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At least 1,531 records · Page 85Linked to original sources
PubMed2001

trans-10,cis-12-Conjugated linoleic acid reduces leptin secretion from 3T3-L1 adipocytes.

The trans10,cis12 (t10c12) isomer of conjugated linoleic acid (CLA) has been shown to inhibit heparin-releasable lipoprotein lipase activity, reduce lipid stores in cultured 3T3-L1 adipocytes, and, when fed to mice, reduce body fat gain. We now report that t10c12 CLA significantly reduced leptin secretion from cultured 3T3-L1 adipocytes, and reduced leptin mRNA levels within the cells. Similar effects were produced by conjugated nonadecadienoic acid (a 19-carbon CLA cognate that is more effective than CLA in reducing body fat gain in mice), the lipoxygenase inhibitor nordihydroguaiaretic acid (which is synergistic with CLA in reducing body fat gain in mice), and ciglitazone (TZD, a PPARgamma agonist). Feeding mice diet supplemented with 0.5% t10c12 CLA for 4 weeks significantly reduced body fat gain, serum leptin levels and adipocyte leptin mRNA expression, without affecting feed intake or body weight. These data provide new insights into apparent mechanistic similarities among t10c12 CLA, CNA, NDGA, and TZD.

3T3 Cells↗
PubMedDate not supplied

[Damage of cell membranes by linoleic acid hydroperoxide].

It has been shown on Ehrlich ascite carcinoma cells that under the effect of linoleic acid hydroperoxides in vitro ionic permeability and membrane capacity of the cells sharply decrease after some threshold concentration of hydroperoxides (greater than 10(-5) M), while the threshold value decreases with the increase of the time of cell incubation in the presence of hydroperoxides. Interrelationship between the development of induced POL processes in the cell membranes and disturbance of their functional-structural state in the living cell is discussed.

Animals↗
PubMed2005

Effect of abomasal infusions of geometric isomers of 10,12 conjugated linoleic acid on milk fat synthesis in dairy cows.

The trans-10,cis-12 isomer of conjugated linoleic acid (CLA) decreases TAG accumulation in 3T3-L1 adipocytes, reduces lipid accretion in growing animals, and inhibits milk fat synthesis in lactating mammals. However, there is evidence to suggest that other FA may also exert antilipogenic effects. In the current experiment, the effects of geometric isomers of 10,12 CLA on milk fat synthesis were examined using four Holstein-British Friesian cows in a 4 x 4 Latin Square experiment with 14-d periods. Treatments consisted of abomasal infusions of skim milk, or skim milk containing trans-10,cis-12 CLA (T1), trans-10,trans-12 CLA (T2), or a mixture of predominantly 10,12 isomers containing (g/l00 g) trans-10,cis-12 (35.0), cis-10,trans-12 (23.2), trans-10,trans-12 (14.9), and cis-10,cis-12 (5.1). CLA supplements were prepared from purified ethyl linoleate and infused as nonesterified FA. Infusions were conducted over a 4-d period with a 10-d interval between treatments and targeted to deliver 4.5 g/d of 10,12 CLA isomers. Compared with the control, trans-10, trans-12 CLA had no effect (P> 0.05) on milk fat yield, whereas treatments T1 and T3 depressed (P < 0.05) milk fat content (19.8 and 22.9%, respectively) and decreased milk fat output (20.8 and 21.3%, respectively). Comparable reductions in milk fat synthesis to 4.14 and 1.80 g trans-10,cis-12/d supplied by treatments T1 and T3 indicate that other 10,12 geometric isomers of CLA have the potential to exert antilipogenic effects. The relative abundance of cis-10,trans-12 CLA in treatment T3 and the low transfer efficiency of this isomer into milk suggest that cis-10,trans-12 CLA was the active component..

Animals↗
PubMed2003

Suppression of free radical-induced DNA strand breaks by linoleic acid and low density lipoprotein in vitro.

