Dietary effects of conjugated octadecatrienoic fatty acid (9 cis, 11 trans, 13 trans) levels on blood lipids and nonenzymatic in vitro lipid peroxidation in rats

Dhar, Pubali; Ghosh, Santinath; Bhattacharyya, Debasish

doi:10.1007/s11745-999-0343-2

Cited by 75 publications

(75 citation statements)

References 31 publications

(25 reference statements)

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“…However, several in vivo studies using 9c, 11t, 13t-CLN or bitter melon oil rich in this fatty acids have been reported. In addition to increase the antioxidant activity of blood and liver lipid in rats [10], 9c, 11t, 13t-CLN has also been reported to modulate the body fat and triglyceride metabolism in a manner that is different from CLA [19]. Although CLN increased serum and liver triglyceride level, it reduced the weight of perirenal and epididymal adipose tissue and enhanced the activity of b-oxidation in liver mitochondria and peroxisomes to a higher extent than CLA [19].…”

Section: Discussionmentioning

confidence: 99%

Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARα in bitter gourd (Momordica charantia L.)

et al. 2006

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SummaryBitter gourd (Momordica charantia L.) is a common vegetable in Asia that has been used in traditional medicine for the treatment of Diabetes. PPARs are ligand-dependent transcription factors that belong to the steroid hormone nuclear receptor family and control lipid and glucose homeostasis in the body. We previously reported that the ethyl acetate (EA) extract of bitter gourd activated peroxisome proliferator receptors (PPARs) a and c. To identify the active compound that activated PPARa, wild bitter gourd EA extract was partitioned between n-hexane and 90% methanol/10% H 2 O, and the n-hexane soluble fraction was further separated by silica gel column chromatography and finally by preparative HPLC. A transactivation assay employing a clone of CHOK1 cells stably transfected with a (UAS) 4 -tk-alkaline phosphatase reporter and a chimeric receptor of GAL4-rPPARa LBD was used to track the active component. Based on Mass, NMR, and IR spectroscopy, 9cis, 11trans, 13trans-conjugated linolenic acid (9c, 11t, 13t-CLN) was identified as a PPARa activator in wild bitter gourd. The isolated 9c, 11t, 13t-CLN rich fraction also significantly induced acyl CoA oxidase (ACO) activity in a peroxisome proliferator-responsive murine hepatoma cell line, H4IIEC3, implying that 9c, 11t, 13t-CLN was able to act on a natural PPARa signaling pathway as well. The content of 9c, 11t, 13t-CLN was estimated to be about 7.1 g/kg of our dried wild bitter gourd sample. The concentration of 9c, 11t, 13t-CLN and activation activity in the hydrolyzed EA extract of the seeds was higher than that of the flesh. The potential health benefits of 9c, 11t, 13t-CLN through the PPARa regulated mechanism are worthy to be further characterized in in vivo studies.

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Section: Discussionmentioning

confidence: 99%

Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARα in bitter gourd (Momordica charantia L.)

et al. 2006

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“…Interestingly, the c9,t11-CLA isomer was incorporated into forestomach phospholipids after CLA intubation in their study. In addition, Dhar et al 56) reported that c9,t11,t13-18:3 from bitter melon acts as an antioxidant. These compounds have more than two conjugated double bonds, and conjugation is known to increase the rate of oxidation.…”

