposure and its implications for metabolic diseases

dc.contributor.advisorHeeren, Jörg
dc.contributor.advisorScheja, Ludger
dc.contributor.advisorBay, Péter
dc.contributor.authorSenkalfa, Berkay Yasar
dc.contributor.departmentDE--Természettudományi és Technológiai Kar--Biológiai és Ökológiai Intézethu_HU
dc.date.accessioned2020-05-14T21:39:42Z
dc.date.available2020-05-14T21:39:42Z
dc.date.created2020-05-14
dc.description.abstractEver since the discovery of active and adequate brown fat depots in adult humans, non-shivering thermogenesis (NST) function of brown adipose tissue (BAT), where oxidation of tissue-stored fats is uncoupled from ATP synthesis and instead used to generate heat for the body, has become a promising avenue for metabolic disease research in the last decade. As BAT utilizes its stored fats for the purpose of generating heat for the body, it also maintains a stable energy storage in the form of fats within brown adipocytes. To prevent replenishment of these fat stores, upon cold stimuli, BAT picks up additional glucose from plasma to be converted into storage triglycerides via de novo lipogenesis (DNL), alongside taking up additional lipids also from plasma. If the cold stimuli are long enough, the same phenomena are observed in white adipose tissue (WAT) as well via a process called browning. These trends make BAT, NST and WAT browning exciting avenues for metabolic disease research targeting type 2 diabetes and obesity, alongside fatty liver diseases and other metabolic conditions. ChREBP, as a glycolytic and lipogenic transcription factor identified more than a decade ago, has been established to be the main driver of DNL in adipocytes and thus has important roles in the processes observed in BAT and WAT during NST and browning, which can have far-reaching implications. The present thesis work evaluates effects and necessity of ChREBP function by analysing its organ-specific roles during metabolic adaptation to cold, in liver, BAT, and WAT via gene expression, protein expression, and tissue uptake data obtained from murine cohorts with ChREBP availability versus deletion, housed under different ambient temperatures.hu_HU
dc.description.courseBiochemical Engineeringhu_HU
dc.description.degreeBSc/BAhu_HU
dc.format.extent91hu_HU
dc.identifier.urihttp://hdl.handle.net/2437/287358
dc.language.isoenhu_HU
dc.subjectbrown adipose tissuehu_HU
dc.subjectde novo lipogenesishu_HU
dc.subjectnon-shivering thermogenesishu_HU
dc.subjectchrebphu_HU
dc.subjectmetabolic disordershu_HU
dc.subjectdiabeteshu_HU
dc.subjectobesityhu_HU
dc.subjectadipose tissueshu_HU
dc.subjectlipid metabolismhu_HU
dc.subjectglucose metabolismhu_HU
dc.subjectgeneticshu_HU
dc.subjecttranscription factorshu_HU
dc.subject.dspaceDEENK Témalista::Biológiai tudományokhu_HU
dc.subject.dspaceDEENK Témalista::Kémiahu_HU
dc.subject.dspaceDEENK Témalista::Orvostudományhu_HU
dc.titleOrgan-specific role of the lipogenic transcription factor ChREBP for metabolic adaptation in response to cold exposure and its implications for metabolic diseaseshu_HU
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