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At least 19 recordsLinked to original sources
PubMed1984

The absorption and transport of dietary cholesterol in the presence of peanut oil or randomized peanut oil.

Peanut oil has been shown to be unexpectedly atherogenic for cholesterol-fed rats, rabbits and rhesus monkeys. However, randomization (rearrangement of fatty acids to random distribution) of peanut oil significantly reduced its atherogenicity for rabbits and monkeys. This study was conducted to investigate whether the absorption and transport of dietary cholesterol was altered in the presence of peanut oil or randomized peanut oil, thereby accounting for the difference in the atherogenicity of the two diets. Intestinal lymph fistula rats were infused intraduodenally with a lipid emulsion at a rate of 3 ml/hr. The lipid emulsion contained either peanut oil (control) or randomized peanut oil (experimental) (10 mM), 14C-cholesterol (1.3 mM) and sodium taurocholate (19 mM) in phosphate-buffered saline, pH 6.4. Lymph triglyceride, cholesterol and phospholipid outputs were similar in both groups of rats during fasting and subsequently during lipid infusion. Comparable recovery of 14C-cholesterol from the intestinal lumen and the intestinal mucosa of the control and the experimental rats showed that the absorption and transport of dietary cholesterol were similar in both groups of rats. Analyses of the fatty acid of both lymph and intestinal mucosal lipid again failed to reveal a difference between the 2 groups of rats. It is concluded that the difference in the atherogenicity between the peanut oil and the randomized peanut oil is probably caused by events subsequent to the release of cholesterol containing chylomicrons and very low density lipoproteins by the small intestinal epithelial cells.

Animals↗
PubMed1998

Lectin may contribute to the atherogenicity of peanut oil.

Peanut oil is unexpectedly atherogenic for rats, rabbits, and primates. The lesions it produces are more fibrous than fatty. The mechanism underlying the atherogenicity of peanut oil has been elusive. Randomization of peanut oil reduces significantly its atherogenic properties, but native and randomized peanut oils have similar rates of lipolysis, and rats fed the two oils absorb and transport lipids in a similar fashion. Peanut oil differs from other oils in having a relatively high lectin content, and the randomization process markedly reduces the lectin content as well. The biologically active lectin of peanut oil has an affinity for glycoproteins found specifically on arterial smooth muscle cells. Peanut lectin has been shown to stimulate growth of smooth muscle and pulmonary arterial cells. Vigorous washing of peanut oil reduces its lectin content by 46%. Compared to rabbits fed cholesterol and peanut oil, rabbits fed cholesterol and washed peanut oil exhibited less severe atherosclerosis in the aortic arch (by 9%) and in the thoracic aorta (by 31%). The data suggest that peanut oils' endogenous lectin may contribute significantly to its atherogenic properties.

Animals↗
PubMedDate not supplied

Cholesterol vehicle in experimental atherosclerosis. Part 18. Comparison of North American, African and South American peanut oils.

Peanut oils were obtained from the United States (NAPNO), Africa (APNO), and South America (SAPNO) and their effects on atherosclerosis in rabbits fed 2% cholesterol were determined. The major differences among the oils were in the content of oleic (NAPNO, 48.9%; APNO, 58.6%; SAPNO, 36.4%) and linoleic (NAPNO, 29.6%; APNO, 21.7%; SAPNO, 41.1%) acids. In a series of 4 experiments it was found that South American peanut oil was 7% more atherogenic than African peanut oil and 18% more atherogenic than North American peanut oil. American peanut oil was 14% more atherogenic that corn oil (CO). South American peanut oil gave highest serum and liver lipid levels. The differences in atherogenicity may be due to the structure of the triglycerides of the various peanut oils.

Africa↗
PubMed1980

Heart pathology in rats fed partially hydrogenated fish oil, rapeseed oil or peanut oil for 30 weeks.

132 male Sprague-Dawley rats were given diets for 30 weeks including rapeseed oil with 41.4% erucic acid, partially hydrogenated fish oil with 15.1% docosenoic acids, or peanut oil with no docosenoic acids. Four diets were isocaloric and contained respectively 21% rapeseed oil (8.7% w/w erucic acid), 10.5% rapeseed oil and 10.5% peanut oil (4.4% w/w erucic acid), 21% partially hydrogenated fish oil (3.2% w/w docosenoic acids) and 21% peanut oil. The fifth diet contained 4.3% peanut oil. The relative heart weights increased in rats fed rapeseed oil and partially hydrogenated fish oil, and abnormally enlarged hearts were found in 32% of the rats fed 21% rapeseed oil and in 5% of those fed 10.5% rapeseed oil. Heart lesions consisting of focal or confluent destruction of muscle cells were seen in all groups. The incidence was 96% and the average severity grade 2.5 when 21% rapeseed oil was given, and 61% and 1.3 respectively when 10.5% rapeseed oil was given. Minor heart lesions were found in 14% of the rats fed 21% partially hydrogenated fish oil, in 39% of those fed 21% peanut oil and in 12% when 4.3% peanut oil was given. It is concluded that partially hydrogenated fish oil is markedly less cardiopathogenic than high erucic rapeseed oil. The heart lesions that were found do not differ in incidence, severity or morphology from those found when peanut oil was given, or from those reported when other control fats and oils are given to rats for prolonged feeding periods.

