Euro Fed Lipid: A lively network for lipids,fats and oils
To investigate the effects of different dietary fat and oils (differing in their degree of As a result of lipid peroxidation, malondialdehyde (MDA, a genotoxic harmful . parameters was determined by the Pearson correlation coefficient method. .. Articles from Asian Pacific Journal of Tropical Biomedicine are provided here. Published Online July in SciRes. dayline.info Evolutionary and Historical Perspectives Concerning Edible Lipids for Human Consumption. Consumption of fats and oils in the ancient world was examined as a connection of excess consumption of omega-6 fatty acid to the. European Journal of Lipid Science and Technology Waste Cooking Oils as . Future studies may find a link between ethanol kinetics in the malaxation.
Contrarily to the stomach, several enzymes could hydrolyze lipids in the small intestine, and their characteristics have been reviewed Armand, ; Bakala N'Goma et al. The HPL is synthetized by the acinar cell of the pancreas and secreted optimally to ensure efficient lipid digestion in healthy adults Armand, Thus, an increase of the HPL secretion has been noticed after the consumption of a high fat diet 45—50 g lipids compared to a low fat one The complex formed by the lipase and co-lipase hydrolyzes the ester bond in sn-1 and sn-3 positions of TAG.
The type of FA impairs the rate of lipolysis: For equivalent lipid intake, small droplets initial droplet size 0. Authors claimed that in physiological condition, lipases are in excess relative to the substrate. Indeed, the specific activity of HPL can vary at pH 8.
This could explain why part of the FAs at position sn-2 of TAG can be exchanged upon digestion, absorption and chylomicron CM synthesis Couedelo et al. To be absorbed by the border brush membrane of the enterocytes, FFA and 2-MAG must be incorporated in nanoscale structures containing bile salts and called mixed micelles 8—20 nm or into larger structures designed as vesicles 40— nm containing phospholipids as well Armand, The rate of appearance and extent of lipid present in the lymphatic system following fat ingestion postprandial state gives an indication of the bioavailability of the dietary lipids Carey et al.
Some data suggest that lipid absorption can be modulated by enhancing the gastrointestinal lipolysis via the emulsification of dietary lipids Couedelo et al. Thus, some studies have evidenced the faster absorption and metabolization of emulsified lipids than unemulsified one Garaiova et al. Additionally, the nature of the emulsifiers can affect the metabolism of lymph CM Daher et al. Indeed, the improvement of intestinal lipid absorption would enhance the accretion of TAG in CM in rat lymph Masuda et al.
The CMs structure can be affected to dietary fat and it turn can impair plasma lipemia Couedelo et al. Conversely, the proportion of n-6 FA in the lymph lipids decreased significantly Sugasini et al.
Comparison of the results obtained on lymph and liver Fig. Similar trends were observed in serum Sugasini et al. Altogether, these results indicate that appropriate formulation of lipid carrier can not only enhance the absorption and accretion of dedicated FA but also their conversion to long chain polyunsaturated FA.
Another promising approach was the design of particular lipid that will be able to address a specific FA such as DHA to a target organ such as brain Lagarde et al. Evolution of the fatty acid composition of lipids of various tissues after 60 days feeding with bulk linseed oil Bulkwhey protein-stabilized emulsion WPI and phospholipid-stabilized emulsion P.
L of the same linseed oil. Adapted from Sugasini et al. The control of lipid bioavailability and lipid absorption is emergently questioned since the middle of the s with a rapid boom of related scientific publications. The lipid bioavailability control addresses two opposite situations as regards of improvement of human health and well-being.
In the first situation, the aim is to increase, promote or optimize the absorption and the use by the body of certain lipids, beneficial for health but under-consumed or of limited bioavailability. Typically, it concerns energy supply by SFAs or indispensable FA supply for preterm infant and new born or for subjects suffering of permanent or transitory digestive insufficiencies. The increase the long-chain omega-3 PUFA intake and absorption to cover the nutritional needs of general or targeted populations for health benefits is also included.