The results of the present study have shown that unoxidized linoleic acid (LA) and low density lipoprotein (LDL) suppressed free radical-induced supercoiled plasmid DNA strand breaks. Unoxidized LA suppressed DNA strand breaks induced by free radicals generated from hydrogen peroxide/Fe(II) ion, 2'-azobis(2-amidinopropane)hydrochloride (AAPH), and 4-(hydroxymethyl)benzene diazonium salt. Thiobarbituric acid reactive substances (TBARS) of LA were increased on treatment with the radical generators. The intensities of the electron spin resonance (ESR) signals of the spin adducts of the radicals were reduced by unoxidized LA. Although LA hydroperoxide caused DNA strand breaks as has already been shown, its strand breaking activity was observed only at the higher concentrations. Unoxidized LDL inhibited ascorbic acid/Cu(II) ion-, ascorbic acid/Fe(II) ion-, peroxynitrite- and AAPH-induced DNA strand breaks. The TBARS of LDL were increased by treatment with the agents. LDL oxidized with Cu(II) ion did not cause DNA strand breaks. The results indicate that the potency of the free radicals to cause DNA strand breaks was attenuated by the fatty acid and the lipoprotein through lipid peroxidation.

DNA Damage↗
PubMed2003

Effects of dietary conjugated linoleic acid on fatty acid composition and cholesterol content of hen egg yolks.

The main objectives of the present study were to determine the effect of dietary conjugated linoleic acid (CLA) isomers on the fatty acid composition and cholesterol content of egg-yolk lipids. Forty-five 25-week-old laying hens were randomly distributed into five groups of nine hens each and maintained in individual laying cages, throughout 12 weeks of the experiment. They were assigned to the five treatments that consisted of commercial layer diets containing 0, 5, 10, 15 or 20 g pure CLA/kg. Feed intake of hens varied little and insignificantly. Egg mass was uniformly lower (P<0.05) in the hens fed the CLA-enriched diets. Feed conversion efficiency, when expressed per kg eggs, was impaired (P<0.05), although without obvious relation to the dietary CLA concentration. Feeding the CLA-enriched diets resulted in gradually increasing deposition of CLA isomers (P<0.01) in egg-yolk lipids. Saturated fatty acids were increased (P<0.01) and monounsaturated fatty acids decreased (P<0.01). Polyunsaturated fatty acids (PUFA), when expressed as non-CLA PUFA, were also significantly decreased (P<0.01). The most striking effects (P<0.01) were observed for palmitic (16 : 0) and stearic (18 : 0) acids, which increased from 23.6 to 34 % and from 7.8 to 18 %, respectively. On the other hand, oleic acid (18 : 1n-9) decreased from 45.8 to 24.3 %. Among non-CLA PUFA, linoleic (18 : 2n-6) and alpha-linolenic (18 : 3n-3) acids were strongly (P<0.01) decreased, from 14.2 to 7.7 % and from 1.3 to 0.3 %, respectively. The same was true for arachidonic (20:4n-6) and docosahexaenoic (22 : 6n-3) acids. The cholesterol content of egg yolks, when expressed in mg/g yolk, was not affected by the dietary CLA concentrations. In conclusion, unless the adverse effects of CLA feeding to laying hens on the fatty acid profile of egg yolks are eliminated, the CLA-enriched eggs cannot be considered functional food products.

Animal Feed↗
PubMed1991

Effect of linoleic acid hydroperoxide on replication of adenovirus DNA in endothelial cells of bovine aorta.

The effect of linoleic acid hydroperoxide on replication of adenovirus type 2 DNA in cultured endothelial cells of bovine aorta was studied to elucidate the deleterious effect of lipid peroxides on replication of DNA in the arterial endothelial cells. When, just after the infection, the cells were incubated with 1 nmol (measured by the thiobarbituric acid reaction and expressed in terms of malondialdehyde) of the hydroperoxide, the replication of adenovirus type 2 DNA was markedly reduced. The level of the messenger RNA for adenovirus type 2 DNA polymerase was also reduced. In accordance with the reduction of the messenger RNA, the synthesis of the polymerase in the cells was reduced. The inhibition of DNA replication in the arterial endothelial cells by lipid peroxides was discussed in relation to atherogenesis.

Adenoviruses, Human↗
PubMed2002

Factors affecting conjugated linoleic acid and trans-C18:1 fatty acid production by mixed ruminal bacteria.

