Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Butter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1998

Physical properties of Malaysian cocoa butter as affected by addition of milkfat and cocoa butter equivalent.

Commercial samples of Malaysian cocoa butter (MCB), anhydrous milkfat (AMF), high melting fraction milkfat42 (HMF42) and cocoa butter equivalent (CBE) were blended in binary and ternary blends. All the fats were then evaluated for their solid fat content, thermal analyses and polymorphic stability. MCB possessed the highest solid followed by CBE, HMF42 and AMF. Data on thermal analyses showed that eutectic interaction was more noticeable when AMF and HMF42 were present in the MCB and CBE system. Moreover, X-ray diffraction patterns also showed that AMF and HMF42 exhibit the presence of beta' polymorph while MCB and CBE exhibit beta polymorph.

Animals↗
PubMedDate not supplied

Development of a rapid method for the detection of cocoa butter equivalents in mixtures with cocoa butter.

A simple and rapid gas chromatographic (GC) method was developed for the detection of cocoa butter equivalents (CBEs) in cocoa buffer (CB). It is based on the use of a 5 m nonpolar capillary column for the separation of the main triglycerides of CB according to their acyl/carbon numbers. The GC procedure was optimized to avoid thermal degradation of the triglycerides. By computing the ratio C54/C50 and (C54/C50) x C52 and by 2-dimensional plotting of these values, authentic CB samples were clearly distinguished from samples containing various CBEs. The detection of little as 1% CBE in CB (corresponding to about 0.3% CBE in chocolate) in a model system was shown to be possible. Under real conditions, for a wide range of CBs, about 2.5% CBEs in CB were detected. With this method, quantitation was possible at a concentration of 5% CBEs in CB mixtures, which corresponds to around 1% in chocolate; this value is far below the maximum level of 5% CBEs allowed to be added to chocolate.

Chromatography, Gas↗
PubMed2005

A worldwide survey of polychlorinated dibenzo-p-dioxins, dibenzofurans, and related contaminants in butter.

The main source of human exposure to persistent organic pollutants (POPs) is, in general, food. In this study, 64 butter samples from 37 countries were analyzed to assess the global contamination of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), biphenyls (PCBs), hexachlorobenzene (HCB), and 2,2-bis (4-chlorophenyl)-1,1,1-trichloroethane (DDT) together with its major metabolites. The objectives of the study were to assess the presence of major organohalogen contaminants in butter, to trace geographical differences, and to determine toxic equivalents (TEQs) of PCDDs/Fs and dioxin-like PCBs in butter. The highest PCDD/F concentrations were found in butter from Korea with an average of 1.4 pg TEQ g(-1) lipid weight (l.w.). from PCDD/F and an additional contribution from the non- and mono-ortho-PCBs of 0.55 pg TEQ g(-1) l.w. Belgian butter showed average levels of 0.53 and 1.2 pg TEQ g(-1) l.w. for PCDDs/Fs and PCBs, respectively, but one sample of Belgium butter had a total TEQ level as high as 4.0 pg TEQ g(-1) l.w. Three out of five butter samples from Portugal showed similarly high PCDD/F TEQ levels. The sigmaPCB levels in European butter appeared to be somewhat higher than in the samples from the rest of the world. The average contribution of CB-153 to the total PCB concentration was 22% (SD 6.4, coefficient of variation 29%). Generally, the PCBs contributed around 60% of the total TEQ value, with CB-126 contributing approximately half of this value. This shows the important TEQ contribution from dioxinlike PCBs to the total TEQs. The highest HCB levels were found in butter samples from Russia, Ukraine, Belgium, and Slovenia. Low levels of HCB in butter were generally found in the Southern Hemisphere. Butter samples from countries from Eastern Europe had elevated sigmaDDT concentrations, with a particularly high concentration in Ukraine butter, followed by some Russian samples, Brazil, and the U.S.

Benzofurans↗
PubMed1981

Composition of cocoa shell fat as related to cocoa butter.

The physical and chemical constants of cocoa shell fat (a by-product resulted during the production of cocoa butter at chocolate factories) were almost identical with those of cocoa butter obtained from the same cocoa beans except for their high acid value. Shell fat contained more amount of phospholipid content (as cephalin) than cocoa butter. The lipid classes were almost the same in cocoa butter and shell fat, however, the latter contained an unidentified constituent which was not found in cocoa butter. The fatty acids were determined quantitatively by GLC, and the results showed that the predominant acids in cocoa butter were palmitic, and oleic. Less amounts of capric, myristic, palmitoleic and linoleic were found in cocoa butter, whereas more amounts of these acids were found in shell fat. Cocoa butter gave higher values of stearic and myristic acids than those of shell fat. Seventeen compounds were detected by GLC in the unsaponifiable matter of both cocoa butter and shell fat from which eight were identified as C30 hydrocarbon, C32 hydrocarbon, squalene, alpha-tocopherol, cholesterol, campsterol, stigmasterol and beta-sitosterol in the two samples. The sterols were determined quantitatively, and it was found that the predominant sterol in cocoa butter and shell fat was B-sitosterol. Cocoa butter contained higher values of stigmasterol than that of shell fat, which contained increasing values of campsterol, low values of cholesterol were found in both samples. Stability of cocoa butter and shell fat towards oxidative rancidity at 100 degrees C was the same (10.5 hrs).