Animal Feed↗
PubMed1999

Effect of peanut oil and randomized peanut oil on cholesterol and oleic acid absorption, transport, and distribution in the lymph of the rat.

Peanut oil was shown to be atherogenic in cholesterol-fed rats, rabbits, and monkeys. However, after randomization, a process in which the fatty acids in peanut oil are randomly rearranged, its atherogenicity was significantly reduced in cholesterol-fed rabbits and monkeys. The mechanism for this effect remains unknown. This study was designed to investigate whether the absorption, transport and distribution of dietary cholesterol and oleic acid in the lymph were altered in the presence of peanut oil or randomized peanut oil. Previous investigators collected lymph through the mesenteric duct for 6 h and analyzed lymph for cholesterol. In the present study, lymph fluids were collected at timed intervals for up to 8 h and then at 24 h via the thoracic duct. Cholesterol and oleic acid (fatty acid) were estimated not only in the whole lymph but also in lymph lipoprotein fractions and in major lipid fractions. A 24-h lymph collection will enhance accuracy as short-term fluctuations in lipid absorption will not affect the results. Thoracic duct lymph collection is quantitative compared to mesenteric duct lymph collection, which provides only a fraction of the total lymph. Rats were given a lipid emulsion containing either peanut oil or randomized peanut oil. The emulsion also contained cholesterol, oleic acid, and sodium taurocholate in saline and was given through a duodenal catheter. Results show that absorption, transport, and distribution of cholesterol and oleic acid in the lymph fluids were similar in both dietary groups. These results suggest that the atherogenicity of peanut oil may be due to other events taking place subsequent to the release of cholesterol-containing chylomicrons and very low density lipoprotein by the small intestinal epithelial cells into the blood or may be due to the triglyceride structure itself.

Animals↗
PubMed1994

Comparison of atherogenicity of soybean oil and peanut oil, and effect of clentiazem on diet-induced atherosclerosis in rabbits.

Rabbits were fed with two kinds of atherogenic diet, one containing 0.5% cholesterol and 3% soybean oil and the other 0.5% cholesterol and 6% peanut oil, for three months to compare the atherogenic property of the diets. The soybean oil diet seemed to be superior to the peanut oil diet for evaluation of the anti-atherogenic effect of drugs, because the former caused milder vascular lesions than the latter. Using this rabbit model for atherosclerosis, the anti-atherogenic effect of clentiazem, a new calcium antagonist, was examined. Clentiazem at an oral dose of 30 mg/kg/day significantly reduced the size of atheromatous lesion in the aortic arch and thoracic aorta, and lowered the collagen content of the aortic intima and media, although it did not decrease serum lipid levels. On the other hand, clentiazem showed no clear effect on reducing the coronary atherosclerotic lesions. These results suggest that clentiazem may inhibit the progression of diet-induced aortic atherosclerosis without normalizing the serum lipid levels.

Analysis of Variance↗
PubMed1978

Cholesterol vehicle in experimental atherosclerosis. Part 16. Effect of peanut oil on pre-established lesions.

Rabbits were fed an atherogenic diet (2% cholesterol and 6% corn oil) for 8 weeks and then divided into groups of equal average serum cholesterol levels. One group was autopsied, and the others were returned to cholesterol-free diets consisting of commercial laboratory ration or ration augmented with 6% corn oil, peanut oil or PGF, a fat designed to resemble peanut oil minus arachidic and behenic acids. The animals were maintained on the diets for 8 more weeks. On all regimens, severity of atherosclerosis was exacerbated. The extent of exacerbation was significantly less in rabbits fed corn oil than in the others. The extent of exacerbation of lesions appears to be a function of the level of unsaturation of the dietary fats.

Animals↗
PubMed1994

Risks of milk formulas containing peanut oil contaminated with peanut allergens in infants with atopic dermatitis.