The objective of this study was to identify environmental factors that influence conjugated linoleic acid (CLA) and trans-C18:1 fatty acid production by mixed ruminal bacteria. Ruminal contents were collected from a 600-kg ruminally fistulated Hereford steer maintained on pasture. Mixed ruminal bacteria were obtained by differential centrifugation under anaerobic conditions and added to a basal medium that contained a commercial emulsified preparation of soybean oil and a mixture of soluble carbohydrates (cellobiose, glucose, maltose, and xylose). Culture samples were collected from batch culture incubations at 0, 2, 4, 6, 8, 12, 24, 26, 28, 30, 32, and 48 h. Continuous culture incubations were conducted at dilution rates of 0.05 and 0.10 h(-1) with extracellular pH values of 5.5 and 6.5, and 0.5 and 1.0 g/L of mixed soluble carbohydrates. Culture samples were obtained from the culture vessel once steady-state conditions had been achieved. In batch culture, trans-C18:1 concentrations increased over time and reached a maximum at 48 h. Little CLA was produced during the first 8 h, but cis-9, trans-11 CLA concentrations remained high between 24 and 30 h. When mixed ruminal bacteria were maintained in continuous culture on 0.5 g/L of mixed soluble carbohydrates, concentrations of trans-C18:1 and cis-9, trans-11 CLA were reduced (P < 0.05) at a dilution rate of 0.05 h(-1) and an extracellular pH of 5.5. Similar effects were also observed when 1.0 g/L of mixed soluble carbohydrates was used. When extracellular pH was lowered to 5.0, neither trans-C18:1 or CLA isomers were detected. In conclusion, our results suggest that culture pH appears to have the most influence on the production of trans-C18:1 and CLA isomers by mixed ruminal bacteria.

Animals↗
PubMed2003

Dietary supplementation of conjugated linoleic acid reduces colon tumor incidence in DMH-treated rats by increasing apoptosis with modulation of biomarkers.

OBJECTIVES: We investigated the effects of conjugated linoleic acid (CLA) on tumor incidence, apoptosis, eicosanoid formation, 1,2-diacylglycerol (DAG), and fatty acid profiles of colonic mucosa in 1,2-dimethylhydrazine-treated rats fed different types of dietary fats. METHODS: One hundred twenty male 7-wk-old Sprague-Dawley rats were assigned to a beef tallow (BT) diet or a fish oil (FO) diet; each group was further divided into two groups, one with CLA supplementation (BTC and FOC) and the other without (BT and FO). All groups were fed for 30 wk on experimental diets that contained 12% (w/w) dietary fat (including 1% CLA for the BTC and FOC groups) and were intramuscularly injected with 1,2-dimethylhydrazine for 6 wk, for a total dose of 180 mg/kg of body weight. RESULTS: Rats fed the FOC, BTC, or FO (omega-3 fatty acids, mainly docosahexaenoic acid) showed a reduced incidence of tumors, increased apoptotic index values (P < 0.05), and lower levels of eicosanoids (prostaglandin E(2) and thromboxane B(2)) and DAG in colonic mucosa (P < 0.05). CLA and docosahexaenoic acid were incorporated into membrane phospholipids and significantly reduced the distribution of arachidonic acid in colonic mucosal phospholipids. Because CLA and omega-3 fatty acids reduced tumor incidence and levels of cell response regulators (prostaglandin E(2), thromboxane B(2), and DAG), they may share at least one common path of action in promoting the apoptotic process of colon carcinogenesis. CONCLUSIONS: These results suggested that increased apoptosis by dietary CLA may be attributed, at least in part, to changes in arachidonic acid metabolism in rats. Therefore, CLA may have anticarcinogenic effects by inducing apoptosis through modification of signal transduction in colonic mucosal cells.

1,2-Dimethylhydrazine↗
PubMed2005

Linoleic acid, but not oleic acid, upregulates production of interleukin-8 by human vascular smooth muscle cells via arachidonic acid metabolites under conditions of oxidative stress.

