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Applied Physiology, Nutrition, and... Dec 2016Carthamus tinctorius L. (common name: safflower) is an herb whose extracted oil (safflower oil) has been employed in both alternative and conventional medicine in the... (Comparative Study)
Comparative Study
Carthamus tinctorius L. (common name: safflower) is an herb whose extracted oil (safflower oil) has been employed in both alternative and conventional medicine in the treatment of disease. Overnutrition during early postnatal life can increase the lifetime risk of obesity and metabolic syndrome. Here we investigate the effect of safflower oil supplementation given during a critical early developmental stage on the eventual occurrence of metabolic disease in overnourished rats. Groups of overnourished or adequately nourished rats were randomly assigned into 2 additional groups for supplementation with either safflower oil (SF) or vehicle for 7 to 30 days. Murinometric data and weights were examined. Serum was collected for measurement of glucose, cholesterol, high-density lipoprotein cholesterol, and triglycerides. Heart and liver oxidative status were also measured. Overnutrition for 7-30 days induced a significant increase in body weight and in values for abdominal circumference, thoracic circumference, body length, and body mass index. SF supplementation did not attenuate the effect of overnutrition on any of these parameters. In addition, overnutrition increased levels of glucose, triglycerides, and very low-density lipid compared with normal controls, but SF supplementation had no effect on these parameters. Measures of oxidative status in heart or liver were not influenced by overnutrition. However, oxidative measures were altered by SF supplementation in both of these organs. The present study reveals that nutritional manipulation during early development induces detrimental effects on metabolism in the adult that are not ameliorated by supplemental SF.
Topics: Animals; Carthamus tinctorius; Dietary Supplements; Fatty Acids, Omega-6; Female; Hyperglycemia; Hyperlipidemias; Lactation; Liver; Male; Maternal Nutritional Physiological Phenomena; Myocardium; Obesity; Overnutrition; Oxidative Stress; Plant Preparations; Pregnancy; Random Allocation; Rats, Wistar; Safflower Oil; Weaning; Weight Gain
PubMed: 27863203
DOI: 10.1139/apnm-2016-0191 -
Journal of Agricultural and Food... Aug 2012Evidence suggests that monounsaturated and polyunsaturated fats facilitate greater absorption of carotenoids than saturated fats. However, the comparison of consuming a... (Comparative Study)
Comparative Study
Evidence suggests that monounsaturated and polyunsaturated fats facilitate greater absorption of carotenoids than saturated fats. However, the comparison of consuming a polyunsaturated fat source versus a saturated fat source on tomato carotenoid bioaccumulation has not been examined. The goal of this study was to determine the influence of coconut oil and safflower oil on tomato carotenoid tissue accumulation in Mongolian gerbils ( Meriones unguiculatus ) fed a 20% fat diet. Coconut oil feeding increased carotenoid concentrations among many compartments including total carotenoids in the serum (p = 0.0003), adrenal glandular phytoene (p = 0.04), hepatic phytofluene (p = 0.0001), testicular all-trans-lycopene (p = 0.01), and cis-lycopene (p = 0.006) in the prostate-seminal vesicle complex compared to safflower oil. Safflower oil-fed gerbils had greater splenic lycopene concentrations (p = 0.006) compared to coconut oil-fed gerbils. Coconut oil feeding increased serum cholesterol (p = 0.0001) and decreased hepatic cholesterol (p = 0.0003) compared to safflower oil. In summary, coconut oil enhanced tissue uptake of tomato carotenoids to a greater degree than safflower oil. These results may have been due to the large proportion of medium-chain fatty acids in coconut oil, which might have caused a shift in cholesterol flux to favor extrahepatic carotenoid tissue deposition.
Topics: Animals; Body Weight; Carotenoids; Cholesterol; Coconut Oil; Fatty Acids; Gerbillinae; Liver; Lycopene; Solanum lycopersicum; Male; Organ Size; Plant Oils; Safflower Oil; Spleen; Testis; Tissue Distribution
PubMed: 22866697
DOI: 10.1021/jf301902k -
Hepatology (Baltimore, Md.) Dec 2007Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). We analyzed the effects of dietary fish oil on fatty liver induced by sucrose,...