The second situation is linked to the over-consumption of junky foods and its deleterious health consequences overweight, metabolic syndrome, diabetes mellitus ….
The objective is either to reduce lipid absorption for overweighed, hyperlipidemics or metabolic syndrome subjects Armand, or to reduce the fat and food intake by increasing the satiety. As recently reviewed, the structure of dietary lipids can affect FA bioavailability and lipid metabolism Michalski et al. Many newly designed lipid structures and formulations paired with generally in vitro digestion trials has been accordingly performed in the objective to take advantage of the two levels of structures previously described, namely i the molecular level, gathering TAGs structured naturally or by the process to control the regio-distribution of FAs on the glycerol backbone and the various classes of lipids Fig.
TAG molecules making up adipose tissue of current livestock animals have predominantly a saturated FA in sn-1 position and an unsaturated FA at sn-2 position.
Seed oils exhibit PUFA mostly esterified at sn-2 position. In vegetable oils, saturated FA occurs primarily at sn-1 position Karupaiah and Sundram, The TAG structure of natural fats and oils and their nutritional properties can be modified either by use of lipases as catalysts or by chemical modifications Linderborg and Kallio, An example of structured fat design for dedicated nutrition is Betapol, a vegetable lipid blend exhibiting similar TAG structure that the ones of human milk.
This structure favors the absorption of palmitic acid, which is esterified in sn-2 position as in human milk and reduces its loss in feces. Fecal losses of saturated lipids are favored by the formation in the GIT of insoluble soaps between calcium or other divalent ions and the SFAs esterified in sn-1 or sn-3 positions of fats, preferentially and rapidly released by the digestive enzymes Linderborg and Kallio, ; Mu and Porsgaard, ; Karupaiah and Sundram, This effect is favored because an increased concentration of bile salts is needed to maintain SFAs with melting point above the body temperature in mixed micelles Linderborg and Kallio, Once in the blood stream, saturated FA in the sn-2 position delay the clearance of CM and lipoproteins remnants, probably due to alteration in the physical properties of CM interface that impair the activity of the LPL Linderborg and Kallio, EPA and DHA are mainly esterified in sn-2 position in fish oils instead of sn-1 or sn-3 position in mammal oils.
After intra-gastric administration of fish or seal oil to rats, the lymphatic transport was found to be higher during the first 8 h with fish oil Christensen et al. Many disease entities that elevate triglyceride levels, such as diabetes mellitus, nephrotic syndrome, chronic renal disease, and certain primary hyperlipidemias, carry an increased risk of CHD. In these situations, the high triglyceride level may be a clue to the presence of other lipoprotein abnormalities that are more directly associated with CHD, such as low HDL-C, elevated apo B or LDL-C, or atherogenic remnant triglyceride-rich lipoprotein particles that have not been well defined.
Thus, whether or not VLDL and triglycerides are directly involved in the atherogenic process, elevated levels can be helpful in identifying people at increased risk of cardiovascular diseases. Clinical-Genetic Evidence of CHD A number of genetic disorders of lipoprotein metabolism have been identified and characterized Brown and Ginsberg, ; Stanbury et al.
The study of these disorders has provided many insights into the structure, metabolism, and regulation of the plasma lipoproteins and apolipoproteins. Several of these disorders are characterized by severe hypercholesterolemia and premature atherosclerosis and CHD. Such disorders include familial hypercholesterolemia FHfamilial combined hyperlipidemia, and familial dysbetalipoproteinemia type 3 hyperlipoproteinemia.
The defective gene results in the receptor being either absent or nonfunctional. One gene for the LDL receptor normally is inherited from each parent. Heterozygous FH occurs in the general population at a frequency of about 1 inmaking FH one of the most common single-gene-determined diseases in humans.
Rarely, about once per million people, individuals inherit two abnormal genes for LDL receptors and hence are homozygous for FH. Severe and often fatal coronary disease frequently develops while these people are in their teens. One homozygote had an acute myocardial infarction as early as 18 months of age; another died of an acute myocardial infarction at 3 years of age. Very few FH homozygotes survive past age 30 Goldstein and Brown, These rabbits have very high TC and LDL-C levels and develop severe atherosclerosis that is similar to that seen in humans.