OBJECTIVE: Preeclampsia is associated with oxidative stress, elevated plasma levels of linoleic acid (LA), and increased vascular smooth muscle expression of the inflammatory chemokine, interleukin-8 (IL-8). We hypothesized that increased levels of LA under conditions of oxidative stress would increased production of IL-8 by vascular smooth muscle cells because LA is the dietary precursor to arachidonic acid (AA) and its metabolites that mediate inflammation. We also hypothesized that oleic acid (OA), which is not metabolized to AA metabolites, would not increase IL-8 under conditions of oxidative stress. METHODS: To test this hypothesis, we cultured placental arterial smooth muscle (PASM) cells with an oxidizing solution enriched with LA (OxLA) or OA (OxOA). Media concentrations were analyzed for IL-8 and AA metabolites. Inhibitors were used to block the lipoxygenase and cyclooxygenase pathways. RESULTS: Exposure of cells to OxLA, but not to OxOA, significantly increased production of IL-8. OxLA also significantly increased production of AA metabolites. Nordihydroguaiaretic acid, an inhibitor of the lipoxygenase pathway, blocked IL-8 and leukotriene B4 (LTB4) production induced by OxLA, whereas indomethacin, an inhibitor of the cyclooxygenase pathway, blocked IL-8, prostaglandin E2 (PGE2), and thromboxane B2 (TXB2) production. Reverse transcriptase-polymerase chain reaction (RT-PCR) demonstrated gene expression in PASM cells for representative lipoxygenase (LTB4) and cyclooxygenase (thromboxane) metabolite receptors. CONCLUSION: PASM cells produced IL-8 in response to LA, but not OA, under conditions of oxidative stress. The IL-8 response was mediated by AA metabolites.

Arachidonic Acid↗
PubMed2002

Influence of dietary conjugated linoleic acid isomers on early inflammatory responses in male broiler chickens.

1. The influence of dietary conjugated linoleic acid isomer (CLA, 0 and 10 g/kg) on the metabolic and physiological responses to immune stimulation induced by a single injection of Salmonella enteritidis lipopolysaccharide (LPS) or repeated injections of LPS and Sephadex G-50 was determined in male broiler chicks. 2. In experiment 1, 10-d-old chicks were fed on experimental diets for 14 d and half of the birds fed on each diet were injected intraperitoneally with LPS (1.5 mg/kg body weight). In experiment 2,7-d-old chicks were fed on experimental diets for 18 d. Immune stimulation was started at 19 d old and continued for 5 d. Half of the birds fed on each diet were injected intraperitoneally with 0.25 mg/kg body weight of LPS at 19, 21 and 23 d of age, and with 250 mg/kg body weight of Sephadex at 20 and 22 d of age to stimulate the immune system. 3. In experiment 1, giving CLA prevented an increase in blood heterophil to lymphocyte ratio 7 h after a single injection of LPS, and increases in plasma ceruloplasmin and alpha 1 acid glycoprotein (AGP) 24 h after the injection, but not 7 h after the injection. CLA also prevented a decrease in food intake for 24 h after LPS injection. 4. In experiment 2, the CLA diet partially prevented reductions in body weight gain and weight gain to feed intake ratio caused by repeated injections of LPS and Sephadex. Feeding CLA prevented increases in plasma ceruloplasmin and AGP at 24 d of age caused by repeated injections of LPS and Sephadex, but not at 20 d of age. 5. These results suggest that feeding CLA alleviates some undesirable metabolic and physiological changes induced by immunological stimulation in male broiler chicks.

Animals↗
PubMed2000

Influence of conjugated linoleic acid (CLA) on establishment and progression of atherosclerosis in rabbits.

OBJECTIVE: To determine effects of conjugated linoleic acid (CLA) on establishment and progression of experimentally-induced atherosclerosis in rabbits. METHODS: For establishment of atherosclerosis, New Zealand White rabbits were fed a semipurified diet containing 0.1% to 0.2% cholesterol for 90 days. Some groups were fed diet and CLA. For effects on progression of atherosclerosis, rabbits with established atherosclerosis were fed a semipurified diet +/- CLA for 90 days. RESULTS: At dietary levels as low as 0.1%, CLA inhibited atherogenesis. At dietary levels of 1%, CLA caused substantial (30%) regression of established atherosclerosis. This is the first example of substantial regression of atherosclerosis being caused by diet alone. CONCLUSION: Dietary CLA is an effective inhibitor of atherogenesis and also causes regression of established atherosclerosis.

Animals↗
PubMed2000

Dietary conjugated linoleic acid protects against end stage disease of systemic lupus erythematosus in the NZB/W F1 mouse.

