Influence of Amount and Type
of Dietary Fat on Plasma Cholesterol Concentrations in African Grey Parrots

 

F. J. Bavelaar, MSc, MVR

Prof. Dr. Ir. A.C. Beynen

 

Department of Nutrition

Faculty of Veterinary Medicine

University of Utrecht, The Netherlands

 

KEY WORDS: African Grey parrot, atherosclerosis, plasma cholesterol concentration, dietary intervention

 

ABSTRACT

The incidence of atherosclerosis in African Grey parrots is high. An important risk factor for atherosclerosis in humans is an elevated plasma cholesterol concentration; this might also hold for parrots. Plasma cholesterol levels in humans can be lowered through dietary intervention. We studied the influence of diets with different dietary fatty acid composition and fat content on plasma cholesterol concentrations in African Grey parrots. Four groups of parrots were fed 4 different diets according to a Latin-square design. There were 2 low- and 2 high-fat diets, and the diets contained either sunflower oil or palm kernel oil as a variable fat source. Sunflower oil is rich in the polyunsaturated fatty acid linoleic acid. Palm kernel oil is rich in the saturated fatty acids lauric acid and myristic acid. Twenty parrots were involved in the entire experiment. The high-fat diet with palm kernel oil resulted in significantly higher plasma cholesterol and phospholipid concentrations when compared with the other 3 diets. The magnitude of the parrots’ cholesterolemic response to the amount and type of fat in the diet appeared to be comparable to that reported in humans. Thus, it is possible to influence plasma cholesterol in parrots through dietary intervention.

 

INTRODUCTION

Atherosclerosis is a common disease in parrots, especially in African Grey and Amazones parrots.1 The incidence is considered to be about 10%,1–3 but Bavelaar and Beynen⁴ found sudanophilic staining in aortas of 84% of parrots presented for autopsy. In parrots, atherosclerosis is mainly located in the beginning of the aorta and the brachiocephalic arteries.1,5,6 The most common sign of atherosclerosis is sudden death.7 However, there can be clinical signs such as hind limb paresis, sudden collapses, dyspnea, and lethargy.1,7,8 The diagnosis of atherosclerosis is rarely made in the living animal,1 and there is no treatment for atherosclerosis in the parrot, which makes prevention particularly relevant.

Regarding the development of atherosclerosis in parrots, possible risk factors such as a high-fat diet, social stress, inactivity, high plasma cholesterol, and high blood pressure have been suggested,1,3,7,9–11 but no experimental evidence is available. One of the most important risk factors of human atherosclerosis is an elevated plasma cholesterol concentration.12 Cholesterol might also be a risk factor in parrots, assuming that they share similarities with budgerigars. Finlayson and Hirchinson13 induced hypercholesterolemia and severe atheroma in female budgerigars by feeding them a diet rich in cholesterol.

Diet composition is an important determinant of plasma cholesterol concentrations in humans. Dietary saturated fatty acids, as opposed to isoenergetic amounts of either carbohydrates or mono- or polyunsaturated fatty acids, increase plasma cholesterol concentrations in humans14,15 We are not aware of literature describing the influence of diet on plasma cholesterol concentrations in parrots. Thus, this experiment was designed to study the effect of the amount and type of dietary fat on plasma cholesterol concentrations in African Grey parrots. As mentioned above, African Grey parrots display a high incidence of atherosclerosis, and dietary intervention would be expected to be most effective in this species. It was anticipated that the results obtained would contribute to the formulation and selection of appropriate diets for parrots.

MATERIALS AND METHODS

Animals and Housing

A total of 30 African Grey parrots (Psittacus erithacus) were used. The parrots were made available by the Dutch Parrot Refuge (Nederlandse Opvang Papegaaien, Veldhoven, the Netherlands) and were housed in groups in 4 aviaries. Each group consisted of 7 or 8 birds. The parrots were of both genders, with ages ranging from 3 to 41 years and body weight from 338 to 571 g. Before the experiment, all parrots had been fed the same diet (Nutribird P15, Versele-Laga, Deinze, Belgium) for at least 2 months. The parrots had been chipped for identification. The aviaries had an indoor and outdoor space. Outside, the floor was covered with sand and inside with wood shavings. Indoors, there was continuous light. Feed and water were provided inside for ad libitum consumption and were refreshed daily. The aviaries were cleaned weekly. Food consumption was recorded per group per day. At the end of each dietary period (described subsequently) all parrots were caught for the collection of blood samples and for the determination of body weight. If a parrot had lost 15% or more of its initial body weight, it was excluded from the experiment. Parrots showing signs of sudden illness and those involved in fighting were excluded as well.