This genetic animal model provides further strong evidence of the causal relationship between high LDL-C levels and atherosclerosis.
The research on FH and on the LDL receptor has provided insights into the mechanisms that might be involved in the more common problem of the mild to moderately elevated blood cholesterol levels that are seen in the general population.
Potential relationships between LDL receptors, diet, and atherosclerosis have been discussed by Brown and Goldstein It is likely that the dietary components that raise plasma TC and LDL-C levels specifically, dietary SFAs and cholesterol, as discussed in detail later in this chapter act, at least in part, by suppressing hepatic LDL receptor activity.
Impact of dietary oils and fats on lipid peroxidation in liver and blood of albino rats
Recent studies Spady and Dietschy, in hamsters powerfully demonstrate the role of dietary saturated triglycerides in augmenting the effect of dietary cholesterol in suppressing hepatic LDL receptor activity and elevating plasma LDL-C levels. Clinical Trials of CHD Small-Scale Trials Angiographic End Points Evidence has been accumulating and a number of studies are under way to determine the effect of lowering TC by diet, drugs, or ileal bypass surgery on the progression or regression of atherosclerotic lesions of coronary and large peripheral arteries as determined by angiography and ultrasound.
As shown angiographically, in the earliest reported randomized controlled trial, patients with intermittent claudication had less angiographic progression and more regression of plaques in the diet- and drug-treated group than did a control group over a month period. In a recently completed randomized controlled trial in which angiographic techniques were used, patients treated with diet and several TC-lowering drugs had less progression and more actual regression of plaques in natural and bypass graft coronary vessels compared to controls over a 2-year period Blankenhorn et al.
These results and those of other systematic studies cited below are generally consistent with the conclusion that reducing LDL-C in hyperlipidemic patients reduces the rate of progression and can induce regression of atherosclerosis according to the degree of blood lipid reduction Arntzenius et al.
Key elements of their designs are summarized in Table In five trials, various methods were used to change the plasma lipid concentrations as the only intervention; in two, diet was used; and in three, drugs. The other four studies, in which diet was also used, were multifactorial trials in which effects of change in plasma lipids were confounded with effects of change in cigarette smoking and blood pressure.
Only one of the six trials involving change in diet—the Los Angeles Veterans Administration Domiciliary Study—was conducted under double-blind conditions Dayton et al. In the others, individuals were randomized. The number of participants in these studies varied from approximately to nearly 50, A negative sign here indicates that the experimental group had a lower mean level than the control group.
These results indicate that the magnitude of the difference in risk of CHD varied directly with the magnitude of the difference in mean TC. Studies that achieved little or no difference in mean TC had little or no difference in rate of CHD, whereas studies that achieved larger difference in mean TC experienced larger differences in CHD rates. Combined with the evidence from epidemiologic, clinical, and laboratory animal studies, this body of evidence establishes unequivocally that lowering serum TC, particularly LDL-C, reduces the incidence of CHD in middle-aged, hypercholesterolemic men.
High-risk populations were used in most of these studies for quite practical reasons; the cost and problems of conducting such a trial in the general population would be very large and the results might well be inconclusive. Results of the Los Angeles Veterans Administration Domiciliary Trial support the inference that the conclusion may extend to people over 65 years of age as well, perhaps with a somewhat smaller effect, but the evidence bearing on this important question is still weak.
Most of the trials listed in Tables and showed an excess of non-CHD deaths in the intervention group as compared to the comparison group. How much of this can be attributed to chance and whether any of it reflects adverse effects of intervention are complex questions that may never be completely resolved. An analysis of 20 randomized controlled clinical trials that involved change in serum TC as the only systematic intervention indicates no statistically significant effect on risk of non-CHD death Richard Peto, University of Oxford, personal communication, In the trials shown in Tablenone of the percentage differences in risk of non-CHD death or total mortality was statistically significant except for the WHO Clofibrate Trial.