Conjugated linoleic acid (CLA) is a naturally occurring fatty acid with anti-carcinogenic, anti-atherosclerotic and immune-enhancing activities. Dietary CLA accelerated the onset of proteinuria in autoimmune-prone NZB/W F1 mice but did not affect anti-DNA antibody production. Body weight of the CLA group was decreased compared to the control group at the time proteinuria first developed. CLA group also had slightly earlier mortality than control fed mice, however the mean days of survival did not differ between CLA and control fed mice. Body weight loss between proteinuria onset and death was approximately twice as much in the control group as in the CLA group. Moreover, duration between proteinuria and death was longer in the CLA than in the control group. Our data suggested that dietary CLA may accelerate the autoimmune symptoms of NZB/W F1 mice, however, CLA protected against the disease related body weight loss and prolonged survival after proteinuria.

Animals↗
PubMed2004

Conjugated linoleic acid reduces parathyroid hormone in health and in polycystic kidney disease in rats.

BACKGROUND: Feeding conjugated linoleic acid (CLA) is reported to reduce prostaglandin E(2) synthesis, which is required for parathyroid hormone (PTH) release. OBJECTIVE: This study was undertaken to determine whether CLA would suppress hyperparathyroidism and the resulting high-turnover bone disease in a rat model of polycystic kidney disease (PKD). DESIGN: Outcome measurements were conducted after 8 wk of feeding diets supplemented with and without CLA (1% of dietary fat) to Han:SPRD-cy male rats (n = 52). PTH, bone formation, and resorption were assessed in addition to femur bone mass with use of dual-energy X-ray absorptiometry. RESULTS: CLA feeding resulted in attenuation of PTH concentrations in both PKD-affected and nonaffected rats (by 60%) but did not significantly alter bone formation and resorption. CONCLUSION: Reduction in PTH may open possibilities for CLA as an adjunctive therapy in secondary hyperparathyroidism.

Absorptiometry, Photon↗
PubMed2006

t10,c12 Conjugated linoleic acid induces compensatory growth after immune challenge.

Previous work demonstrated that feeding commercial preparations of conjugated linoleic acid (CLA) [a 50:50 mixture of c9,t11 and t10,c12 CLA (cCLA)] partially overcame lipopolysaccharide (LPS)-induced growth depression. The objective of this study was to determine which CLA isomer was responsible for the reduction of LPS-induced growth depression. Dietary cCLA supplementation for 3 weeks protected mice from LPS-induced weight loss 24 h after injection compared to mice fed isocaloric and isonitrogenous control diets supplemented with either corn oil (CO) or a mixture of CO and olive oil. Dietary c9,t11 or t10,c12 CLA led to body weight loss intermediate to controls and cCLA. After LPS-induced weight loss, the t10,c12 CLA fed mice regained weight faster than the control or c9,t11 CLA fed mice. Dietary t10,c12 CLA and cCLA reduced plasma tumor necrosis factor 2 h after LPS stimulation. While neither c9,t11 nor t10,c12 CLA isomers alone protected from immune-induced weight loss, the t10,c12 CLA isomer induced compensatory gain.

Animals↗
PubMed2004

Red cell membrane and plasma linoleic acid nitration products: synthesis, clinical identification, and quantitation.

Nitric oxide (*NO) and its reactive metabolites mediate the oxidation, nitration, and nitrosation of DNA bases, amino acids, and lipids. Here, we report the structural characterization and quantitation of two allylic nitro derivatives of linoleic acid (LNO(2)), present as both free and esterified species in human red cell membranes and plasma lipids. The LNO(2) isomers 10-nitro-9-cis, 12-cis-octadecadienoic acid and 12-nitro-9-cis, 12-cis-octadecadienoic acid were synthesized and compared with red cell and plasma LNO(2) species based on chromatographic elution and mass spectral properties. Collision-induced dissociation fragmentation patterns from synthetic LNO(2) isomers were identical to those of the two most prevalent LNO(2) positional isomers found in red cells and plasma. By using [(13)C]LNO(2) as an internal standard, red cell free and esterified LNO(2) content was 50 +/- 17 and 249 +/- 104 nM, respectively. The free and esterified LNO(2) content of plasma was 79 +/- 35 and 550 +/- 275 nM, respectively. Nitrated fatty acids, thus, represent the single largest pool of bioactive oxides of nitrogen in the vasculature, with a net LNO(2) concentration of 477 +/- 128 nM, excluding buffy coat cells. These observations affirm that basal oxidative and nitrating conditions occur in healthy humans to an extent that is sufficient to induce abundant membrane and lipoprotein-fatty acid nitration. Given that LNO(2) is capable of mediating cGMP and non-cGMP-dependent signaling reactions, fatty acid nitration products are species representing the convergence of ()NO and oxygenated lipid cell-signaling pathways.

