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* Comparative Nutrition Laboratory and College of Veterinary Medicine, Texas A&M University, College Station, TX 77843-4474 and ** Nestle-Purina PetCare, St. Louis, MO 63102
3 To whom correspondence should be addressed. E-mail: jbauer{at}cvm.tamu.edu.
KEY WORDS: • canine • puppy • fatty acids • suckling • lipoprotein • plasma • cholesterol
Polyunsaturated fatty acids (PUFAs)4 are important for neonatal growth and development in all mammalian species studied to date. Normal fetal development requires the 18-carbon essential fatty acids as well as long-chain polyunsaturated fatty acids (LCPUFAs) with 20- and 22-carbon–chain lengths (1). Provision of both dietary (n-3) and (n-6) PUFAs in appropriate amounts are needed to optimize development of nervous system tissue and to promote kidney, liver, and skin functions. Two LCPUFAs, arachidonic acid of the (n-6) series and docosahexaenoic acid of the (n-3) series, which are synthesized by chain elongation and desaturation of essential fatty acids, have received increasing interest recently because they are found in high concentrations in the phospholipids of normal cell membranes of the central nervous system (2). It was shown (3) that human infants who consume low LCPUFA levels also have lower LCPUFA levels in the phospholipids of the cerebral cortex. The clinical relevance of this finding is the subject of various growth and neurodevelopment studies.
Because the PUFAs are transported via plasma lipoproteins (LPs), the effects of dietary fatty acids on LP metabolism may play an important role in development. In dogs, high-density lipoproteins (HDLs) are the predominant plasma LP fraction (75–85%) (4). This differs from humans, where low-density lipoproteins (LDLs) predominate. For this reason, dogs are considered to be "HDL mammals" (5,6) and also exhibit atherosclerosis-resistance properties (4).
However, as in humans, diet can alter canine LP cholesterol distributions. For example, a study by Bauer (7) demonstrated that dogs fed a diet that is high in saturated fat (primarily from beef tallow) show an increase in both LDL and HDL fractions, and all LP fractions tend to shift toward a lower density. Dreon et. al. (8) also reported that feeding saturated fat increases both LDL and HDL concentrations in humans. Replacing saturated fat with unsaturated fat in the diet decreases LDL more than HDL in humans. Polyunsaturated fatty acids are the most potent fatty acids for reducing LDL cholesterol (9).
An early study of canine LP metabolism showed that immature dogs had greater hepatic LDL receptor activity than mature dogs. This activity was undetectable by 24 mo of age. Canine liver contains two distinct LP receptors. There is an apoprotein-B,E (apo-B,E) receptor, which binds both LDL and HDL cholesterol, and an apo-E receptor, which binds only HDL cholesterol. The apo-B,E receptor is seen in immature, growing dogs, whereas only the apo-E receptor is found in adult dogs (10). This same study also revealed that feeding cholesterol can suppress apo-B,E receptors in immature dogs, whereas in mature dogs, prolonged fasting can induce expression of apo-B,E receptors. The apo-E hepatic membrane receptors remain constant in both immature and adult dogs or decrease only slightly with age (10). Thus, the possibility exists that immature dogs have greater concentrations of LDL fractions during early life, and dietary fatty acids may further modify plasma LP fractions overall.
The present study was conducted to investigate plasma LP distribution changes during suckling and early adolescence of puppies born to bitches that were fed diets that varied only in fatty acid composition and were otherwise identical.
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MATERIALS AND METHODS |
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 TOP MATERIALS AND METHODS RESULTSDISCUSSIONLITERATURE CITED |
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-linolenic acid (ALA) using linseed oil and (n-3) LCPUFAs (i.e., 20/22-carbon (n-3) fatty acids) from menhaden fish oil. The groups were designated Lo/Lo, Hi/Lo, Lo/Mod, and Lo/Hi, according to their ALA/(n-3) LCPUFA concentrations (Table 1). All other diet ingredients including protein, nitrogen-free extract, and vitamin and mineral sources were identical, which resulted in diets with similar nutrient concentrations except for fatty acid types. The diet compositions are described in a companion article (11). Each bitch was fed her randomly assigned diet from the time of insemination throughout gestation, parturition, and lactation according to her body condition. Sufficient quantities of the diets were fed to maintain a 25% weight gain of each bitch's nonpregnant body weight during the latter stages of gestation by adjusting the amounts fed as necessary. At 21 d of age, gruel consisting of the mothers' respective diets and water were offered to the puppies three times a day in addition to suckling. Gradually, the time the puppies spent suckling was decreased until they were completely weaned by d 42. Upon weaning, puppies were continued on the same diet as their mothers until 10 wk of age.