In the final mortality follow-up, however, the Committee of Principal Investigators of that study found that the excess mortality in the clofibrate-treated group did not continue after the end of treatment, and they could not find a reasonable explanation for the excess mortality that did occur during the period of active treatment.
The excess deaths were due to a variety of non-CHD causes and had no apparent association either with the extent of reduction in TC or with duration of treatment with clofibrate. These results do not rule out the possibility of a toxic effect, but seem more consistent with the hypothesis that the excess of deaths in the treated group was the result of random sampling variation.
The possible adverse effects of the drugs used in these trials are not strictly relevant to a report on diet and health and are not discussed further. The safety of dietary changes to lower serum TC is discussed in Chapter 28 of this report. There is no firm evidence to indicate that any of the dietary interventions used in the trials described above increased the risk of non-CHD deaths.
Also, results from other clinical trials did not indicate an excess of cancer deaths in groups assigned to a high-PUFA diet Ederer et al. These considerations support the conclusion that the excess of cancer deaths observed in the Los Angeles study did not result from the high-PUFA diet. The extensive literature that has since developed on this topic has been reviewed by McMichael et al. In some studies, an inverse association was found over a protracted period; in others, an inverse association was observed during the first few years of follow-up but disappeared during continued follow-up; in yet others, no association was observed between initial serum TC level and subsequent risk of cancer.
Some of the results may have reflected a preclinical effect of cancer on serum TC and some may have been due to metabolic characteristics e. There is no evidence from studies in humans that low consumption of SFAs and cholesterol are positively correlated with rates of mortality from colon cancer Liu et al.
This evidence is discussed in more detail later in this chapter and in Chapter Richard Peto Oxford University, personal communication, contends that the primary information to be obtained from the randomized clinical trials is the time required for changes in TC to have an effect on CHD rates. He has obtained information on 18 published and 2 unpublished randomized trials that involved changes in TC as the only systematic intervention, regardless of the mode of intervention diet or drugs and regardless of whether they were trials of disease prevention or disease treatment.
Peto also noted that the reduction in risk varied according to the duration of treatment: In the Framingham Study, the year cumulative incidence of intermittent claudication showed a concentration of cases in the upper part of the distribution for TC values in men but not in women i.
The results are, however, inconsistent among studies. For example, serum cholesterol was strongly related in some studies Bothig et al. In a British in-patient case-control study, there was a suggestion that prebetalipoprotein i. Clustering of intermittent claudication with other atherosclerotic diseases was also very strong in the Framingham Study. Overt coronary disease, cerebrovascular disease, or congestive heart failure were found in one out of three cases of intermittent claudication at the time of diagnosis, indicating the strong likelihood of common risk characteristics Kannel and McGee, The linkage in the basic processes leading to manifestations of PVD and CHD is further suggested by the finding of a strong curvilinear relationship between a Framingham risk index involving multiple risk characteristics for coronary disease and the incidence over time of manifest intermittent claudication, primarily due to an excess risk of intermittent claudication in the upper quintile of the coronary index Kannel and McGee, A similar predominance of hypertriglyceridemia was observed in older men and in women among a series of Swedish patients with PVD Leren and Haabrekke, This is also suggested by the epidemiologic evidence about PVD, i.
Finally, although the pathogenesis of atherosclerosis is similar in the different arterial beds, the relative importance of different risk factors in causing the disease process clearly differs among different anatomic sites.
This issue is discussed further in Chapter Stroke There are few systematic data relating blood lipids and lipoproteins to stroke incidence. A U-shaped relationship between lipids and stroke was suggested in the Chicago Stroke Study, in which a lower stroke risk was found in the central part of the TC distribution Ostfeld et al.
This U-shaped relationship was stronger for acute brain infarction than for all strokes. The left side of the U-shaped relationship to stroke in the Honolulu Study was due primarily to the inverse relationship between TC and hemorrhagic stroke Kagan et al. In later studies involving improved ability to discriminate between intracerebral hemorrhage and thrombosis by the use of computed tomography CT scanning, a clearer epidemiologic picture emerges.