UNLABELLED
Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). We analyzed the effects of dietary fish oil on fatty liver induced by sucrose, safflower oil, and butter in ddY mice. In experiment I, mice were fed a high-starch diet [70 energy% (en%) starch] plus 20% (wt/wt) sucrose in the drinking water or fed a high-safflower oil diet (60 en%) for 11 weeks. As a control, mice were fed a high-starch diet with drinking water. Fish oil (10 en%) was either supplemented or not. Mice supplemented with sucrose or fed safflower oil showed a 1.7-fold or 2.2-fold increased liver triglyceride content, respectively, compared with that of control mice. Fish oil completely prevented sucrose-induced fatty liver, whereas it exacerbated safflower oil-induced fatty liver. Sucrose increased SREBP-1c and target gene messenger RNAs (mRNAs), and fish oil completely inhibited these increases. In experiment II, mice were fed a high-safflower oil or a high-butter diet, with or without fish oil supplementation. Fish oil exacerbated safflower oil-induced fatty liver but did not affect butter-induced fatty liver. Fish oil increased expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and target CD36 mRNA in safflower oil-fed mice. These increases were not observed in sucrose-supplemented or butter-fed mice.
CONCLUSION
The effects of dietary fish oil on fatty liver differ according to the cause of fatty liver; fish oil prevents sucrose-induced fatty liver but exacerbates safflower oil-induced fatty liver. The exacerbation of fatty liver may be due, at least in part, to increased expression of liver PPARgamma.
Topics: Animals; Butter; Fatty Liver; Fish Oils; Male; Mice; Safflower Oil; Sucrose; Sweetening Agents
PubMed: 17935225
DOI: 10.1002/hep.21934 -
Caries Research 2012The prevalence of dental erosion is still increasing. A possible preventive approach might be rinsing with edible oils to improve the protective properties of the...
AIM
The prevalence of dental erosion is still increasing. A possible preventive approach might be rinsing with edible oils to improve the protective properties of the pellicle layer. This was tested in the present in situ study using safflower oil.
METHODS
Pellicle formation was carried out in situ on bovine enamel slabs fixed buccally to individual upper jaw splints (6 subjects). After 1 min of pellicle formation subjects rinsed with safflower oil for 10 min, subsequently the samples were exposed in the oral cavity for another 19 min. Enamel slabs without oral exposure and slabs exposed to the oral cavity for 30 min without any rinse served as controls. After pellicle formation in situ, slabs were incubated in HCl (pH 2; 2.3; 3) for 120 s, and kinetics of calcium and phosphate release were measured photometrically (arsenazo III, malachite green). Furthermore, the ultrastructure of the pellicles was evaluated by transmission electron microscopy (TEM).
RESULTS
Pellicle alone reduced erosive calcium and phosphate release significantly at all pH values. Pellicle modification by safflower oil resulted in an enhanced calcium loss at all pH values and caused an enhanced phosphate loss at pH 2.3. TEM indicated scattered accumulation of lipid micelles and irregular vesicle-like structures attached to the oil-treated pellicle layer. Acid etching affected the ultrastructure of the pellicle irrespective of oil rinsing.
CONCLUSION
The protective properties of the pellicle layer against extensive erosive attacks are limited and mainly determined by pH. The protective effects are modified and reduced by rinses with safflower oil.
Topics: Adult; Animals; Arsenazo III; Calcium; Cattle; Coloring Agents; Dental Enamel; Dental Pellicle; Humans; Hydrochloric Acid; Hydrogen-Ion Concentration; Lipids; Materials Testing; Micelles; Microscopy, Electron, Transmission; Mouth; Phosphorus; Photometry; Protective Agents; Rosaniline Dyes; Safflower Oil; Tooth Erosion; Young Adult
PubMed: 22813924
DOI: 10.1159/000339924 -
Molecular Human Reproduction Apr 2010Aberrant arachidonic acid and nitric oxide (NO) metabolic pathways are involved in diabetic embryopathy. Previous works have found diminished concentrations of PGE(2)...
