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Unidad de Investigación en Nutrición, Instituto Mexicano del Seguro Social, Apartado Postal 7–1069, Mexico, DF 06700
3To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • mammary gland • lipoprotein lipase • lactation • dietary fat • lipogenesis • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Lipid in the chylomicrons is derived from intestinal
absorption, while lipid in VLDL may arise from hepatic synthesis or
from nonesterified-fatty acids originally released from adipose
tissue.
In animals and humans, the fatty acid composition of milk lipids is
highly variable and depends on the lipid composition of the diet, the
maternal energy balance and the relative proportions of carbohydrate
and lipid in the maternal diet. When mothers are in a negative energy
balance, the fatty acids in milk reflect the composition of the
maternal fat depots (Insull et al. 1958
). If the
maternal diet is low in fat and high in carbohydrate and provides
adequate energy, the proportion of medium-chain fatty acids in the
milk increases. Medium-chain fatty acids are synthesized by the
mammary gland. When a diet high in fat is consumed, fatty acid milk
composition resembles that of the lipid in the diet, and the proportion
of medium-chain fatty acids in milk is lower (Green et al. 1981
, Hachey et al. 1989
, Ross et al. 1985
, Tead et al. 1965
). Changes in the
composition or energy content of the maternal diet were not related to
either an increase in the volume or the total milk lipid concentration
(Insull et al. 1958
, Ross et al. 1985
).
The changes in fatty acid composition of milk reported in animals fed
high lipid diets are indicative of an associated decrease in fatty acid
synthesis by the mammary gland and of an increase in its uptake of
fatty acid (Grigor and Warren 1980
). An oral load of
either long- or medium-chain triglycerides or the administration of
diets with a high concentration of fat to lactating rats inhibits the
rate of mammary gland lipogenesis in vivo (Grigor and Warren 1980
, Agius and Williamson 1980
).
We have shown in rats fed a diet high in lipid concentration, that milk
output and lipid concentration are greater than that of rats fed with a
normal, high carbohydrate, low lipid diet. In addition, pups of
high-fat diet fed dams grew faster than controls (Del Prado et al. 1997
).
This study was designed to better understand the mechanisms controlling the lipid concentration of milk. It was designed to test whether alterations in mammary gland lipid uptake and lipoprotein lipase activity caused by changes in the lipid concentration of the diet are related to an increase in milk lipid concentration. The working hypothesis was that a higher intake of fat during pregnancy and lactation increases mammary gland lipid uptake and lipoprotein lipase activity.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Female Sprague-Dawley rats (Charles River Breeding Laboratories, Wilmington, MA) housed in group cages, under controlled temperature (22 ± 2°C) and 12- light-dark cycles (lights on from 0700 h) were used for all experiments. The rats were randomly assigned to one of three experimental groups. In the first group, the 14C-triolein uptake and oxidation and the mammary gland lipoprotein lipase (LPL)4 activity was measured. In the second group, mammary gland lipogenesis was determined, and in the third group, milk composition and production were evaluated. Rats were maintained and handled in accordance with the guidelines for experimental animals of the NIH and Secretaria de Salubridad of México. From weaning to 12 wk of age, rats were fed a pelleted, nonpurified diet (Purina, Guadalajara, México) containing 24 g protein/100 g dry weight, 61 g carbohydrate /100 g dry weight and 2.5g fat/100 g dry weight. For 2 wk before mating, rats were fed a pelleted purified diet containing the same proximate composition as the pelleted commercial diet.
Animals at 14 wk of age, weighing 220–280 g, were mated. The day on which sperm was identified in vaginal smears was designated as d 1 of pregnancy. Breed females were housed individually. The day of parturition, designated as day 1 of lactation, litters were weighed and then adjusted to 8 pups per dam. No gender differentiation was done.
Experimental diets.
After mating, rats were randomly assigned to one of two purified diets
containing 2.5 (low-fat diet, LL) or 20 g fat/100 g dry weight
(high-fat diet, HL). Both provided 14.64 kJ of digestible energy/g
of dry diet. Lipid contributed 42% to the total energy in the
high-fat diet and with 3% to the low-fat diet. Casein
contributed 30% to the total energy density in both diets. The diets
were prepared as pellets and stored at 4°C until subsequent used.
Rats had free access to diet and water at all times. The composition of
the experimental diets was previously described (Del Prado et al. 1997
).
Measurement of [14C] lipid accumulation in tissues and oxidation.
