L
Lutz W. D. Weber
Researcher at University of Kansas
Publications - 42
Citations - 3058
Lutz W. D. Weber is an academic researcher from University of Kansas. The author has contributed to research in topics: Toxicity & Gluconeogenesis. The author has an hindex of 19, co-authored 42 publications receiving 2841 citations.
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Journal ArticleDOI
Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model.
TL;DR: CCl4 activates tumor necrosis factor (TNF)alpha, nitric oxide (NO), and transforming growth factors (TGF)-alpha and -beta in the cell, processes that appear to direct the cell primarily toward (self-)destruction or fibrosis.
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Mechanism of carbon tetrachloride-induced hepatotoxicity. Hepatocellular damage by reactive carbon tetrachloride metabolites.
TL;DR: The results confirm that covalent binding of the CCl3* radical to cell components initiates the inhibition of lipoprotein secretion and thus steatosis, whereas reaction with oxygen, to form CCI3*-OO*, initiates lipid peroxidation.
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Maintaining cholesterol homeostasis: sterol regulatory element-binding proteins.
TL;DR: It appears that SREBPs alone, in the sequence described above, can exert complete control over cholesterol synthesis, whereas many additional factors are required for complete control of lipid metabolism.
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The toxicity of brominated and mixed-halogenated dibenzo-p-dioxins and dibenzofurans: an overview.
Lutz W. D. Weber,H. Greim +1 more
TL;DR: Considering the overall similarity in action of chlorinated and brominated dibenzo-p-dioxins and dibenzofurans, environmental and health assessments should be based on molar body burdens without discrimination for the nature of the halogen.
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Reduced activities of key enzymes of gluconeogenesis as possible cause of acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in rats.
Lutz W. D. Weber,Margitta Lebofsky,Bernhard U. Stahl,Joel R. Gorski,Giacomo Muzi,Karl K. Rozman +5 more
TL;DR: The hypothesis that reduced in vivo rates of gluconeogenesis in TCDD-treated rats are due to decreased activities of gluc oneogenic enzymes is confirmed and appetite suppression and reduced total PEPCK activity in whole livers occurred in the same dose-ranges of T CDD, suggesting the possibility of a cause-effect relationship.