Aberrant arachidonic acid and nitric oxide (NO) metabolic pathways are involved in diabetic embryopathy. Previous works have found diminished concentrations of PGE(2) and PGI(2) in embryos from diabetic rats, and that PGI(2) is capable of increasing embryonic PGE(2) concentrations through the activation of the nuclear receptor PPARdelta. PPARdelta activators are lipid molecules such as oleic and linoleic acids, present in high concentrations in olive and safflower oils, respectively. The aim of this study was to analyze the capability of dietary supplementation with either 6% olive or 6% safflower oils to regulate PGE(2), PGI(2) and NO concentrations in embryos and deciduas from control and diabetic rats during early organogenesis. Diabetes was induced by a single injection of streptozotocin (55 mg/kg) 1 week before mating. Animals were fed with the oil-supplemented diets from Days 0.5 to 10.5 of gestation. PGI(2) and PGE(2) were measured by EIA and NO through the evaluation of its stable metabolites nitrates-nitrites in 10.5 day embryos and deciduas. We found that the olive and safflower oil-supplemented treatments highly reduced resorption and malformation rates in diabetic animals, and that they were able to prevent maternal diabetes-induced alterations in embryonic and decidual PGI(2) and PGE(2) concentrations. Moreover, these dietary treatments prevented NO overproduction in embryos and deciduas from diabetic rats. These data indicate that in maternal diabetes both the embryo and the decidua benefit from the olive and safflower oil supplementation probably through mechanisms that involve the rescue of aberrant prostaglandin and NO generation and that prevent developmental damage during early organogenesis.
Topics: Animals; Arachidonic Acid; Diabetes Mellitus, Experimental; Dietary Fats; Dietary Supplements; Dinoprostone; Embryo, Mammalian; Female; Fetal Diseases; Male; Models, Biological; Nitric Oxide; Olive Oil; Plant Oils; Pregnancy; Pregnancy in Diabetics; Rats; Rats, Wistar; Safflower Oil
PubMed: 20051498
DOI: 10.1093/molehr/gap109 -
Journal of Medicinal Food Aug 2020The study aims to establish how feasible a natural therapy option (safflower oil) is in the treatment of postoperative pain. Naproxen sodium has already been...
The study aims to establish how feasible a natural therapy option (safflower oil) is in the treatment of postoperative pain. Naproxen sodium has already been experimentally proven to be effective for this purpose. Accordingly, the analgesic and anti-inflammatory effects of safflower oil were compared with those obtained with benzydamine HCl and naproxen sodium. Forty-two, healthy, adult female rats of Wistar albino species were divided at random into six groups of seven rats. The intervention allocation was as follows: Group No. 1-physiological saline 0.9%; Group No. 2-safflower oil 100 mg/kg; Group No. 3-safflower oil 300 mg/kg; Group No. 4-benzydamine HCl 30 mg/kg; Group No. 5-benzydamine HCl 100 mg/kg; and Group No. 6-naproxen sodium 10 mg/kg. Following allocation of treatment, pain was induced experimentally and tested in various ways (hot plate test, tail-pinching test, and writhing test) and the efficacy of each treatment in providing peripheral and central analgesia was evaluated. The second stage consisted of providing different treatments to four groups (groups 7-10) of seven rats each, chosen at random. The allocations were as follows: Group No. 7-physiological saline 0.9%; Group No. 8-safflower oil 300 mg/kg; Group No. 9-benzydamine HCl 100 mg/kg; and Group No. 10-naproxen sodium 10 mg/kg. To create experimental inflammation, 2% formaldehyde was injected into the experimental animal's paw and the resulting edema was measured and recorded for a 10-day period. Edema inhibition was calculated as a percentage. The rats were sacrificed and the paw and stomach dissected for histopathological examination. The data were used for statistical analysis, using the Shapiro-Wilk, Kruskal-Wallis test, and two-way analysis of variance. In the tail-pinching test, it was determined that a 300 mg/kg dose of safflower oil shows central spinal analgesic efficacy and this effect is close in magnitude to 10 mg/kg of the reference material, naproxen sodium. In the squirming test, it was observed that the 100 and 300 