The metabolic fate of an oral load of [1-14C]triolein was
determined by the method previously described by Oller do Nascimento
and Williamson (1986)
. All experimental procedures started at 0900 h. Food was not withheld before the experiment, and the rats had free
access to food during the procedure. After intragastric administration
of [1-14C] triolein (glycerol tri [1-14C]
oleate; 0.5 g, 29.6 kBq per rat), the
14CO2 production (oxidation of the oral lipid
load) was measured every hour for 5 h in a glass desiccator
connected to a wash bottle fitted with a sintered-glass tube that
contained ethanolamine to absorb the CO2. A portion of the
ethanolamine was added directly to the scintillation fluid for
measurement of radioactivity. After 5 h (1400 h), rats were
anesthetized with pentobarbital (60 mg/kg body weight), and a sample of
mammary gland was freeze-clamped for LPL activity measurement.
Arterial blood was collected to measure triacylglycerol concentration
by using an enzymatic method (Triacylglyceride-UV, cat no. 334,
Sigma-Aldrich, St Louis, MO). The whole intestinal tract, the
mammary gland, the liver and the parametrial adipose tissue were
dissected. The carcass was homogenized in water. The intestinal tract
was homogenized in 30g HClO4/L (wt/v). Pups were killed
while under diethyl ether anesthesia, and the stomachs were dissected.
Milk clots were removed, weighed and mixed. The remaining pup was
homogenized in water. After saponification with 300 g KOH/L,
lipids were extracted in duplicate samples from the homogenates of the
intestinal tract, maternal and pups carcass, and 0.5-g samples of
mammary gland, milk clot, liver and parametrial adipose tissue
(Stansbie et al. 1976
). The radioactivity in the
extracted fatty acids was measured, and the [14C]lipid
accumulated by the tissues was calculated. The amount of the
[1-14C]triolein absorbed was determined as the difference
between the radioactivity in the total dose and the radioactivity
remaining in the intestinal tract.
Measurement of mammary gland LPL activity.
The LPL (clearing factor lipase, EC 3.1.1.34) activity was measured in
acetone/ether dried powder of the mammary gland by using
[9,10-3H]triolein as substrate (Nilsson-Ehle and Schotz, 1976
). The activity is expressed as nmol of fatty acid
released/(min·mg of acetone-dried tissue).
Measurement of mammary gland lipogenesis.
Lipogenesis was measured in vivo by using tritiated water as described
by Robinson and Williamson (1978)
. In short, rats were injected
intraperitoneally with 74 Bq (in 0.2 mL) of
3H2O. the Mammary gland was removed from the
anesthetized rats 60 min after 3H2O
administration. Lipids were extracted from duplicate samples of the
tissue, and the radioactivity in the lipid fraction was measured
(Stansbie et al. 1976
).
Measurement of milk production.
Daily milk production was measured on d 14 of lactation by the
tritiated water method described by Godbole et al. (1981)
, modified by
Warman and Rasmussen (1983)
. The rats received 37 Bq of
3H2O (0.2 mL) intraperitoneally followed by
free intake of 3H2O diluted in the drinking
water. Its specific activity was individually adjusted to equal the
specific activity in the plasma of the dam 1 h after injection.
Twenty-four h later, tritium specific activity in the blood of dams
and pups was measured. The estimates of metabolic water needed for the
calculations were obtained with the average values for milk composition
for each diet group and the factors reported by Schmidt-Nielsen (1964)
.
Milk lipid concentration and fatty acid composition.
Milk samples were collected between 12 and 14 d postpartum in 8 rats from each dietary group. The dams were separated from their litters for a period of 4 h (0900–1300 h) before milking. The milk was expressed manually from all teats while the rats were under pentobarbital anesthesia (35 mg/kg body weight) and after an injection of oxytocin (4 UI per rat) intraperitoneally. Milk samples were frozen at -20°C until further analyses.
Milk lipid concentration was measured gravimetrically after
chloroform-methanol extraction by a modified Folch method
(Jensen 1989
).
Fatty acids were transesterified and methylated by using methanolic
H2SO4 (Knapp 1979
). The
resulting fatty acids methyl esters (FAME) were separated by using a
100-m cyanopropyl silicone capillary column in a gas chromatograph
(Hewlett-Packard model 5890, Avondale, PA) equipped with a flame
ionization detector. Individual FAME were identified by comparing their
retention times to those of commercial standards. The injector and
detector were at 300°C; the column temperature was programmed to rise
from 195 to 240°C at a rate of 15°C/min with an hydrogen flow rate
of 1.5 mL/min. All of the lipid samples contained a known amount of an
internal standard (heptadecanoic acid). The results from gas
chromatography were expressed as percentage composition.
Statistical analysis.
