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4 hydroxyanisole/гојазност

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ЧланциКлиничка испитивањаПатенти
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Antioxidants delay the onset of thyroiditis in obese strain chickens.

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Dietary iodine has been shown to be important in the induction of thyroiditis in susceptible chicken strains although the underlying mechanism remains unknown. Iodine may exert its effects through the formation of reactive oxidative radicals which would cause thyroidal injury and initiate

Perturbation of 3-tert-butyl-4-hydroxyanisole in adipogenesis of male mice with normal and high fat diets.

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As one of the widely used anthropogenic food additives, 3-tert-butyl-4-hydroxyanisole (3-BHA) has been found to perturb adipogenesis in vitro and induce lipid accumulation in some strains of oleaginous microalgae. The impact of this chemical on adipocyte development and lipid metabolism in mammals

Butylated hydroxyanisole isomers induce distinct adipogenesis in 3T3-L1 cells.

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Butylated hydroxyanisole (BHA) isomers, as the widely used anthropogenic antioxidants in food, have been revealed to induce endocrine disrupting effects, while the mechanism how BHA isomers regulate the lipogenic differentiation remains to be elucidated. Using 3T3-L1 differentiation model, the

Hepatic glutathione contributes to attenuation of thioacetamide-induced hepatic necrosis due to suppression of oxidative stress in diet-induced obese mice.

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We previously reported that hepatic necrosis induced by thioacetamide (TA), a hepatotoxicant, was attenuated in mice fed a high-fat diet (HFD mice) in comparison with mice fed a normal rodent diet (ND mice). In this study, we focused on investigation of the mechanism of the attenuation. Hepatic

Influence of nutrients and other dietary materials on cytochrome P-450 enzymes.

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The cytochrome P-450 (P-450) enzymes are collectively responsible for the bulk of oxidation of xenobiotic chemicals, including drugs, pesticides, and carcinogens. This biotransformation can result in either increased or decreased toxicity, depending on the situation. The regulation of individual

Sestrin2 inhibits uncoupling protein 1 expression through suppressing reactive oxygen species.

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Uncoupling protein 1 (Ucp1), which is localized in the mitochondrial inner membrane of mammalian brown adipose tissue (BAT), generates heat by uncoupling oxidative phosphorylation. Upon cold exposure or nutritional abundance, sympathetic neurons stimulate BAT to express Ucp1 to induce energy
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