Experimental Design

The experiment was approved by the animal experiments committee of the Faculty of Veterinary Medicine, Utrecht, the Netherlands. The trial was performed from the beginning of February to the end of May 2001. To eliminate any effects of animal baseline value, diet sequence, and time, the experiment had a 4 x 4 Latin-square design. There were 4 dietary treatments and the 4 groups of parrots were randomly allocated to the 4 diet orders. The first 2 experimental periods lasted 28 days each, the third lasted 32 days, and the last period was 24 days. On the last day of each experimental period, blood samples were collected from the jugular vein of each parrot, and the birds were weighed. The blood samples, ranging from about 0.1 to 1.5 mL, were collected in heparinized tubes. Blood was centrifuged (10.000 x g, 10 minutes) and the plasma was stored at -20˚C until further analyses.

Diet Formulation

The experimental diets differed in fat content and fatty acid composition. There were 2 low- and 2 high-fat diets with sunflower oil and palm kernel oil as variable fat sources. To formulate the low-fat diets, glucose was isoenergetically substituted for part of the variable fat source in the high-fat diets. For the isoenergetic substitution, the energy densities of glucose and fat were taken to be 17 and 39 kJ gross energy per gram. The composition of the experimental diets and their constant components are given in Tables 1 and 2. The diets were composed so as to meet the assumed nutrient requirements of parrots.16 The diets were fed as extruded pellets.

Feed Analyses

Dry matter, crude protein, crude fiber, and crude ash in the diets were analyzed according to the Weende analysis. Crude fat was extracted from the feed with chloroform:methanol (2:1, v/v) as described by Folch et al,17 and the extracted fat was weighed. For determination of the fatty acid composition of the fat sources, the oils were saponified using methanolic sodium hydroxide and the constituent fatty acids were converted into their methyl esters using boronitrifluoride in methanol. Fatty acid analyses were performed by gas-liquid chromatography using a flame ionization detector, a Chromopack column (Fused silica, no. 7485, CP.FFAPCB 25 m x 0.32 mm, Chromopack, Middelburg, the Netherlands) and H₂ as carrier gas.18 The individual fatty acids are expressed as weight percentage of total methyl esters. The fatty acid composition of the fat sources (Table 3) and that of the other ingredients, as derived from the Dutch Feedstuff Table 199919 and from the USDA nutrient database (www.nal.usda. gov/fnic/foodcomp), were used to calculate the fatty acid composition of the whole diets (Table 4).

Blood Analyses

Plasma total cholesterol, phospholipids, and triglycerides were determined with commercial test combinations and the Cobas-Bio centrifugal analyser (Roche Diagnostics, Basel, Switzerland). For the cholesterol and phospholipid determination, Precinorm U (cat. nr. 171743, Boehringer, Mannheim, Germany) was used as the control serum, and Precinorm L (cat. nr. 781827) was used for the triglyceride determination. If more than 150 mL plasma was available, high-density lipoprotein (HDL) cholesterol was determined as soluble cholesterol after precipitation of apoB-containing lipoproteins (cat. nr. 543004, Roche, Mannheim, Germany) using the Cobas-Bio autoanalyser and Precinorm L as the control serum. Low-density lipoprotein (LDL) cholesterol was calculated with the formula of Friedewald et al20 as LDL-cholesterol (mmol/L) = total cholesterol (mmol/L) - triglycerides (mmol/L) / 2.2 - HDL-cholesterol (mmol/L).