Chromatography, High Pressure Liquid↗
PubMed2002

Methylation methods for the quantitative analysis of conjugated linoleic acid (CLA) isomers in various lipid samples.

Precise methylation methods for various chemical forms of conjugated linoleic acid (CLA), which minimize the formation of t,t isomers and allylmethoxy derivatives (AMD) with the completion of methylation, were developed using a 50 mg lipid sample, 3 mL of 1.0 N H(2)SO(4)/methanol, and/or 3 mL of 20% tetramethylguanidine (TMG)/methanol solution(s). Free CLA (FCLA) was methylated with 1.0 N H(2)SO(4)/methanol (55 degrees C, 5 min). CLA esterified in safflower oil (CLA-SO) was methylated with 20% TMG/methanol (100 degrees C, 5 min), whereas CLA esterified in phospholipid (CLA-PL) was methylated with 20% TMG/methanol (100 degrees C, 10 min), followed by an additional reaction with 1.0 N H(2)SO(4)/methanol (55 degrees C, 5 min). Similarly, CLA esterified in egg yolk lipid (CLA-EYL) was methylated by base hydrolysis, followed by reaction with 1.0 N H(2)SO(4)/methanol (55 degrees C, 5 min). These results suggest that for the quantitative analysis of CLA in lipid samples by GC, proper methylation methods should be chosen on the basis of the chemical forms of CLA in samples.

Chromatography, Gas↗
PubMed2005

Peritoneal metastasis inhibition by linoleic acid with activation of PPARgamma in human gastrointestinal cancer cells.

The effect on peritoneal metastasis of linoleic acid (LA) was examined using in vitro treatment of cancer cells and mouse peritoneal metastasis models. Firstly, cell growth of MKN28 human gastric cancer cells and Colo320 human colon cancer cells was suppressed by LA in a dose-dependent manner with increment of apoptosis. LA-induced growth inhibition was recovered by the exposure to antisense S-oligodeoxynucleotide for peroxisome proliferator-activated receptor gamma (PPARgamma) or 15-lipoxygenase-1, which converts LA to PPARgamma ligands. LA significantly inhibited invasion into type-IV collagen-coated membrane of MKN28 and Colo320 cells (p<0.05). BALB/c nu/nu mice inoculated with MKN28 and Colo320 cells into their peritoneal cavities were administrated with LA intraperitoneally (weekly, four times). The LA treatment significantly diminished the number of metastatic foci of both cells in the peritoneal cavity (p<0.05). Protein production in MKN28 and Colo320 cells treated with LA showed a decrease of epidermal growth factor receptor and an increase of Bax. These findings suggest that LA inhibits invasion and metastasis of human gastric and colon cancer cells by nondietary administration.

Animals↗
PubMed2004

Isomers of conjugated linoleic acid differ in their effects on angiogenesis and survival of mouse mammary adipose vasculature.

Dietary conjugated linoleic acid (CLA) is a cancer chemopreventive agent that has been shown to inhibit angiogenesis in vivo and in vitro, and to decrease vascular endothelial growth factor (VEGF) and Flk-1 concentrations in the mouse mammary gland. To determine which isomer mediates the antiangiogenic effects of CLA in vivo, the effects of diets supplemented with 5 or 10 g/kg c9,t11- or t10,c12-CLA isomers were compared in CD2F1Cr mice. Both isomers inhibited functional vascularization of a matrigel pellet in vivo and decreased serum VEGF concentrations; the t10,c12 isomer also decreased the proangiogenic hormone leptin (P < 0.05). Additionally, the t10,c12 isomer, but not c9,t11-CLA, rapidly induced apoptosis of the white and brown adipocytes as well as the preexisting supporting vasculature of the mammary fat pad (P < 0.05). Independent of this isomer-specific adipose apoptotic effect, both isomers induced a rapid and reversible decrease in the diameter of the unilocular adipocytes (P < 0.05). The ability of both CLA isomers to inhibit angiogenesis in vivo may contribute to their ability to inhibit carcinogenesis. Moreover, we propose that each CLA isomer uniquely modifies the mammary stromal "soil" in a manner that is useful for chemoprevention of breast cancer.

Adipocytes↗