Section: Discussionmentioning

confidence: 99%

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

et al. 2004

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Pomegranate (Punica granatum L.) seed oil (PGO) contains more than 70% cis(c)9,trans(t)11,c13-18:3 as conjugated linolenic acids (CLN). Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in c9,t11,t13-CLN, inhibited the occurrence of colonic aberrant crypt foci (ACF) induced by azoxymethane (AOM). In this study, we investigated the effect of dietary PGO on the development of AOM-induced colonic malignancies and compared it with that of conjugated linoleic acid (CLA). To induce colonic tumors, 6-week old male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks. One week before the AOM treatment they were started on diet containing 0.01%, 0.1%, or 1% PGO or 1% CLA for 32 weeks. Upon termination of the bioassay (32 weeks) colon tumors were evaluated histopathologically. AOM exposure produced colonic adenocarcinoma with an incidence of 81% and multiplicity of 1.88 ± ± ± ±1.54 at week 32. Administration of PGO in the diet significantly inhibited the incidence (AOM + + + +0.01% PGO, 44%, P < < < <0.05; AOM + + + +0.1% PGO, 38%, P < < < <0.01; AOM + + + +1% PGO, 56%) and the multiplicity (AOM + + + +0.01% PGO, 0.56 ± ± ± ±0.73, P < < < <0.01; AOM + + + +0.1% PGO, 0.50 ± ± ± ±0.73, P < < < <0.005; AOM + + + +1% PGO, 0.88 ± ± ± ±0.96, P < < < <0.05) of colonic adenocarcinomas, although a clear dose-response relationship was not observed at these dose levels. CLA feeding also slightly, but not significantly, reduced the incidence and multiplicity of colonic adenocarcinomas. The inhibition of colonic tumors by PGO was associated with an increased content of CLA (c9,t11-18:2) in the lipid fraction of colonic mucosa and liver. Also, administration of PGO in the diet elevated expression of peroxisome proliferator-activated receptor ( olon cancer is one of the leading causes of cancer deaths in Western countries. Globally, more than 875,000 men and women were afflicted with this cancer in 1996 and more than 510,000 died in the same year.

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“…Ha et al 17 demonstrated that CLA may act by antioxidant mechanisms cytotoxicity. In addition, Dhar et al 44 reported that c9,t11,t13-18:3 from BMO acts as an antioxidant. In compounds with more than 2 conjugated double bond, conjugation increases the rate of oxidation.…”

Section: Discussionmentioning

confidence: 99%

Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane‐induced rat colon carcinogenesis through elevation of colonic PPARγ expression and alteration of lipid composition

Kohno

Yasui

Suzuki

et al. 2004

Intl Journal of Cancer

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Our previous short-term experiment demonstrated that seed oil from bitter melon (Momordica charantia) (BMO), which is rich in cis(c)9, trans(t)11, t13-conjugated linolenic acid (CLN), inhibited the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF). In our study, the possible inhibitory effect of dietary administration of BMO on the development of colonic neoplasms was investigated using an animal colon carcinogenesis model initiated with a colon carcinogen AOM. Male F344 rats were given subcutaneous injections of AOM (20 mg/kg body weight) once a week for 2 weeks to induce colon neoplasms. They also received diets containing 0.01%, 0.1% or 1% BMO for 32 weeks, starting 1 week before the first dosing of AOM. At the termination of the study (32 weeks), AOM induced 83% incidence (15/18 rats) of colonic adenocarcinoma. Dietary supplementation with 0.01% and 0.1% BMO caused significant reduction in the incidence (47% inhibition by 0.01% BMO, p<0.02; 40% inhibition by 0.1% BMO, p<0.05; and 17% inhibition by 1% BMO) and the multiplicity (64% inhibition by 0.01% BMO, p<0.005; 58% inhibition by 0.1% BMO, p<0.02; and 48% inhibition by 1% BMO, p<0.05) of colonic adenocarcinoma, though a clear dose response was not observed. Such inhibition was associated with the increased content of CLA (c9,t11-18:2) in the lipid composition in colonic mucosa and liver. Also, BMO administration in diet enhanced expression of peroxisome proliferator-activated receptor (PPAR) ␥ protein in the nonlesional colonic mucosa. These findings suggest that BMO rich in CLN can suppress AOM-induced colon carcinogenesis and the inhibition might be caused, in part, by modification of lipid composition in the colon and liver and/or increased expression of PPAR␥ protein level in the colon mucosa.

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Dietary effects of conjugated octadecatrienoic fatty acid (9 cis, 11 trans, 13 trans) levels on blood lipids and nonenzymatic in vitro lipid peroxidation in rats

Cited by 75 publications

References 31 publications

Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARα in bitter gourd (Momordica charantia L.)

Fractionation and identification of 9c, 11t, 13t-conjugated linolenic acid as an activator of PPARα in bitter gourd (Momordica charantia L.)

Pomegranate seed oil rich in conjugated linolenic acid suppresses chemically induced colon carcinogenesis in rats

Dietary seed oil rich in conjugated linolenic acid from bitter melon inhibits azoxymethane‐induced rat colon carcinogenesis through elevation of colonic PPARγ expression and alteration of lipid composition

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