Statistical Analyses

Individual parrots were considered as experimental units. Data were used from 20 birds that had participated in the entire experiment. Plasma lipid values and body weights were subjected to a univariate analysis of variance. The plasma values were logarithmically transformed so that they showed a normal distribution. Group, carry-over effect, dietary treatment, and feeding period were used as fixed factors, and the parrots as a random factor. If a significant (P<0.05) effect of one of the fixed factors was observed by analysis of variance, a least significant difference (LSD) test was then used to identify group differences. The statistical analyses were performed with the computer program SPSS (SPSS Inc, Chicago, IL).

RESULTS

Chemical Analyses of Diets

The results of the chemical analyses of the experimental diets are given in Table 1. The low and high-fat diets contained about 69 and 193 g fat/kg, respectively. The fatty acid composition of the variable fat sources is given in Table 3. As would be anticipated, the palm kernel oil was rich in lauric acid and the sunflower oil was rich in linoleic acid. The calculated fatty acid composition of the whole diets is shown in Table 4. The high-fat diets resembled the variable fats more closely than did the low-fat diets, in which the fatty acid composition of the other ingredients had a greater impact.

Feed Consumption and Weight Changes

Of the 30 parrots, 20 animals finished the experiment. Seven parrots were excluded because of unacceptable weight loss or illness, one parrot escaped, one was removed because of fighting, and one parrot was found dead. The mean daily feed consumption per animal was 39.3 g for the low-fat diet with sunflower oil, 36.7 g for the low-fat diet with palm kernel oil, 31.1 g for the high-fat diet with sunflower oil, and 34.7 g for the high-fat diet with palm kernel oil. Because the parrots could not be fed individually, body weight served as an indicator of individual feed consumption. The experimental diets had no differential influence on body weight (P=0.32), but feeding period was associated with a significant difference in weight (P=0.014); body weight was significantly higher during the third period. Because there was no diet effect on body weight, it is concluded that the parrots consumed equal amounts of energy with the 4 diets and that there was no difference in palatability. This conclusion is supported by the feed intake values given previously and the calculated energy contents of the diets (Table 1).

Plasma Lipids

The plasma values at the beginning of the experiment (n = 30) were 8.39 ± 2.57 (range, 5.31–18.62) mmol/L for total cholesterol, 5.33 ± 1.00 (range, 3.48–8.49) mmol/L for phospholipids, and 2.27 ± 1.33 (range, 0.59–5.63) mmol/L for triglycerides.

The plasma values per dietary treatment are given in Table 5. No group effect and no carry-over effect were found. The diet had a significant influence on plasma cholesterol concentrations (P=0.006). The high-fat diet rich in saturated fatty acids lauric and myristic acid, added in the form of palm kernel oil, produced significantly higher levels of plasma cholesterol than did the other 3 diets.

Both dietary treatment and feeding period had a significant influence on plasma phospholipid levels (P<0.001 and P=0.014, respectively). Feeding the high-fat diet with palm kernel oil resulted in significantly higher plasma phospholipid concentrations when compared with the other 3 diets. The first feeding period was associated with lower phospholipid concentrations when compared with the other 3 periods. No significant differences among the dietary treatments were found for plasma triglyceride levels.

In many cases, there was not enough plasma to determine HDL-cholesterol. Therefore, the statistical power was low, and it was decided not to analyze the values for HDL-cholesterol statistically. LDL-cholesterol was not determined but was calculated from HDL-cholesterol. Therefore, no statistical analyses were performed for LDL-cholesterol either. In general, HDL was the main cholesterol carrier in the blood of the parrots; the average percentage of total cholesterol in HDL was 56%. Two parrots had LDL as the main cholesterol carrier, with this lipoprotein providing 56% and 65% of the total cholesterol. Throughout the experiment, the mean LDL to HDL cholesterol ratio in individual parrots varied from 0.17 to 2.81.