The results are mean ± SD Differences between groups were analyzed by Student's t test for independent samples with an alpha of 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The intestinal absorption of [1-14C] triolein
was 14% higher in the rats fed the HL diet (Table 1
). To correct for differences in absorption between experimental groups,
all the results are expressed as the percentage of the dose absorbed.
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. The amount of
[1-14C] triolein accumulated in the carcass of
the pups and the total amount of the 14C-lipid
transferred to the pups, defined as the sum of the radioactivity in the
milk clot and in the carcass of the pups, (22.89 ± 9.13 vs. 15.56
± 6.24, P < 0.05) were significantly higher in
the HL rats . 14CO2 production and 14C-lipid accumulation in maternal carcasses and liver.
The percentage of the 14C-dose accumulated in the
liver was 33% lower in the HL group than in the LL group, and there
were no differences in the amount of
[1-14C]triolein accumulated in the maternal
carcass or in the parametrial adipose tissue (Table 2
). The rate of 14CO2
production in the dams fed with the HL diet was 100% faster than in
rats fed the LL diet.
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Mammary gland lipogenesis was 75% lower [22.9 ± 10.0 vs. 88.3 ± 33.0 µmol of 3H2O incorporated/(h · g tissue), P < 0.01], while LPL activity and plasma triglycerides were 30 and 133% higher in the HL group than those in the LL group [2.87 ± 0.41 vs. 2.19 ± 0.43 nmol/(min·mg acetone powder), P < 0.05 and 2.37 ± 0.84 vs. 1.02 ± 0.38 mmol/L, P < 0.05, respectively].
Milk fatty acid composition and production.
Fatty acid composition in the milk of the HL group showed a
preponderance of palmitic, oleic and linoleic acid, reflecting the
fatty acid composition of the corn oil used in the preparation of the
diet (Fig. 1
). In the LL group the proportions of medium-chain fatty acids
(C8–C14) were higher than in the HL group. The HL group had greater
milk volume and milk lipid concentration than did the rats fed the LL
diet (Table 3
). When milk fatty acids were pooled in groups based on to their
metabolic origin, i.e., C8–C14 indicate synthesis the novo by the
mammary gland, and fatty acids of 16 carbons or longer indicate the
contribution of the diet, the excretion (g/d) of long-chain fatty
acids by the HL group was more than twice that in the LL group (P
< 0.001). The daily excretion of medium-chain fatty acids by
the HL group was 46% lower than that in the LL group (P < 0.001).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The notion that the increased production of total lipid in milk was of biological importance for the pups is supported strongly by the intense accumulation of labeled triolein in the milk clot and in the carcass of the pups in the HL group.
The milk fat of HL rats contained ~80% of long-chain fatty acids
(>C18), with the remaining as medium-chain fatty acids (C8–C14).
It was demonstrated that oral loads of lipid (both medium-chain or
long-chain triacylglycerols) or chronic feeding on a high-fat
diet depresses the rate of mammary gland lipogenesis (Agius and Williamson 1980
, Grigor and Warren 1980
). Our
results corroborated those findings by showing that feeding a
high-fat diet during pregnancy and lactation decreased mammary
gland lipogenesis 75%. Thus, we can conclude that the larger milk fat
production in the HL rats was achieved by a larger extraction of lipid
from plasma associated with a very low rate of lipogenesis in the
mammary gland.
The association between a high concentration of plasma triglycerides
and the larger total lipid concentration in the milk of rats fed the HL
diet is congruent with the higher LPL activity found in their mammary
glands. Lipoprotein lipase hydrolyses the triacylglycerol component of
circulating chylomicrons and VLDL to provide free fatty acids and
2-monoacylglycerol for tissue utilization. The activity of the enzyme
was described as the key factor in the uptake of circulating lipid by
the lactating mammary gland (Scow et al. 1977
). To our
knowledge there is no evidence in the literature concerning the effect
of a high lipid intake and the LPL activity in the mammary gland. In
the HL rats, the LPL activity was modestly greater (30%), while the
concentration and the daily output of long-chain fatty acids in the
milk was much greater than in the LL rats (68% and 43% respectively).
