Dietary conjugated linolenic acid in relation to CLA differently modifies body fat mass and serum and liver lipid levels in rats

Koba, Kazunori; Akahoshi, Asuka; Yamasaki, Masao; Tanaka, Kazunari; Yamada, Koji; Iwata, Toshio; Kamegai, Takeshi; Tsutsumi, K.; Sugano, Michihiro

doi:10.1007/s11745-002-0901-7

Cited by 116 publications

(115 citation 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%

“…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]. Noguchi et al fed rats with bitter gourd oil (BGO) diets for 4 weeks and found occurrence of c9, t11-conjugated linoleic acid (c9,t11-CLA) in the liver of rats [26], and the conversion of c9,t11, t13-CLN to CLA by an enzymatic biohydrogenation in rat tissue was confirmed later [34,35].…”

Section: Discussionmentioning

confidence: 99%

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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%

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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“…Similar effects have been observed in another study in the same animal model. 94 Results of these studies suggest that reductions in fat mass due to CLA (or reduced food intake) are associated with reductions in leptin, which induces insulin resistance.…”

Section: Cla Induces Insulin Resistancementioning

confidence: 99%

Conjugated linoleic acid and obesity control: efficacy and mechanisms

2004

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Obesity is associated with high blood cholesterol and high risk for developing diabetes and cardiovascular disease. Therefore, management of body weight and obesity are increasingly considered as an important approach to maintaining healthy cholesterol profiles and reducing cardiovascular risk. The present review addresses the effects of conjugated linoleic acid (CLA) on fat deposition, body weight and composition, safety, as well as mechanisms involved in animals and humans. Animal studies have shown promising effects of CLA on body weight and fat deposition. The majority of the animal studies have been conducted using CLA mixtures that contained approximately equal amounts of trans-10, cis-12 (t10c12) and cis-9, trans-11 (c9t11) isomers. Results of a few studies in mice fed CLA mixtures with different ratios of c9t11 and t10c12 isomers have indicated that the t10c12 isomer CLA may be the active form of CLA affecting weight gain and fat deposition. Inductions of leptin reduction and insulin resistance are the adverse effects of CLA observed in only mice. In pigs, the effects of CLA on weight gain and fat deposition are inconsistent, and no adverse effects of CLA have been reported. A number of human studies suggest that CLA supplementation has no effect on body weight and insulin sensitivity. Although it is suggested that the t10c12 CLA is the antiadipogenic isomer of CLA in humans, the effects of CLA on fat deposition are marginal and more equivocal as compared to results observed in animal studies. Mechanisms through which CLA reduces body weight and fat deposition remain to be fully understood. Proposed antiobesity mechanisms of CLA include decreased energy/food intake and increased energy expenditure, decreased preadipocyte differentiation and proliferation, decreased lipogenesis, and increased lipolysis and fat oxidation. In summary, CLA reduces weight gain and fat deposition in rodents, while produces less significant and inconsistent effects on body weight and composition in pigs and humans. New studies are required to examine isomer-specific effects and mechanisms of CLA in animals and humans using purified individual CLA isomers.

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“…The seed oils of pomegranate, catalpa, and pot marigold contain 83.0% punicic acid (9c,11t,13c-CLN), 42.3% catalpic acid (9t,11t,13c-CLN), and 62.2% calendic acid (8t,10t,12c-CLN), respectively (14). As for the biological activity of CLN, dietary CLN produced by alkaline isomerization of linolenic acid (LN) reduces fat content in the body (15). Purified punicic acid has a hypolipidemic effect (16).…”

Section: Introductionmentioning

confidence: 99%

Catalpa seed oil rich in 9t,11t,13c-conjugated linolenic acid suppresses the development of colonic aberrant crypt foci induced by azoxymethane in rats

Suzuki

Yasui²,

Kohno³

et al. 2006

Oncol Rep

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Abstract. Catalpa (Catalpa ovata) seed oil (CPO) is a unique oil that contains a high amount of 9trans,11trans,13cis-conjugated linolenic acid. In the present study, we investigated whether dietary administration with CPO affects the development of azoxymethane (AOM)-induced colonic aberrant crypt foci (ACF) in male F344 rats to elucidate its possible cancer chemopreventive efficiency. Also, the effect of CPO on the fatty acid composition of liver tissue and colonic mucosa, the serum levels of total cholesterol and triglyceride, and the mRNA expression of cyclooxygenase (COX)-2 in the colonic mucosa were measured. In addition, the cell proliferation activity and apoptotic index in the colonic mucosa were estimated immunohistochemically. Animals were given two weekly subcutaneous injections of AOM (20 mg/kg body weight). They also received the experimental diet containing 0.01%, 0.1% or 1% CPO for 4 weeks, starting one week before the first dosing of AOM. AOM exposure produced a substantial number of ACF (99±28) at the end of the study (week 4). Dietary administration of CPO reduced the number of ACF (AOM + 0.01% CPO, 32±11, P<0.001; AOM + 0.1% CPO, 35±18, P<0.001; AOM + 1% CPO, 18±10, P<0.001). 9t,11t-conjugated linoleic acid was detected in the liver tissue and colonic mucosa of rats fed the CPO-containing diet. Additionally, dietary administration with CPO decreased the serum triglyceride level and the expression of COX-2 mRNA in the colonic mucosa. The indices of cell proliferation and apoptosis in the colonic mucosa of rats treated with AOM and 1% CPO have significant differences when compared with the AOM alone group. These findings suggest the possible chemopreventive activity of CPO in the early phase of colon carcinogenesis.

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Dietary conjugated linolenic acid in relation to CLA differently modifies body fat mass and serum and liver lipid levels in rats

Cited by 116 publications

References 50 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.)

Conjugated linoleic acid and obesity control: efficacy and mechanisms

Catalpa seed oil rich in 9t,11t,13c-conjugated linolenic acid suppresses the development of colonic aberrant crypt foci induced by azoxymethane in rats

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