DISCUSSION

Initial plasma lipid values and those seen in the course of the experiment showed great inter-individual variation. During the experiment, the lowest average plasma cholesterol concentration in an individual parrot was 4.64 mmol/L and the highest value was 18.62 mmol/L. Polo et al21 reported that the plasma concentration of cholesterol was 6.8 ± 0.7 (range, 5.8–8.2) mmol/L for African Grey parrots fed a mixed diet. The plasma concentrations of cholesterol found in this study are generally higher and show a much greater range. Polo et al21 gave no information about the number of birds examined, their age and gender, or their housing conditions. Researchers believe that in middle-aged humans, the risk for coronary heart disease is increased when plasma cholesterol concentrations are higher than 5.17 mmol/L (200 mg/dL)22 and that the risk increases progressively above this concentration.23 All of the parrots in this experiment and all of those studied by Polo et al21 had a plasma cholesterol value higher than 4.64 mmol/L. It appears relevant to know at which level an individual parrot should be considered hypercholesterolemic.

In birds on a cholesterol-free diet, the main carrier of blood cholesterol is HDL.24–26 In general, the parrots in this experiment also had HDL as main cholesterol carrier, but in 2 parrots, most plasma cholesterol was carried in LDL. The LDL/HDL cholesterol ratios showed great variation among the parrots. This ratio is of interest because it is considered to be a risk factor for atherosclerosis in humans that is more predictive than total cholesterol.27 A low ratio of LDL/HDL cholesterol may prevent the development of atherosclerosis. Unfortunately, we cannot conclude whether or not the experimental diets affected the LDL/HDL cholesterol ratio in these parrots.

Plasma phospholipids are mainly transported by HDL particles. Indeed, the high-fat diet with palm kernel oil significantly raised phospholipids and also increased group-mean plasma HDL cholesterol concentrations. In humans, plasma HDL cholesterol and triglyceride concentrations are inversely related,28 but this was not seen in the parrots. However, it should be noted that the parrots were not fasted before blood sampling and thus may have been in different feeding states, increasing the variation in plasma triglyceride concentrations.

The major objective of this experiment was to examine the effect of amount and type of dietary fat on plasma total cholesterol concentrations in parrots. Plasma cholesterol concentrations were found to be significantly higher when the parrots were fed the high-fat diet rich in saturated fatty acids (lauric and myristic acid) in the form of palm kernel oil. No difference in plasma cholesterol was found for the two low-fat diets versus the high-fat diet rich in the polyunsaturated fatty acid linoleic acid (in the form of sunflower oil). It can be concluded that, for low-fat diets, the type of dietary fat has no important influence on plasma cholesterol concentration. However, when a high-fat diet is given, polyunsaturated fatty acids versus saturated fatty acids may lower plasma cholesterol concentrations in parrots. A high-fat diet rich in polyunsaturated fatty acids may lower cholesterol to levels seen for low-fat diets. Thus, both the amount and type of dietary fat should be considered in relation to plasma cholesterol concentrations.

Mensink and Katan15 conducted a meta-analysis of 27 trials in humans. They came up with a formula to predict the changes in plasma cholesterol concentration when carbohydrates are replaced by fatty acids. The equation is change in total cholesterol (mmol/L) = 0.039 ¥ (carbÆsat) - 0.003 ¥ (carbÆmono) - 0.015 ¥ (carbÆpoly), in which (carbÆsat) refers to the isoenergetic replacement of carbohydrates by saturated fatty acids, (carbÆmono) to the replacement by monounsaturated fatty acids and (carbÆpoly) to the replacement by polyunsaturated fatty acids. The amounts of carbohydrates and fatty acids and their replacements are expressed as percent contribution to total daily energy intake. We have used the equation of Mensink and Katan15 to predict the diet-induced differences in plasma cholesterol in this study. The isoenergetic replacement of glucose and fatty acids was expressed in terms of gross energy. The analyzed amounts of macronutrients (Table 1) and calculated fatty acid composition of the diets (Table 4) were used. Between the high-fat diet with palm kernel oil and the low-fat diets with either sunflower or palm kernel oil, the predicted differences in plasma cholesterol are 0.78 and 0.65 mmol/L, respectively. In this study, the measured differences were 0.68 and 1.06 mmol/L, respectively. It would appear that the cholesterol response to the amount and type of dietary fat in parrots is of the same order of magnitude as that in humans, but the lower group-mean cholesterol concentration for the low-fat diet with palm kernel oil instead of the sunflower oil was unexpected.