Cacao↗
PubMed2000

Fate of Campylobacter jejuni in butter.

An outbreak of Campylobacter enteritis was associated with a restaurant in Louisiana during the summer of 1995. Thirty cases were identified, and four required hospitalization. Campylobacter jejuni was isolated from the patients, and epidemiologic studies revealed illness associated with eating garlic butter served at the restaurant. Three batches of garlic butter prepared by the restaurant associated with the outbreak and a C. jejuni isolate obtained from a patient involved in the outbreak were used for studies to determine the fate of C. jejuni in garlic butter. Studies also were done to determine the efficacy of the heat treatment used by the restaurant to prepare garlic bread to kill C. jejuni. Garlic butter was inoculated with approximately 10(4) and 10(6) CFU/g of C. jejuni and held at 5 or 21 degrees C. Results revealed that the survival of C. jejuni differed greatly, depending on the presence or absence of garlic. At 5 degrees C, C. jejuni populations decreased to an undetectable level (<10 CFU/g) within 3 h for two batches and within 24 h for another batch. In contrast, C. jejuni could survive at 5 degrees C for 13 days in butter with no garlic. At 21 degrees C, C. jejuni populations decreased to an undetectable level within 5 h for two batches and to 50 CFU/g in 5 h for another batch. In contrast, C. jejuni was detected at 500 CFU/g at 28 h after inoculation but was undetectable at 3 days in butter with no garlic held at 21 degrees C. The heating procedure (135 degrees C, 4 min) used to make garlic bread by the implicated restaurant was determined not to be sufficient for killing C. jejuni, with the internal temperature of the buttered bread after heating ranging from 19 to 22 degrees C. This study revealed that C. jejuni can survive for many days in refrigerated butter, but large populations (10(3) to 10(5) CFU/g) are killed within a few hours in butter that contains garlic. Furthermore, the heat treatment used by the restaurant to melt garlic butter in making garlic bread was not adequate to kill C. jejuni.

Animals↗
PubMedDate not supplied

[A new type of creamery butter for pediatric and dietetic nutrition].

The paper presents the data on the chemical composition and the technology of manufacturing a new sort of butter for child's and dietetic nutrition. The butter has high biological value due to the introduction of polyunsaturated fatty acids (PUSFA) with vegetable oils and milk-protein ingredients. The milk-protein ingredients also play the role of the butter structure stabilizers. The chemical composition of the new sort of butter, including the vitamin and mineral content, as well as the amino-acid composition of the butter plasma are described. It is shown that the content of PUSFA in the new sort of butter is 10-fold higher than in the routine butter. Various kinds of dessert butter have been developed with different flavoring additives. One of the butter variant has been enriched with bifidobacteria. The new sort of butter is recommended for the dietetic nutrition of children and adults suffering from obesity, as well as for the nutrition of the middle- and old-aged subjects to prevent lipid metabolism disorders.

Bifidobacterium↗
PubMed1997

Butter, margarine and serum lipoproteins.

Intake of trans fatty acids unfavorably affects blood lipoproteins. As margarines are a major source of trans, claims for the advantages of margarines over butter need to be scrutinized. Here we review dietary trials that directly compared the effects of butter and margarine on blood lipids. We identified 20 studies in which subjects had stable body weights, and margarine and butter were exchanged in the diet at constant energy and fat intake. We calculated the changes in average blood lipid levels between study diets (49 comparisons) as a function of the percentage of calories as margarine substituted for butter. Replacing 10% of calories from butter by hard high-trans stick margarines lowered total serum cholesterol by 0.19, LDL by 0.11, and HDL by 0.02 mmol/l, and did not affect the total/HDL cholesterol ratio. Soft low-trans tub margarines decreased total cholesterol by 0.25 and LDL by 0.20 mmol/l, did not affect HDL, and decreased the total/HDL cholesterol ratio by 0.20. Based on the total/HDL cholesterol ratio, replacement of 30 g of butter per day by soft tub margarines would theoretically predict a reduction in coronary heart disease risk of 10%, while replacement of butter by hard, high-trans margarines would have no effect. Replacing butter by low-trans soft margarines favorably affects the blood lipoprotein profile and may reduce the predicted risk of coronary heart disease, but high-trans hard margarines probably confer no benefit over butter.

Butter↗
PubMed2001

Exposure of Listeria monocytogenes within an epidemic caused by butter in Finland.