For example, in recent data from the Multiple Risk Factor Intervention Trial on more thanscreenees observed for 10 years, there is a clear, positive, monotonic, linear relationship between TC level and death ascribed to cerebral thrombosis Iso et al. This explains the right side of the U-shaped distribution of TC to overall stroke risk. A strong linear negative relationship was found between TC level and deaths coded to cerebral hemorrhage, the major explanation for the left side of the U-shaped TC-stroke risk curve.
Animal Studies of Atherosclerosis Hypercholesterolemia has been the common denominator of experimental atherosclerosis in a variety of animal species since shortly after the turn of the century reviewed by Anitschkow, ; Duff, ; Jokinen et al. In most species, hypercholesterolemia is induced by a diet enriched in cholesterol, SFAs, or both.
Some animal species, such as the rat and the dog, are resistant to diet-induced hypercholesterolemia and develop atherosclerotic lesions when hormonal or other manipulations are used in conjunction with diet to induce hypercholesterolemia.
When hypercholesterolemia is prolonged over several years, these animals develop all the complications seen in advanced atherosclerosis in humans and, eventually, myocardial infarction and other clinical manifestations of atherosclerosis in humans Taylor et al. Not only has hypercholesterolemia been the sine qua non of experimental atherosclerosis, but the relationship of the specific plasma lipoproteins to atherosclerosis in animals is similar to that in humans.
For example, in humans and nonhuman primates, LDL is positively, and HDL is negatively, associated with atherosclerosis. In some experiments, physical characteristics of LDL, such as molecular size, are also associated with atherosclerosis Rudel et al. When diet-induced hypercholesterolemia is combined with other conditions known to augment atherosclerosis in humans, such as hypertension, the experimental lesions also are increased in extent and severity McGill et al.
Thus, the association of altered plasma lipoprotein concentrations in laboratory animals is not only strong and consistent, but the pattern of the association is similar to that in humans. Furthermore, many studies have demonstrated that reduction of plasma cholesterol concentrations by withdrawal of cholesterol or fat, or both, from the diet, or by administration of drugs, leads to regression of experimental atherosclerosis reviewed by Malinow, These regression studies, which were conducted in nonhuman primates, gave considerable support to the concept that the progression of atherosclerosis in humans can be retarded and possibly that lesions can be reversed by treating hyperlipidemia with diet and drugs.
In Vitro Studies of Atherogenesis The strong relationship between high levels of plasma LDL and atherosclerosis has provided an important background for in vitro studies dealing with the cellular and molecular mechanisms of atherogenesis. These in vitro studies have sought to determine how LDL and other atherogenic lipoproteins could lead to the formation of cholesteryl ester-filled macrophages foam cells and other elements of the atherosclerotic lesion. The results of such studies have, in turn, supported data on humans and animals that suggest a primary etiologic role for LDL and related lipoproteins in the development of atherosclerosis.
A prominent and early feature of atherosclerotic lesions is the foam cell.
Fats and Other Lipids - Diet and Health - NCBI Bookshelf
In order to understand the mechanisms of foam cell formation, investigators have studied the interaction of plasma lipoproteins with various types of cultured macrophages. Native LDL does not lead to the accumulation of cholesteryl ester in many types of macrophages reviewed in Brown and Goldstein, This lack of native LDL-induced cholesteryl ester accumulation is due, at least in part, to down-regulation of the LDL receptor on these cells by small amounts of excess cellular cholesterol, thus preventing a large influx of LDL-C.
These modified forms of LDL enter the cell by a receptor called the scavenger receptor that is distinct from the LDL receptor and that is not subject to down-regulation Brown and Goldstein, Thus, cellular influx of these modifled forms of LDL continues at a high rate, leading to significant accumulation of cholesteryl ester. These in vitro observations have spawned a widespread search for evidence of LDL modification in vivo.
