Dietary lipids induce Phase 2 enzymes in rat small intestine

Dannenberg, Andrew J.; Yang, Eun Kyung; Aharon, Deborah

doi:10.1016/0005-2760(93)90042-8

Cited by 6 publications

(1 citation statement)

References 27 publications

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“…Several CYP isoforms and phase II enzymes can be induced or suppressed by micro- and macronutrients. Dietary fats, for example, with different amounts of and/or different fatty acid compositions, can change the activities of certain CYP enzymes, UGT, and GST , . In addition, vitamin E and retinoids are shown to activate the nuclear receptors and induce CYP3A expression at mRNA as well as enzyme activity , .…”

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confidence: 99%

Effect of Chitosan on Hepatic Drug-Metabolizing Enzymes and Oxidative Stress in Rats Fed Low- and High-Fat Diets

Yao

Lii

Chou

et al. 2010

J. Agric. Food Chem.

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Chitosan is sold worldwide as a lipid-lowering functional food and may be taken with certain medications. To investigate the effect of chitosan on drug-metabolizing enzymes and oxidative stress in the liver, male Wistar rats were fed a low- or high-fat diet with cellulose or chitosan for 4 weeks. A significant decrease in cytochrome P450 (CYP) 3A-catalyzed testosterone 6beta-hydroxylation in liver microsomes was observed in rats fed the chitosan with low- and high-fat diets. The expression of CYP 3A1 and 3A2, however, was suppressed by chitosan in rats fed the low-fat diet only. Furthermore, rats fed the low-fat diet with chitosan had lower hepatic glutathione S-transferase (GST) activity and superoxide dismutase activity and higher total tissue and microsomal lipid hydroperoxides. Hepatic alpha-tocopherol was lower in rats fed the chitosan-containing diet. The results suggest that chitosan is likely to modulate CYP 3A activity and protein expression and GST activity partially in a dietary fat-dependent manner. This change may cause a decrease in the metabolism of drugs catalyzed by these enzymes in liver tissues. Moreover, decrease of alpha-tocopherol level and SOD activity by chitosan partly accounts for the increase of hepatic lipid peroxidation.

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Section: Introductionmentioning

confidence: 99%

Effect of Chitosan on Hepatic Drug-Metabolizing Enzymes and Oxidative Stress in Rats Fed Low- and High-Fat Diets

Yao

Lii

Chou

et al. 2010

J. Agric. Food Chem.

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Ah receptor involvement in mediation of pyruvate carboxylase levels and activity in mice given 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin

Ryu

Roy

Sparrow

et al. 1995

J. Biochem. Toxicol.

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The arylhydrocarbon receptor (AhR) plays a central role in mediating 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity in animals. The investigations described here provide evidence that support a role for the AhR in TCDD-mediated pyruvate carboxylase (PC) level/activity reductions in mice. Pyruvate carboxylase plays a pivotal role in gluconeogenesis and in supplying carbon units for the citric acid cycle. Delivered ip in a corn oil carrier, TCDD suppresses PC activity/amount at doses as low as 1 microgram/kg in responsive C57BL/6J(Ahb/b) mice. Corn oil alone injected ip into mice at 4 mL/kg appears to be an inducer that increases the amount and activity of PC. However, TCDD suppresses this induction. In the Ahb/b mouse, PC levels and activity are reduced to 10% of control values at a dose of 75 micrograms/kg. A time-course experiment shows that the PC reductions are apparent within 16 hours post-TCDD exposure. Here we report investigations on the PC/TCDD response using a congenic C57BL/6J(Ahd/d) mouse strain having an AhR with a low affinity for TCDD. If the PC/TCDD response is AhR mediated, the congenic mouse strain (Ahd/d) would require much higher doses of TCDD to suppress PC. In the Ahd/d mice, we observe that an approximately 60-fold increase in TCDD dose is necessary to produce a PC/TCDD effect. We also find that in Ahd/d mice, corn oil does not induce an increase in PC activity/amounts, as reported for Ahb/b mice.

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Comparative effects of omeprazole on xenobiotic metabolizing enzymes in the rat and human*

Kashfi

McDougall

Dannenberg

1995

Clin Pharmacol Ther

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Omeprazole induces CYP1A in the human liver and gut, which has led to concern about possible side effects. The purpose of this study was to compare the effects of omeprazole on phase 1 and phase 2 enzymes in the rat and human. Male rats were treated with intraperitoneal (40 or 80 mg/kg) or oral omeprazole (40 mg/kg) for 5 or 14 days, respectively. The activities and amounts of CYP1A, uridine diphosphate-glucuronosyltransferase, and glutathione transferase were determined in liver and gut. Enzyme activities were also determined in duodenal biopsy specimens from six healthy human volunteers before and after treatment with omeprazole (20 mg/day) for 10 days. Treatment with intraperitoneal omeprazole (40 mg/kg; 80 mg/kg) coinduced uridine diphosphate-glucuronosyltransferase (36%; 66%), glutathione transferase (22%; 50%), and CYP1A (26%; 50%) in rat liver. In rat small intestine, comparable levels of induction were observed for uridine diphosphate-glucuronosyltransferase and glutathione transferase; CYP1A was unaffected. Oral omeprazole had similar effects. Immunoblotting showed corresponding changes in the amounts of these enzymes. Omeprazole increased the activities of CYP1A (19% to 167%; p = 0.014) and uridine diphosphate-glucuronosyltransferase (11% to 68%; p = 0.04) in the duodenal biopsy specimens of all six human volunteers; glutathione transferase was unaffected. Thus, omeprazole coinduced multiple xenobiotic metabolizing enzymes in the rat and human. The pattern of induction differed in the rat and human, consistent with known differences in genetic regulatory elements in the two species.

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Dietary lipids induce Phase 2 enzymes in rat small intestine

Cited by 6 publications

References 27 publications

Effect of Chitosan on Hepatic Drug-Metabolizing Enzymes and Oxidative Stress in Rats Fed Low- and High-Fat Diets

Effect of Chitosan on Hepatic Drug-Metabolizing Enzymes and Oxidative Stress in Rats Fed Low- and High-Fat Diets

Ah receptor involvement in mediation of pyruvate carboxylase levels and activity in mice given 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin

Comparative effects of omeprazole on xenobiotic metabolizing enzymes in the rat and human*

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