Conclusions

In conclusion, this experiment shows that it is possible to influence plasma cholesterol concentrations in parrots through the composition of the diet. Dietary intervention might be an approach to decrease the risk for atherosclerosis in parrots. To lower plasma cholesterol in parrots, the diet should either have a low fat content or be rich in polyunsaturated fatty acids. In pelleted parrot feeds, the fat concentration ranges between 5% and 15%, whereas in seed diets, the fat content may be much higher, but the proportion of polyunsaturated fatty acids is often also high. To give a solid recommendation as to an appropriate diet for parrots, more research is necessary. For the time being, it would appear advisable to use diets with up to 10% fat in the dry matter.

ACKNOWLEDGMENTS

We thank the Dutch Parrot Refuge for their cooperation and the use of their parrots. Furthermore, we want to thank Hedwig Van der Horst, DVM, for her assistance during the experiment, Jan Van der Kuilen, Inez Lemmens, and Robert Hovenier for their analytical assistance, and Eloy Cruz for extrusion of the diets.

REFERENCES

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2. Dorrestein GM, Zwart P, Borst GHA, et al: Ziekte- en doodsoorzaken van vogels. Tijdschr Diergeneesk 102:437–447, 1977.

3. Griner LA: Pathology of zoo animals: A review of necropsies conducted over a 14-year period at the San Diego zoo, an San Diego wild animal park. San Diego: Zoological society of San Diego, 1983.

4. Bavelaar FJ, Beynen AC: Severity of atherosclerosis in parrots in relation to fatty acid composition of breast muscle or adipose tissue as biomarkers of fatty acid intake. Avian Dis 2003; submitted.

5. Grünberg W: Arteriosklerose beim Wildtieren. Klin Wochenschr 43:479–488, 1965.

6. Fiennes RNTW: Atherosclerosis in wild animals. In: Roberts JC, Strauss R, eds: Comparative Atherosclerosis. New York: Harper and Row; 113–126, 1965.

7. Johnson JH, Phalen DN, Kondik VH, et al: Atherosclerosis in psittacine birds. Proc Assoc Avian Vet 87–93, 1992.

8. Phalen DN, Hays HB, Filippich LJ, et al: Heart failure in a macaw with atherosclerosis in the aorta and brachiocephalic arteries. J Am Vet Med Assoc 209:1435–1440, 1996.

9. Bohorquez F, Stout C: Aortic atherosclerosis in exotic avians. Exp Mol Pathol 17:261–273, 1972.

10. Ratcliffe HL: Arterial lesions of zoo birds: Responses to environmental factors. Acta Zool Pathol Antverp 39:3–26, 1966.

11. Wolkoff K: Uber die Atherosklerose beim Papagei. Virch Arch 256:751–758, 1925.

12. Consensus Conference: Lowering blood cholesterol to prevent heart disease. J Am Med Assoc 253:2080–2086, 1985.

13. Finlayson R, Hirchinson V: Experimental atheroma in budgerigars. Nature 192:369–370, 1961.

14. Kris-Etherton PM, Yu S: Individual fatty acids effects on plasma and plasma lipoproteins: Human studies. Am J Clin Nutr 65:1628S–1644S, 1997.

15. Mensink RP, Katan MB: Effect of dietary fatty acids on serum lipids and lipoproteins. Arterioscl Thromb 12:911–919, 1992.

16. Schoemaker NJ, Lumeij JT, Dorrestein GM, Beynen AC: Voedingsgerelateerde problemen bij gezelschapsvogels. Tijdschr Diergeneesk 124:39–43, 1999.

17. Folch J, Lees M, Sloane Stanley GH: A simple method for the isolation and purification of total lipids from animal tissues. J Biol Chem 226:497–509, 1957.

18. Metcalfe LD, Schmitz AA, Pelka JR: Rapid preparation of fatty acid esters from lipids for gaschromatographic analysis. Anal Chem 318:514–515, 1966.

