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Article: Supplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspring

TitleSupplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspring
Authors
Issue Date2011
PublisherAmerican Society for Nutrition. The Journal's web site is located at http://jn.nutrition.org
Citation
Journal Of Nutrition, 2011, v. 141 n. 9, p. 1664-1672 How to Cite?
AbstractThis study examined the impact of maternal high-fructose intake and if metabolic control in the offspring could benefit from supplementing bioactive food components such as bitter melon (BM) to the maternal diet. In Expt. 1, virgin female rats received control (C), high-fructose (F; 60%), or BM-supplemented fructose (FBM; 1%) diet before conception until d 21 of lactation.Weaned male offspring were fed the C diet for 11 wk, forming C/C, F/C, and FBM/C groups. The F/C group had elevated serum insulin, TG, and FFA concentrations and hepatic lipid alterations compared with the C/C and FBM/C groups (P, 0.05). The 2 latter groups did not differ. Expt. 2 had similar dam treatment groups, but offspring were weaned to the C or F diet, forming C/C, C/F, F/F, and FBM/F groups, and the dietary treatment was extended to 20 wk. The hepatic levels of stearyl-CoA desaturase and microsomal TG transfer protein mRNA were lower, but that of PPARg coactivator 1-a and fibroblast growth factor 21 mRNA and fatty acid binding protein 1 protein were higher in the FBM/F group compared with the C/F and F/F groups (P, 0.05), indicating that maternal BM supplementation may reduce lipogenesis and promote lipid oxidation in offspring. The FBM/F group had significantly higher activities of liver glutathione peroxidase, superoxide dismutase, and catalase than the F/F group. The results indicate that supplementing BM to dams could offset the adverse effects of maternal high-fructose intake on lipid metabolism and antioxidant status in adult offspring. © 2011 American Society for Nutrition.
Persistent Identifierhttp://hdl.handle.net/10722/179253
ISSN
2015 Impact Factor: 3.74
2015 SCImago Journal Rankings: 2.040
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChing, RHHen_US
dc.contributor.authorYeung, LOYen_US
dc.contributor.authorTse, IMYen_US
dc.contributor.authorSit, WHen_US
dc.contributor.authorLi, ETSen_US
dc.date.accessioned2012-12-19T09:53:23Z-
dc.date.available2012-12-19T09:53:23Z-
dc.date.issued2011en_US
dc.identifier.citationJournal Of Nutrition, 2011, v. 141 n. 9, p. 1664-1672en_US
dc.identifier.issn0022-3166en_US
dc.identifier.urihttp://hdl.handle.net/10722/179253-
dc.description.abstractThis study examined the impact of maternal high-fructose intake and if metabolic control in the offspring could benefit from supplementing bioactive food components such as bitter melon (BM) to the maternal diet. In Expt. 1, virgin female rats received control (C), high-fructose (F; 60%), or BM-supplemented fructose (FBM; 1%) diet before conception until d 21 of lactation.Weaned male offspring were fed the C diet for 11 wk, forming C/C, F/C, and FBM/C groups. The F/C group had elevated serum insulin, TG, and FFA concentrations and hepatic lipid alterations compared with the C/C and FBM/C groups (P, 0.05). The 2 latter groups did not differ. Expt. 2 had similar dam treatment groups, but offspring were weaned to the C or F diet, forming C/C, C/F, F/F, and FBM/F groups, and the dietary treatment was extended to 20 wk. The hepatic levels of stearyl-CoA desaturase and microsomal TG transfer protein mRNA were lower, but that of PPARg coactivator 1-a and fibroblast growth factor 21 mRNA and fatty acid binding protein 1 protein were higher in the FBM/F group compared with the C/F and F/F groups (P, 0.05), indicating that maternal BM supplementation may reduce lipogenesis and promote lipid oxidation in offspring. The FBM/F group had significantly higher activities of liver glutathione peroxidase, superoxide dismutase, and catalase than the F/F group. The results indicate that supplementing BM to dams could offset the adverse effects of maternal high-fructose intake on lipid metabolism and antioxidant status in adult offspring. © 2011 American Society for Nutrition.en_US
dc.languageengen_US
dc.publisherAmerican Society for Nutrition. The Journal's web site is located at http://jn.nutrition.orgen_US
dc.relation.ispartofJournal of Nutritionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Markers - Metabolismen_US
dc.subject.meshDieten_US
dc.subject.meshDietary Carbohydrates - Adverse Effectsen_US
dc.subject.meshDyslipidemias - Chemically Induced - Prevention & Controlen_US
dc.subject.meshFemaleen_US
dc.subject.meshFructose - Administration & Dosage - Adverse Effectsen_US
dc.subject.meshLactationen_US
dc.subject.meshLipid Peroxidationen_US
dc.subject.meshLiver - Drug Effects - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMomordica Charantiaen_US
dc.subject.meshOxidative Stress - Drug Effectsen_US
dc.subject.meshPregnancyen_US
dc.subject.meshPrenatal Exposure Delayed Effectsen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshWeaningen_US
dc.titleSupplementation of bitter melon to rats fed a high-fructose diet during gestation and lactation ameliorates fructose-induced dyslipidemia and hepatic oxidative stress in male offspringen_US
dc.typeArticleen_US
dc.identifier.emailLi, ETS: etsli@hku.hken_US
dc.identifier.authorityLi, ETS=rp00737en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.3945/jn.111.142299en_US
dc.identifier.pmid21813810-
dc.identifier.scopuseid_2-s2.0-80052557042en_US
dc.identifier.hkuros198775-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80052557042&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume141en_US
dc.identifier.issue9en_US
dc.identifier.spage1664en_US
dc.identifier.epage1672en_US
dc.identifier.eissn1541-6100-
dc.identifier.isiWOS:000294523500012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChing, RH=54388743000en_US
dc.identifier.scopusauthoridYeung, LO=54390529200en_US
dc.identifier.scopusauthoridTse, IM=14635211700en_US
dc.identifier.scopusauthoridSit, WH=8528923000en_US
dc.identifier.scopusauthoridLi, ET=14018169600en_US

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