Because the increment seen in the activity of LPL was not proportional
to the changes in long-chain fatty acids output in milk, fatty
acids may be transported through the mammary epithelium membrane by
pathways different than those mediated by LPL. Free fatty acids (FFA)
are derived from triglyceride hydrolysis in adipose tissue and their
uptake by individual tissues is a function of their concentration in
the blood (Fredrickson and Gordon 1958
, Scow and Chernick 1970
). Long-chain fatty acids are carried in the
circulation as FFA bound to albumin or as triglyceride-fatty acids
within chylomicrons and VLDL. We did not measure the plasma
concentration of FFA. However, studies from our laboratory (Del Prado et al. 1995
) and from others (Naismith et al. 1982
) have demonstrated that the body fat stores in rat dams
are depleted at the end of one lactation cycle, indicating an intense
mobilization of FFA into the circulation. In this regard it is
important to estimate, in the future, the rate of transference of
plasma FFA into milk because it is likely that in lactating rats, FFA
might contribute significantly to milk fat production (Nielsen and Hajibsen 1994
). It also has to be considered that
nonesterified fatty acids liberated from fat stores during lactation
are incorporated in VLDL by the liver and can be taken up by the
mammary gland in a mechanism mediated by LPL (Scow and Chernick 1987
).
Such a massive transport of fat to the mammary epithelium needed for
the daily milk fat excretion requires other, more efficient, mechanisms
of transmembrane transport. Fielding et al. (1979)
have demonstrated
high-affinity binding of chylomicra to vascular endothelial cells
in culture. After binding, the triglyceride moieties are internalized
and hydrolyzed by a lysosome-dependent pathway. It may be that this
process occur in mammary tissues as well. Two other findings merit some
discussion. One is that 14C-triolein absorbed was
14% greater in the rats fed the HL diet than in the LL-fed rats.
Other investigators have found that the activity of pancreatic lipase
and lingual lipase in adult rats significantly increased when the fat
content of the diet is ~20% or more (Armand et al. 1990
, Gidez 1973
and Saab et al. 1986
), enabling an almost complete assimilation of dietary fat
and increasing its availability to tissues.
The second finding is that the amount of
14C-triolein accumulated in the carcass and in
the adipose tissue of the rat dams was not affected by diet lipid
level. However, HL-fed rats expired more than twice as much
14CO2, indicating a greater
dietary fat oxidation rate. Other investigators have found a decreased
rate of dietary fat oxidation during lactation (Oller Do Nascimento and Williamson 1986
), in part as a result of the
high lipid uptake by the mammary gland. It was interpreted as a
mechanism that was used by lactating rats to spare lipids for the
synthesis of milk fat. Souza and Williamson (1993)
showed that the
lactating rats fed, from d 8 to 10 of lactation, a diet with 20%
triolein or medium-chain triglycerides did not have a greater rate
of oxidation and accumulation of [1-14C]
triolein in the mammary gland than did rats fed a low-lipid diet.
Such apparent contradictions with our results are probably caused by
methodological differences; in, particular, the large difference in
dietary fat concentrations [20 vs. 4%, (Oller Do Nascimento and Williamson 1986
)] or the duration of the intervention [5
wk vs. 10 d (Souza 1993
)].
In summary, rats fed a high-lipid diet along pregnancy and lactation develop high- plasma triglyceride concentrations associated with higher concentrations and daily output of total lipid in milk. The fatty acid composition of milk was similar to that of the diet. The LPL activity in the mammary tissue was also higher in the HL-fed rats. These facts imply a greater transference of plasma lipid into the mammary cells. Accordingly, the relative content of fatty acids derived from mammary lipogenesis and the actual lipogenesis rate were very low. Further research is needed to understand the mechanisms controlling the total content of milk fat and the flux of lipid through the membrane.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Dedicated to Professor Dermot H.
Williamson.
4 Abbreviations used: FAME, fatty acids methyl
esters; FFA, free fatty acids; HL, high-fat diet (20 g corn oil/100
g dry weight); LL, low-fat diet (2.5 g corn oil/100 g dry weight);
LPL, lipoprotein lipase.
Manuscript received December 17, 1998. Initial review completed February 15, 1999. Revision accepted April 7, 1999.
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REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Agius L. Y., Williamson D. H. Rapid inhibition of lipogenesis in vivo in lactating rat mammary gland by medium chain triacylglycerols and partial reversal by insulin. Biochem. J. 1980;192:361-364[Medline]
2. Armand M., Borel P., Cara L., Senft M., Chautan M., Lafont H., Lairon D. Adaptation of lingual lipase to dietary fat in rats. J. Nutr. 1990;120:1148-1156
3. Del Prado M., Delgado G., Gonzalez M., Villalpando S. Effect of high fat diet during pregnancy and lactation on maternal and litter body composition. FASEB J 1995;9:494(abs)
4. Del Prado M., Delgado G., Villalpando S. Maternal lipid intake during pregnancy and lactation alters milk composition and production and litter growth in rats. J. Nutr. 1997;127:456-462
5. Fielding C. J., Vlodavsky I., Fielding P. E., Gospodarowicz D. Characteristics of chylomicron binding and lipid uptake by endothelial cells in culture. J. Biol. Chem. 1979;154:8861-8868
6.