19. Centraal Veevoeder Bureau: Veevoedertabel. Lelystad, the Netherlands: 1999.

20. Friedewald WT, Levy RI, Fredrickson DS: Estimation of the concentration of low density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 18:499–502, 1972.

21. Polo FJ, Peinade VI, Viscor G, Palomeque J: Hematologic and plasma chemistry values in captive psittacine birds. Avian Dis 42: 523–535, 1998.

22. Grundy SM, Bilheimer D, Blackburn H, et al: Rationale of the diet-heart statement of the American Heart Association. Circulation 65:839A–851A, 1982.

23. Martin MJ, Hulley SB, Browner WS, et al: Serum cholesterol, blood pressure, and mortality: Implications from a cohort of 316.662 men. Lancet 8513:933–939, 1986.

24. Hammad SM, Siegel HS, Marks HL: Total cholesterol, total triglycerides, and cholesterol distribution and lipoproteins as predictors of atherosclerosis in selected lines of Japanese quail. Mol Integr Physiol 119:485–492, 1998.

25. Oku H, Ishikawa M, Nagata J, et al: Lipoprotein and apoprotein profile of Japanese quail. Biochim Biophys Acta 1167:22–28, 1993.

26. Radcliffe JD, Liebsch KS: Dietary influence on hypercholesterolemia and atherosclerosis in Japanese quail of strain SEA. J Nutr 115:1154–1161, 1985.

27. Manninen V, Elo MO, Frick MH, et al: Lipid alterations and decline in the incidence of coronary heart disease in the Helsinki Heart Study. J Am Med Assoc 260:641–651, 1988.

28. Austin M: Plasma triglyceride as a risk factor for coronary heart disease: The epidemiologic evidence and beyond. Am J Epidemiol 129:249–259, 1989.

 

 

Table 1. The Ingredients, Analyzed Composition, and Calculated Energy Contents of the Diets

 

Table 2. The Ingredient Composition of the Constant Components in the Experimental Diets

 

                                                  Low-Fat                  High-Fat

                                  Low-Fat     Palm     High-Fat     Palm

  Ingredients

     (g/kg)

    Sunflower oil           15.0           —          132.0         —

    Palm kernel oil            —           15.0           —         132.0

    Glucose                  228.5       228.5          —            —

    Constant                 756.5       756.5       868.0       868.0

    Total                       1000.0     1000.0     1000.0     1000.0

 

  Chemical analysis

     (g/kg)

    Dry matter                898          897          897          903

    Crude ash                41.3         40.8         46.9         47.5

    Crude protein          154.8       158.5       181.4       183.5

    Crude fiber               55.9         54.8         58.7         60.9

    Crude fat                  68.2         69.9        193.6       192.2

    Carbohydrates†      577.9       573.2       417.1       419.3

    Gross energy‡        16.2         16.2         19.0         19.0

     (MJ/kg)

 

  *Glucose and the variable fats were exchanged on an energy basis so that on a weight basis the amount of constant components in the high-fat diets was greater than in the low-fat diets.

  †Calculated as residual fraction.

  ‡The gross energy values (MJ/kg) used were as follows: protein 23.8; fat 39; carbohydrates 17.

 

 

  Corn oil                                           6.6

  Corn                                           132.2

  Wheat                                        119.0

  Oats                                             66.1

  Wheat middlings                           52.9

  Corn glutenmeal                           92.5

  Whole egg                                    46.3

  Sugarbeet pulp, dehydrated      125.6

  Soy beans, extracted                  92.5

  Corn starch                                  33.0

  Wheat germs                               26.4

  Molasses, cane                             6.6

  Yeast, dehydrated                       19.8

  Barley                                          39.7

  Peas                                             27.1

  Rice                                                1.3

  Alfalfa meal, dehydrated             72.7

  Trace-element premix*                 10.6

  Vitamin premix†                           13.2

  Lime                                             13.5

  Salt                                                 2.4

 

  *Trace-element premix contained per kg: 49.8 g FeSO4.7H2O, 12.9 g MnO2, 17.1 g ZnSO4.H2O, 3.9 g CuSO4.5H2O, 62.5 mg KI, 37.5 mg Na2SeO3.5H2O, 1.6 g NiSO4.5H2O, 0.3 g NaF, 0.2 g CrCl3.6H20, 0.2 g SnCl2.2H2O, 25 mg NH4VO3 and 913.875 g corn starch as carrier.