Several recent studies have shed light on this topic. These investigators demonstrated that probucol treatment of LDL receptor-deficient WHHL rabbits decreased LDL uptake in foam cell lesions and reduced the rate of development of these lesions independently of plasma cholesterol levels. These results are consistent with the hypothesis that oxidative modification of LDL may be important in the development of foam cell lesions. Malondialdehyde is a byproduct of arachidonic acid metabolism, which is an active process in the arterial wall.
Whether malondialdehyde-LDL is involved in foam cell formation in vivo has yet to be determined. A potential role for native LDL in foam cell formation has recently been suggested by findings that another cultured macrophage, the J macrophage, accumulates large amounts of cholesteryl ester in the presence of native LDL Tabas et al. In this case, the LDL receptor is poorly down-regulated by LDL-C because of intracellular shunting of cholesterol away from the regulatory pathway into a hyperactive cholesterol esterification pathway.
Since LDL receptors are abundant on foam cells in vivo see belowindicative of poor LDL receptor down-regulation, this mechanism of foam cell formation may help explain the atherogenic effects of native LDL. Foam cell formation has also been demonstrated in vitro by lipoproteins other than native and modified forms of LDL.
These and other findings have led some investigators to speculate that postprandial lipoproteins, particularly cholesterol-enriched particles such as chylomicron remnants, may be atherogenic in humans. Foam cell research is an active area of in vitro investigation exploring the relationship between LDL and atherogenesis.
However, other areas of study have also focused on this relationship reviewed in Steinberg, For instance, LDL, either native or oxidized, causes endothelial cell injury in vitro. Endothelial injury, in turn, has been hypothesized to initiate atherogenesis by causing platelet adherence to the vessel wall and release of growth factors. In addition, LDL has been reported to directly augment platelet aggregation and to stimulate the growth of smooth muscle cells—two important features of the atherosclerotic lesion.
The antioxidant system involves both enzymatic and non-enzymatic antioxidants. The conversion of H2O to H2O2 by either glutathione peroxidase GPx or catalase forms the second step of enzymatic system. Superoxide dismutase and GPx enzyme activities and the balance between them are very crucial protection against oxidative stress  — . Lipid-soluble vitamin E is a non-enzymatic antioxidant which plays a significant role in the protection of the cell membrane and against LDL cholesterol as well.
It can reduce free radicals and it has the most action to break the chain reaction in lipid peroxidation  — . The measure of total antioxidant capacity TACwhich is the cumulative action of all the antioxidants present in plasma, provides an insight into the delicate balance in vivo between oxidants and antioxidants .
The objectives of this study were to demonstrate the influence of dietary butter, margarine, olive oil, sunflower oil and corn oil on liver and blood lipid peroxidation in albino rats by measuring MDA levels in blood and liver, and to assess the antioxidant activity in these animals by measuring SOD and GPx activities as well as, vitamin E and TAC levels in blood to determine the dietary oils most susceptible to lipid peroxidation.
Materials and methods 2. Fats and oils Corn oil, sunflower oil, olive oil, butter and margarine were obtained from local market in Kingdom of Saudi Arabia. The flow rate of the carrier gas helium was 0.
A comparison between the retention times of the samples with those of authentic standard mixture Sigma, St. Reagents and chemicals used in the study were of the highest purity available. Experimental animal protocol Fifty white albino rats of both sexes were used in this study. All animals were kept under normal healthy conditions and fed on a basal diet for one week.
The animals were randomly allocated into five groups each group of 10 of approximately equal average body weight g. Utmost care was taken to provide equal physical and environmental housing conditions namely size of units, light, temperature and aeration.
The units were illuminated 24 h a day. Tap water supply for all rats was adjusted by calculating the volume of fluid intake per day per rat as follows: The volume of fluid intake was calculated per day and divided by the number of rats per cage to get the average volume of fluid intake per day per rat. All experimental procedures used were in accordance with the published ethical guidelines for the animal use and care. In the first week, all groups were fed a basal diet composed of The selected lipids were added to respective diets as 5.
Margarine and butter were added to each diet after solubilization at low temperature. Basal diet was mixed with lipids completely and rats were provided with this diet ad libitum.
Rats were sacrificed after 12 h of food deprivation.