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LP distribution was determined by electrophoresis on 1% agarose gel on each blood collection day and was quantified by scanning densitometry (12). Total cholesterol values were determined enzymatically using a microplate reader (12). Results were compared using Statistix software by two-factor ANOVA for diet, time, and diet x time interaction effects and subsequently with Tukey's comparison of means where necessary. A P-value was set at P < 0.05 for all data to determine statistical significance.
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RESULTS |
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TOPMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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-LP cholesterol levels remained unchanged during the suckling period but decreased after weaning (Fig. 3). The only statistically significant diet effect observed was decreased total plasma cholesterol (Fig. 2) and all LP cholesterol fractions in puppies whose mothers were fed either of the menhaden fish–oil diets (Lo/Mod and Lo/Hi groups) compared with the diets of the Lo/Lo and Hi/Lo groups (Figs. 1 and 2).
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DISCUSSION |
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TOPMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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In addition to age-related effects, the results of the present study also show alterations in LP metabolism due to differences in maternal dietary fatty acids. These findings are consistent with the cholesterol-lowering effects and reduction of post-prandial LP fractions of dietary marine oils that are reported for adult humans and other species (16–18).
In human neonates (which differ from canine neonates), only a minor part of total cholesterol is transported via the ß-LP fraction (19). Immature canines have a high ß-LP concentration during early life (d 4 and 10). As a dog matures, the ß-LP fraction decreases. However, in humans, the ß-LP fraction increases with maturity; adult humans carry 
75% of their cholesterol in the LDL fraction (4). Mao and Hamosh (15) concluded that the enzymes associated with the metabolism of cholesterol are well developed in Sprague-Dawley rats shortly after birth. Based on the findings of our study, it is reasonable to also suggest that cholesterol metabolic enzymes are also well developed in puppies shortly after birth. The reduction in total plasma cholesterol concentration as the puppies mature indicates that the receptors and enzymes necessary for lipid metabolism are active in young puppies.
Studies designed to investigate LP metabolism and diet modifications in dogs during the early neonatal period can provide useful new information for the growth and development of dogs used in service activities as well as provide a model for later gestational development of humans. Several studies suggest that in different species, dietary intake during early life may have long-term effects on metabolic systems such as cholesterol and LP metabolism and offer evidence that breastfed neonates are provided with a better defense against atherosclerosis than those fed formula (20–22). This is interesting, because breast milk contains higher cholesterol and saturated fat compared with formula, but that is apparently more beneficial in the long term (23,24).
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FOOTNOTES |
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2 This work was supported in part by Nestle-Purina PetCare and the Mark L. Morris Professorship in Clinical Nutrition at Texas A&M University.
4 Abbreviations used: ALA, -linolenic acid; HDL, high-density lipoprotein; LA, linoleic acid; LCPUFA, long-chain polyunsaturated fatty acids; LDL, low-density lipoprotein; LP, lipoprotein; PUFA, polyunsaturated fatty acids.
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LITERATURE CITED |
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1. Herrera, E. (2002) Lipid metabolism in pregnancy and its consequences in the fetus and newborn. Endocrine 19: 43–55.[Medline]
2. Uauy, R. & Castillo, C. (2003) Lipid requirements of infants: implications for nutrient composition of fortified complementary foods. J. Nutr. 133: 2962S–2972S.
3. Fewtrell, M. S., Morley, R., Abbott, R. A., Singhal, A., Isaacs, E. B., Stephenson, T., MacFadyen, U. & Lucas, A. (2002) Double-blind, randomized trial of long-chain polyunsaturated fatty acid supplementation in formula fed to preterm infants. Pediatrics 110: 73–82.
4. Wagner, J. D., Greaves, K. A., Schwenke, D. C. & Bauer, J. E. (1999) Lipids and lipoproteins. In: The Clinical Chemistry of Laboratory Animals, 2nd ed. (Loeb, W. F. & Quimby, F. W.), chap. 11, pp. 181–207. Taylor & Francis, Philadelphia, PA.
5. Chapman, M. J. (1986) Comparative analysis of mammalian plasma lipoproteins. In: Methods in Enzymology, Vol. 128A (Segrest, J. P. & Alberts, J. J.), pp. 70–143. Academic Press, Boston, MA.
6. Maldonado, E. N., Romero, J. R., Ochoa, B. & Aveldano, M. I. (2001) Lipid and fatty acid composition of canine lipoproteins. Comp. Biochem. Physiol. B Biochem. Mol. Biol. 128: 719–729.[Medline]
7. Bauer, J. E. (1991) Single spin density gradient systems and micropreparative ultracentrifugation. In: Analysis of Fats, Lipids, and Lipoproteins (Perkins, E. G.), p. 555. American Oil Chemists' Society, Champaign, IN.