  †Vitamin premix contained per kg: 1.6 g vitamin A (500 IU/g), 0.25 g vitamin D3 (500 IU/g), 10 g vitamin E (purity 50 %), 0.1 g vitamin K, 25 mg biotin, 0.15 g folic acid, 1.0 g vitamin B12 (purity 0.1%), 300 g choline chloride (purity 50%), 0.4 g thiamin, 0.6 g riboflavin, 5.0 g niacin, 0.6 g pyridoxin, 4.4 g (purity 45%) panthotenic acid and 675.875 g corn starch as carrier.

 

 

 

 

Table 3. Contents of Selected Fatty Acids in the Variable Fat Sources

 

Table 4. Contents of Selected Fatty Acids in the Experimental Diets

 

                                              Palm Kernel

 

  Lauric acid             0.0                 53.8

   (C12:0)

 

  Myristic acid           0.0                 15.5

   (C14:0)

 

  Palmitic acid           5.7                   7.5

   (C16:0)

 

  Stearic acid            3.0                   1.7

   (C18:0)

 

  Oleic acid             21.7                 13.3

   (C18:1 n-9)

 

  Linoleic acid         68.1                   2.1

   (C18:2 n-6)

 

  a-Linolenic acid     0.0                   0.0

   (C18:3n-3)

 

                                                 Palm

                                                 kernel               

                          Low fat          g/100g         High fat     Palm

 

  Lauric acid          0.1               17.0               0.0         41.9

   (C12:0)

 

  Myristic acid        0.3                5.2                0.1         12.2

   (C14:0)

 

  Palmitic acid       15.2              15.8               8.7         10.2

   (C16:0)

                               

  Stearic acid         4.2                3.8                3.4          2.4

   (C18:0)

 

  Oleic acid           27.5              24.8              23.5        17.0

   (C18:1 n-9)

 

  Linoleic acid       44.3              23.5              60.4         9.0

   (C18:2 n-6)

 

  a-Linolenic acid  1.4                1.4                0.4          0.4

   (C18:3n-3)

 

  P/S*                     2.9                0.7                6.9          0.2

 

  *P/S is the polyunsaturated to saturated fatty acid ratio. P is the sum of C18:2 and C18:3 and S is the sum of C12:0. C14:0 and C16:0.

 

 

 

Table 5. Mean Plasma Values of Total Cholesterol, Phospholipids, Triglycerides, High-Density Lipoprotein (HDL) Cholesterol and Low-Density Lipoprotein (LDL) Cholesterol for the Four
Dietary Treatments

 

                                        Low-Fat                      Low-Fat                     High-Fat                     High-Fat

                                    Sunflower Oil            Palm Kernel Oil            Sunflower Oil            Palm Kernel Oil

 

  Cholesterol              20 8.15a ± 2.25          20 7.77b ± 1.93          20 7.43c ± 1.25        19 8.83abc ± 1.30

  Phospholipids          20 5.14d ± 0.64          20 5.15e ± 0.65          20 5.01f ± 0.47        20 5.74edf ± 0.70

  Triglycerides             20 2.37 ± 2.14            20 2.01 ± 0.65            20 1.68 ± 0.48            20 1.67 ± 1.01

  HDL-cholesterol1      12 4.49 ± 1.43            10 4.44 ± 0.95            13 4.10 ± 0.64            10 5.85 ± 1.05

  LDL-cholesterol1      11 3.19 ± 2.45            10 2.37 ± 0.95            13 2.61 ± 1.36            10 2.44 ± 0.65

 

  1 The sample size was considered to be too small for appropriate statistical analyses

  Statistical differences between values is shown with the same letters: a, P=0.019; b, P=0.001; cdef P<0.001.