mg/kg doses of safflower oil had a peripheral analgesic effect when compared with the serum physiological (placebo) group. The peripheral efficacy of 300 mg/kg safflower oil was found to approximate that of 10 mg/kg naproxen sodium. In rats treated with benzydamine HCl 100 mg/kg, similar peripheral analgesic efficacy to naproxen sodium 10 mg/kg was noted. In the hot plate test, no difference in the analgesic efficacy between the various agents was found. The change in inhibition of edema between the 1st and 10th days was most marked in rats receiving naproxen sodium 10 mg/kg. A significant difference was determined in the safflower oil 300 mg/kg and benzydamine HCl 100 mg/kg groups ( < .001). Regarding histopathology findings in the rat paw, significant differences were seen in venous congestion between placebo and safflower oil 300 mg/kg and in inflammation between the control and benzydamine HCl 100 mg/kg groups. Regarding the histopathology findings in the rat stomach, significant differences were observed in venous congestion between placebo and safflower oil 300 mg/kg; in damage to the epithelium between placebo and safflower oil 300 mg/kg and between naproxen sodium 10 mg/kg and safflower oil; and in cell infiltration and development of edema between placebo and safflower oil 300 mg/kg. It is predicted that further research into safflower oil and benzydamine HCl will create opportunities to develop analgesic-anti-inflammatory therapeutics of a novel kind for the treatment of postoperative pain and inflammation.
Topics: Analgesics; Animals; Anti-Inflammatory Agents; Benzydamine; Female; Inflammation; Naproxen; Pain; Rats; Rats, Wistar; Safflower Oil
PubMed: 32216647
DOI: 10.1089/jmf.2019.0157 -
Journal of Dairy Science Feb 2006Conjugated linoleic acid (CLA) refers to a mixture of conjugated octadecadienoic acids of predominantly ruminant origin. The main isomer in bovine milk fat is the cis-9,... (Randomized Controlled Trial)
Randomized Controlled Trial
Conjugated linoleic acid (CLA) refers to a mixture of conjugated octadecadienoic acids of predominantly ruminant origin. The main isomer in bovine milk fat is the cis-9, trans-11 CLA. Interest in CLA increased after the discovery of its health-promoting properties, including potent anticarcinogenic activity. Two experiments were conducted to evaluate dietary strategies aimed at increasing the concentration of CLA in bovine milk fat. Both experiments were organized as a randomized complete block design with a repeated measures treatment structure. In Experiment 1, 28 Holstein cows received either a control diet or one of 3 treatments for a period of 2 wk. The control diet consisted of 60% forage (barley silage, alfalfa silage, and alfalfa hay) and 40% concentrate on a dry matter (DM) basis, fed as a total mixed ration (TMR). The concentrate was partially replaced in the treatment groups with 24 ppm of monensin (MON), 6% of DM safflower oil (SAFF), or 6% of DM safflower oil plus 24 ppm of monensin (SAFF/M). Average cis-9, trans-11 CLA levels in milk fat after 2 wk of feeding were 0.45, 0.52, 3.36, and 5.15% of total fatty acids for control, MON, SAFF, and SAFF/M, respectively. In Experiment 2, 62 Holstein cows received either a control diet or one of 5 treatment diets for a period of 9 wk. The control diet consisted of 60% forage (barley silage, alfalfa silage, and alfalfa hay) and 40% concentrate on a DM basis, fed as a TMR. The concentrate was partially replaced in the treatment groups with 6% of DM safflower oil (SAFF), 6% of DM safflower oil plus 150 IU of vitamin E/kg of DM (SAFF/E), 6% of DM safflower oil plus 24 ppm of monensin (SAFF/M), 6% of DM safflower oil plus 24 ppm of monensin plus 150 IU of vitamin E/kg of DM (SAFF/ME), or 6% of DM flaxseed oil plus 150 IU of vitamin E/kg of DM (FLAX/E). Average cis-9, trans-11 CLA levels during the treatment period were 0.68, 4.12, 3.48, 4.55, 4.75, and 2.80% of total fatty acids for control, SAFF, SAFF/E, SAFF/M, SAFF/ME, and FLAX/E, respectively. The combination of safflower oil with monensin was particularly effective at increasing milk fat CLA. The addition of vitamin E to the diet partially prevented the depression in milk fat associated with oilseed feeding, but had no significant effect on the concentration of CLA in milk.