Four cases of infants with atopic dermatitis are reported. In all cases, a sensitization to peanut is demonstrated. Any ingestion of peanuts can be excluded, with the exception of a daily consumption of peanut oil, contained in milk formulas. Oral challenges with peanut oil induce a rash, and elimination of these brands is followed by the disappearance of eczematous lesions. The presence of residual allergenic proteins in peanut oil is thus suspected. Owing to the growing incidence of peanut hypersensitivity, the elimination of peanut oil from all milk formulas, food for babies, and ointments, seems to be highly advisable.

Allergens↗
PubMed2001

Final report on the safety assessment of Peanut (Arachis hypogaea) Oil, Hydrogenated Peanut Oil, Peanut Acid, Peanut Glycerides, and Peanut (Arachis hypogaea) Flour.

Peanut (Arachis Hypogaea) Oil is the refined fixed oil obtained from the seed kernels of Arachis hypogaea. Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides are all derived from Peanut Oil. Peanut Flour is a powder obtained by the grinding of peanuts. The oils and glycerides function in cosmetic formulations as skin-conditioning agents. The acid functions as a surfactant-cleansing agent, and the flour functions as an abrasive, bulking agent and/or viscosity-increasing agent. In 1998, only Peanut Oil and Hydrogenated Peanut Oil were reported in use. When applied to the skin, Peanut Oil can enhance the absorption of other compounds. Hepatic changes were noted at microscopic examination of rats fed diets containing 15% edible Peanut Oil for 28 days, although no control group was maintained and the findings were also noted in rats fed fresh corn oil. United States Pharmacopeia (USP)-grade Peanut Oil was considered relatively nonirritating when injected into guinea pigs and monkeys. Technical-grade Peanut Oil was moderately irritating to rabbits and guinea pigs and mildly irritating to rats following dermal exposure. This same oil produced reactions in < or = 10% of 50 human males. Peanut Oil was not an ocular irritant in rabbits. Peanut Oil, either "laboratory expressed" or extracted using a food-grade solvent, was not carcinogenic to mice. Peanut Oil exerted anticarcinogenic activity when tested against known carcinogens. Peanuts are the food most likely to produce allergic and anaphylactic reactions. The major allergen is a protein that does not partition into Peanut Oil, Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides. Aflatoxins can be produced in stored agricultural crops such as peanuts, but do not partition into the oils, acids, or glycerides. Manufacturers were cautioned to make certain that the oils, acids, and glycerides are free of aflatoxins and protein. Formulators were cautioned that the oils, acids, or glycerides may enhance penetration and can affect the use of other ingredients whose safety assessment was based on their lack of absorption. The available studies on Peanut Oil supported the conclusion that Peanut Oil, Hydrogenated Peanut Oil, Peanut Acid, and Peanut Glycerides are safe for use in cosmetic formulations. Peanut (Arachis Hypogaea) Flour, however, is sufficiently different from the above ingredients such that its safety can not be supported by studies using the oil. The additional data needed for Peanut (Arachis Hypogaea) Flour are (1) concentration of use; (2) chemical specifications (i.e., aflatoxin and protein levels); (3) method of preparation; and (4) contact urticaria and dermal sensitization at concentration of use. Although data on aflatoxin levels are sought, it is expected that concentrations of aflatoxin should comply with U.S. government stipulations. Absent the additional data, it was concluded that the available data are insufficient to support the safety of Peanut (Arachis Hypogaea) Flour for use in cosmetic products.

Administration, Cutaneous↗
PubMed1987

Biological observations from feeding heated corn oil and heated peanut oil to rats.

Five groups of male weanling rats were provided purified diets containing 15% by weight of either fresh or laboratory-heated corn oil (FCO, HCO) or fresh, laboratory-heated, or commercial pressure deep-fry peanut oil (FPO, HPO, PPO). Total weight gain, feed consumption, and feed efficiency were consistently greater for the FCO, FPO, and PPO groups. Although relative heart weights were unaffected, the HCO and HPO produced elevated liver and kidney weights. The dietary fats had no effect on the hematological status of the animals or the proportions of cells comprising the total leukocytes of the blood. Physical, chemical, and microscopic evaluation of the urine detected no pathologic conditions. Rats fed diets containing HCO or HPO demonstrated toxicity of thermally oxidized fats by the appearance of diarrhea, dermatitis, seborrhea, and hair loss. Histological examinations revealed injury of the thymus by all fat samples except the FCO; the liver was damaged by the HCO, HPO, and PPO, and the testes and epididymides by HPO and PPO. In the latter case there was complete cessation of spermatogenesis.

Animals↗