Data on the levels of bacteria and the amounts of food consumed in food-borne outbreaks provides an excellent opportunity to study the effects of exposure to Listeria monocytogenes. Between June 1998 and April 1999, an outbreak caused by L. monocytogenes serotype 3a in butter occurred in Finland. The majority of the cases were immunocompromised and hospitalized at the Helsinki University Central Hospital (HUCH), where 7-g butter packages produced by a dairy plant were used as the only butter brand. The butter had also been sold to 10 other central hospitals as well as to the retail market. Based on the data on hospital stay, butter consumption and the qualitative and quantitative analyses of L. monocytogenes in butter, the attack rates and exposure were estimated. Incubation studies on the naturally contaminated small butter packages showed that the levels found in the packages at the time of detection of the outbreak could reliably be used for these estimations. However, the levels of L. monocytogenes in 500-g packages increased. The attack rate among HUCH patients varied from 70 to 117 cases per 1000 patients at risk, depending on which estimate of the contamination level of butter (100-60%) was used. The highest single dose (7.7 x 10(4) CFU in one meal) could have been sufficient to cause the listeriosis cases at HUCH. However, this data also supports another hypothesis, according to which these listeriosis cases were caused by a prolonged daily consumption of contaminated butter during the hospital stay. The estimated daily dose, based on the hospital kitchen data or the highest detected level in a wholesale sample (11,000 CFU/g), would have varied from 1.4 x 10(1) to 2.2 x 10(3) CFU/day or from 2.2 x 10(4) to 3.1 x 10(5) CFU/day, respectively. The choice of the hypothesis has a crucial impact on the interpretation of this data for the dose-response estimations as well as for the discussion on Food Safety Objectives. Due to the susceptibility of hospital patients, special care must be taken in order to avoid even low levels of L. monocytogenes in food served.

Butter↗
PubMed2005

Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects.

OBJECTIVE: To determine whether dairy fat in cheese raises low-density lipoprotein (LDL) cholesterol as much as in butter, since epidemiology suggests a different impact on cardiovascular disease. DESIGN: A randomised crossover trial testing the daily consumption of 40 g dairy fat as butter or as matured cheddar cheese, each of 4 weeks duration, was preceded by and separated by 2-week periods when dietary fat was less saturated. SETTING: Free-living volunteers. SUBJECTS: A total of 14 men and five women of mean age 56+/-8 y, with mean total cholesterol of 5.6+/-0.8 mmol/l. MAIN OUTCOME MEASURES: Plasma cholesterol, LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), triacylglycerol and glucose. RESULTS: Saturated fat intake was significantly lower during the run-in than during the cheese and butter periods. Mean lipid values did not differ significantly between the cheese and run-in periods, but total cholesterol and LDL-C were significantly higher with butter: total cholesterol (mmol/l): butter 6.1+/-0.7; run-in 5.6+/-0.8 (P < 0.05; ANOVA with Bonferroni adjustment); vs cheese 5.8+/-0.6 (P > 0.05); median LDL-C (mmol/l): butter 3.9 (3.5-4.1) vs run-in 3.4 (3.0-4.1) (P < 0.05; Tukey test); vs cheese 3.7 (3.3-3.9) (P > 0.05). Among 13 subjects whose initial LDL-C was >4 mmol/l, the difference between butter (4.4+/-0.3 mmol/l) and cheese (3.9+/-0.3 mmol/l) was significant (P = 0.014). HDL-C was highest with butter and triacylglycerol with cheese (neither was significant). CONCLUSION: A total of 40 g dairy fat eaten daily for 4 weeks as butter, but not as cheese, raised total and LDL cholesterol significantly compared with a diet containing significantly less saturated fat. Dietary advice regarding cheese consumption may require modification.

Analysis of Variance↗
PubMedDate not supplied

Evaluation of APHA and AOAC II methods for phosphatase in butter and differentiation of milk and microbial phosphatases by agarose-gel electrophoresis.

Salted and unsalted butters with 3 levels of phosphatase were prepared with both raw and pasteurized cream containing 36% fat. Test samples were analyzed for phosphatase by the modified method of the American Public Health Association (APHA) and the official AOAC method, 16.256 (1984, 14th Ed., 1990 15th Ed., 946.02). In the APHA method, weighing of solid frozen butter for testing yielded repeatable results. Addition of 0.0-1.0 mg magnesium to the butter had little effect on phosphatase activity in the APHA modified rapid colorimetric method (MRCM), but caused the phosphatase activity to decrease in the AOAC method. Phosphatase in salted and unsalted butters was quite stable at -17 +/- 1 degrees C and at 3.0 +/- 0.5 degrees C; however, within 2 to 4 days, freshly prepared butters stored at 22 +/- 1 degrees C developed reactivated and/or microbial phosphatases that were both heat-labile and heat-stable. At 22 +/- 1 degrees C, frozen butters showed decreased milk phosphatase activity before producing microbial phosphatase. Heat-labile phosphatases in salted and unsalted butters were inactivated at 62.8 degrees C for 10 min, and the phosphatase lability was partially due to the heat-denaturing effect of NaCl in salted butter. Some heat-stable phosphatases in unsalted butter survived at 66 degrees C for 30 min. Differentiation of milk phosphatase from microbial phosphatases was difficult by both methods; however, they were successfully differentiated by the agarose-gel electrophoretic technique.

Animals↗