title: Curcumin improves the metabolic syndrome in high-fructose-diet-fed rats: role of TNF-α, NF-κB, and oxidative stress.
abstract: This study aimed to investigate effects of curcumin on high fructose diet (HFD)-induced metabolic syndrome (MetS) in rats and the possible mechanisms involved. MetS was induced in male albino rats (n = 20), over 8 weeks, by 65% HFD. For 8-week experiment period, rats were assigned to 2 equal groups: curcumin-treated rats received curcumin (200 mg/kg, p.o, once daily) along with HFD, and untreated rats were fed with HFD only. We evaluated body mass (BM), systolic blood pressure (SBP), homeostasis model assessment of insulin resistance (HOMA-IR), and serum levels of glucose, insulin, leptin, total cholesterol (TC), triglycerides (TGs), uric acid, malondialdehyde (MDA; lipid peroxidation product), and tumor necrosis factor-α (TNF-α; inflammatory cytokine), and serum catalase (endogenous antioxidant) activity and immunohistochemical expression of nuclear factor κB (NF-κB; inflammation-related transcription factor) in hepatocytes. HFD produced increases in BM, SBP, HOMA-IR, and serum levels of glucose, insulin, leptin, TC, TGs, uric acid, MDA, and TNF-α, a decrease in catalase activity, and strong positive expression of NF-κB in hepatocytes. Curcumin, in presence of HFD, produced significant improvements in all glucose and fat metabolism parameters, and in oxidative stress and inflammation biomarkers. Curcumin may potentially be useful in the treatment of MetS through its ability to modulate oxidation stress status and inflammation cascades.
authors.affiliation: a Clinical Pharmacology Department, Faculty of Medicine, Zagazig University, Egypt.
authors.forename: Mohamed Elsayed
authors.initials: ME
authors.lastname: Kelany
authors.affiliation: b Clinical Pharmacology Department, Faculty of Medicine, Jazan University, Saudi Arabia.
authors.forename: Tahir M
authors.initials: TM
authors.lastname: Hakami
authors.affiliation: c Clinical Pharmacology Department, Faculty of Medicine, Menoufeya University, Egypt.
authors.forename: Adel H
authors.initials: AH
authors.lastname: Omar
mesh_terms: D000818:Animals; D001786:Blood Glucose; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003474:Curcumin / Q000494:pharmacology / Q000627:therapeutic use*; D005632:Fructose / Q000009:adverse effects*; D022781:Hepatocytes / Q000378:metabolism; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008099:Liver / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D024821:Metabolic Syndrome / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism*; D014527:Uric Acid / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D014527:Uric Acid; D005632:Fructose; D008315:Malondialdehyde; D002784:Cholesterol; D002374:Catalase; D003474:Curcumin
keywords: curcumin; curcumine; fructose; insulin resistance; metabolic syndrome; rats; résistance à l’insuline; syndrome métabolique