Topics: Animal Feed; Animals; Cattle; Cell Count; Fats; Fatty Acids; Female; Hydrogenation; Lactation; Lactose; Linoleic Acids, Conjugated; Linseed Oil; Milk; Milk Proteins; Monensin; Rumen; Safflower Oil; Vitamin E
PubMed: 16428641
DOI: 10.3168/jds.S0022-0302(06)72135-X -
The Journal of Nutrition Oct 1991Studies were conducted to explore the mechanisms by which dietary fish oil decreases hepatic triglyceride secretion. Forty-five rats (15/group) were fed purified diets... (Comparative Study)
Comparative Study
Studies were conducted to explore the mechanisms by which dietary fish oil decreases hepatic triglyceride secretion. Forty-five rats (15/group) were fed purified diets containing 10% fat as either fish oil, safflower oil or palm oil for 10 d. Plasma triglyceride concentration was lowest in the fish oil-fed group followed by the groups fed safflower oil and palm oil. The liver's capacity to oxidize fatty acids was assessed by assays of mitochondrial and peroxisomal beta-oxidation pathways in whole homogenates. Additionally, key enzymatic activities in the biosynthesis of triglyceride (diacylglycerol acyltransferase, phosphatidate hydrolysis) and phosphatidylcholine (CTP:phosphocholine cytidylyltransferase) were assayed. Compared with those fed palm oil the fish oil-fed animals showed 25% greater mitochondrial beta-oxidation but this difference was not statistically significant (P = 0.1). Fish oil feeding led to 45% greater (P less than 0.05) peroxisomal beta-oxidation. Diacylglycerol acyltransferase activity was unaffected by the type of dietary fat and slightly (13%) but significantly (P less than 0.02) lower cytidylyltransferase activity due to fish oil feeding was observed. More strikingly, both fish oil and safflower oil diets significantly lowered phosphatidate hydrolysis by 37 and 22%, respectively, compared with the palm oil diet. This activity directly correlated (r = 0.68; P less than 0.001) with plasma triglyceride concentration. Thus, dietary fish oil might suppress triglyceride secretion by decreasing glycerolipid synthesis, an effect mediated by changes in one or more enzymes involved in phosphatidate catabolism.
Topics: Animals; Body Weight; Dietary Fats; Fatty Acids; Fish Oils; Liver; Male; Palm Oil; Plant Oils; Rats; Rats, Inbred Strains; Safflower Oil; Triglycerides
PubMed: 1765819
DOI: 10.1093/jn/121.10.1554 -
Annals of Surgery Aug 1991With the advent of cyclosporin A, accelerated coronary arteriosclerosis has become the major impediment to the long-term survival of heart transplant recipients. Due to...