8. Dreon, D. M., Fernstrom, H. A., Campos, H., Blanche, P., Williams, P. T. & Krauss, R. M. (1998) Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am. J. Clin. Nutr. 67: 828–836.[Abstract]
9. Sacks, F. M. & Katan, M. (2002) Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am. J. Med. 113: 13S–24S.
10. Mahley, R. W., Hui, D. Y. & Innerarity, T. L. (1981) Two independent lipoprotein receptors on hepatic membranes of dog, swine, and man. Apo-B,E and apo-E receptors. J. Clin. Invest. 68: 1197–1206.
11. Bauer, J. E., Heinemann, K. M., Bigley, K. E., Lees, G. E. & Waldron, M. K. (2004) Maternal diet -linoleic acid during gestation and lactation does not increase canine milk docosahexaenoic acid. J. Nutr. 134: 2035S–2038S, 2004.
12. McAlister, K. G., Bauer, J. E., Harte, J., Rawlings, J. M. & Markwell, P. (1996) Canine plasma lipoproteins and lecithin:cholesterol acyltransferase activities in dietary oil supplemented dogs. Vet. Clin. Nutr. 3: 50–56.
13. Mott, G. E., Lewis, D. S. & McMahan, C. A. (1993) Infant diet affects serum lipoprotein concentrations and cholesterol esterifying enzymes in baboons. J. Nutr. 123: 155–163.
14. Butterwick, R. F., McConnell, M., Markwell, P. J. & Watson, T. D. G. (2001) Influence of age and sex on plasma lipid and lipoprotein concentrations and associated enzyme activities in cats. Am. J. Vet. Res. 62: 331–336.[Medline]
15. Mao, J. & Hamosh, M. (1992) Postnatal development of plasma-lipid-clearing enzymes (lipoprotein lipase, hepatic lipase and lecithin:cholesterol acyltransferase) and lipid profiles in suckling rats. Biol. Neonate 62: 1–9.[Medline]
16. Piolot, A., Blanche, D., Boulet, L., Fortin, L. J., Dubreuil, D., Marcoux, C., Davignon, J. & Lussier-Cacan, S. (2003) Effect of fish oil on LDL oxidation and plasma homocysteine concentrations in health. J. Lab. Clin. Med. 141: 41–49.[Medline]
17. Subbaiah, P. V., Kaufman, D. & Bagdade, J. D. (1993) Incorporation of dietary n-3 fatty acids into molecular species of phosphatidylcholine and cholesteryl ester in normal human plasma. Am. J. Clin. Nutr. 58: 360–368.
18. Groot, P. H., Scheek, L. M., Dubelaar, M. L., Verdouw, P. D., Hartog, J. M. & Lamers, J. M. (1989) Effects of diets supplemented with lard fat or mackerel oil on plasma lipoprotein lipid concentrations and lipoprotein lipase activities in domestic swine. Atherosclerosis 77: 1–6.[Medline]
19. Kaser, S., Ebenbichler, C. F., Wolf, H. J., Sandhofer, A., Stanzl, U., Ritsch, A. & Patsch, J. R. (2001) Lipoprotein profile and cholesteryl ester transfer protein in neonates. Metabolism 50: 723–728.[Medline]
20. Mott, G. E., Jackson, E. M., McMahan, C. A. & McGill, H. C., Jr. (1990) Cholesterol metabolism in adult baboons is influenced by infant diet. J. Nutr. 120: 243–251.
21. Lanting, C. I. & Beorsma, E. R. (1996) Lipids in infant nutrition and their impact on later development. Curr. Opin. Lipidol. 7: 43–47.[Medline]
22. Hahn, P. (1982) Development of lipid metabolism. Annu. Rev. Nutr. 2: 91–111.[Medline]
23. McGill, H. C., Mott, G. E., Lewis, D. S., McMahan, C. A. & Jackson, E. M. (1996) Early determinants of adult metabolic regulation: effects of infant nutrition on adult lipid and lipoprotein metabolism. Nutr. Rev. 54: S31–S40.[Medline]
24. Mott, G. E., DeLallo, L., Driscoll, D. M., McMahan, C. A. & Lewis, D. S. (1993) Influence of breast and formula feeding on hepatic concentrations of apolipoproteins and low-density lipoprotein receptor mRNAs. Biochim. Biophys. Acta 21: 59–65.
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