With the advent of cyclosporin A, accelerated coronary arteriosclerosis has become the major impediment to the long-term survival of heart transplant recipients. Due to epidemiologic reports suggesting a salutary effect of fish oil, the dose response of fish oil on graft coronary arteriosclerosis in a rabbit heterotopic cardiac allograft model was assessed using safflower oil as a caloric control. Seven groups of New Zealand White rabbits (n = 10/group) received heterotropic heart transplants from Dutch-Belted donors and were immunosuppressed with low-dose cyclosporin A (7.5 mg/kg/day). Group 1 animals were fed a normal diet and served as control. Group 2, 3, and 4 animals received a daily supplement of low- (0.25 mL/kg/day), medium- (0.75 mL/kg/day), and high- (1.5 mL/kg/day) dose fish oil (116 mg n-3 polyunsaturated fatty acid/mL), respectively. Group 5, 6, and 7 animals were supplemented with equivalent dose of safflower oil (i.e., 0.25, 0.75, and 1.5 mL/kg/day). Oil-supplemented rabbits were pretreated for 3 weeks before transplantation and maintained on the same diet for 6 weeks after operation. The extent of graft coronary arteriosclerosis was quantified using computer-assisted, morphometric planimetry. When the animals were killed, cyclosporin A was associated with elevated plasma total cholesterol and triglyceride levels in the control group. While safflower oil prevented the increase in plasma lipids at all dosages, fish oil ameliorated the cyclosporin-induced increase in total cholesterol only with high doses. Compared to control animals, there was a trend for more graft vessel disease with increasing fish oil dose, as assessed by mean luminal occlusion and intimal thickness. A steeper trend was observed for increasing doses of safflower oil; compared to the high-dose safflower oil group, animals supplemented with low-dose safflower oil had less mean luminal occlusion (16.3% +/- 5.9% versus 41.4% +/- 7.6%, p less than 0.017) and intimal thickness (7.9 +/- 1.9 microns versus 34.0 +/- 13.0 microns, analysis of variance: p = 0.054). Low-dose safflower oil also had a slight, but nonsignificant, beneficial effect on graft vessel disease when compared to control rabbits. The same trends were observed in the degree of histologic rejection (0 = none to 3 = severe) in fish oil- and safflower oil-treated animals. Rejection score correlated weakly but significantly (p = 0.0001) with mean luminal occlusion (r = 0.52) and intimal thickness (r = 0.46). Therefore allograft coronary disease in this model appeared to exhibit an unfavorable, direct-dose response to fish oil and safflower oil, independent of effects on plasma lipids.(ABSTRACT TRUNCATED AT 400 WORDS)
Topics: Animals; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Copper; Coronary Artery Disease; Cyclosporins; Fatty Acids; Fish Oils; Graft Rejection; Heart Transplantation; Oxidation-Reduction; Rabbits; Safflower Oil; Thromboxanes; Transplantation, Heterotopic; Transplantation, Homologous; Triglycerides
PubMed: 1867523
DOI: 10.1097/00000658-199108000-00010 -
The American Journal of Clinical... Feb 1998Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid (LA) with conjugated double bonds. CLA has anticarcinogenic properties... (Clinical Trial)
Clinical Trial
Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid (LA) with conjugated double bonds. CLA has anticarcinogenic properties and has been identified in human tissues, dairy products, meats, and certain vegetable oils. A variety of animal products are good sources of CLA, but plant oils contain much less. However, plant oils are a rich source of LA, which may be isomerized to CLA by intestinal microorganisms in humans. To investigate the effect of triacylglycerol-esterified LA consumption on plasma concentrations of esterified CLA in total lipids, a dietary intervention (6 wk) was conducted with six men and six women. During the intervention period a salad dressing containing 21 g safflower oil providing 16 g LA/d was added to the subjects' daily diets. Three-day diet records and fasting blood were obtained initially and during dietary and postdietary intervention periods. Although LA intake increased significantly during the dietary intervention, plasma CLA concentrations were not affected. Plasma total cholesterol and LDL-cholesterol concentrations were significantly lower after addition of safflower oil to the diet. In summary, consumption of triacylglycerol-esterified LA in safflower oil did not increase plasma concentrations of esterified CLA in total lipids.
Topics: Adult; Anthropometry; Cholesterol; Dietary Fats; Female; Humans; Intestinal Mucosa; Intestines; Linoleic Acid; Male; Safflower Oil
PubMed: 9459383
DOI: 10.1093/ajcn/67.2.332