Fredrickson D. S., Gordon R. S. Transport of fatty acids. Physiol. Rev. 1958;38:585-630
7. Gidez L. I. Effect of dietary fat on pancreatic lipase levels in the rat. J. Lipid Res. 1973;14:169-177
8. Godbole V. Y., Grundleger M. L., Pasquine T., Thenen S. W. Composition of rat milk from day 5 to 20 of lactation and milk intake of lean and preobese Zucker pups. J. Nutr. 1981;111:480-487
9. Green M. H., Dohner E. L., Green J. B. Influence of dietary fat and cholesterol on milk lipids and on cholesterol metabolism in the rat. J. Nutr. 1981;111:276-286
10. Grigor M., Warren S. M. Dietary regulation of mammary lipogenesis in lactating rats. Biochem. J. 1980;188:61-65[Medline]
11. Hachey D. L., Silber G. H., Wong G. H., Garza C. Human lactation II. Endogenous fatty acid synthesis by the mammary gland. Pediatr. Res. 1989;25:63-68[Medline]
12. Insull W., Jr, Hirsch J., James T., Ahrens E. H., Jr The fatty acids of human milk. Alterations produced by manipulation of caloric balance an exchange of dietary fats. J. Clin. Invest. 1958;38:443-450
13. Jensen R. G. eds. The Lipids of Human Milk 1989 CRC Press Inc Boca Raton, FL.
14. Knapp D. R. Handbook of Analytical Derivatization Reactions 1979 John Wiley and Sons New York, NY.
15. Naismith D., Richardson D., Pritchard A. The utilization of protein and energy during lactation in the rat with particular regard to the use of fat accumulated in pregnancy. Br. J. Nutr. 1982;48:433-441[Medline]
16. Neville M. C. Allen J. C. Watters S. C. eds. Lactation: Physiology, Nutrition and Breast Feeding 1980 Plenum Press New York, NY.
17. Nielsen M. O., Hajibsen K. Changes in mammary uptake of free fatty acids, triglyceride, cholesterol and phospholipid in relation to milk synthesis during lactation in goats. Comp. Biochem. Physiol. 1994;109A:857-867
18. Nilsson-Ehle P., Schotz M. A stable, radioactive substrate emulsion for assay of lipoprotein lipase. J. Lipid Res. 1976;17:536-541[Abstract]
19. Oller Do Nascimento C., Williamson D. H. Evidence for conservation of dietary lipid in the rat during lactation and the immediate period after removal of the litter. Decreased oxidation of oral [1–14C]triolein. Biochem. J. 1986;239:233-236[Medline]
20. Robinson A. M., Williamson D. H. Measurements of lipogenesis in vivo and plasma hormone concentrations in response to starvation and refeeding. Biochem. J. 1978;176:343-346[Medline]
21. Ross A. C., Davila M. E., Clearly M. P. Fatty acids and retinyl esters of rat milk. Effects of diet and duration of lactation. J. Nutr. 1985;115:1488-1497
22. Saab J. E., Godfrey P. M., Brannon P. M. Adaptative response of rat pancreatic lipase to dietary fat: effects of amount and type of fat. J. Nutr. 1986;116:892-899
23. Schmidt-Nielsen, K. (1964) Terrestrial animals in dry heat: Desert rodents. In: Handbook of Physiology (Dill, D. B., Adolph, E. F. & Wilbur, C. G., eds.), Section 4, p 501. American Physiological Society, Washington DC.
24. Scow R. O., Chernick S. S. Mobilization, transport and utilization of free fatty acids. Florkin M. Stotz E. H. eds. Comprehensive Biochemistry 1970;Vol. 18:19-49 Elsevier Amsterdam, The Netherlands.
25. Scow R. O., Chernick S. S. Role of lipoprotein lipase during lactation. Borensztajn J. eds. Lipoprotein Lipase 1987:149-185 Evener Chicago, IL.
26. Scow R., Chernick S., Fleck R. Lipoprotein lipase and uptake of triacylglycerol cholesterol and phosphatidylcholine from chylomicrons by mammary and adipose tissue of lactating rats in vivo. Biochim. Biophys. Acta 1977;487:297-306[Medline]
27. Souza F.A.P., Williamson D. H. Effects of feeding medium-chain triacylglycerols on maternal lipid metabolism and pup growth in lactating rats. Br. J. Nutr. 1993;69:779-787[Medline]
28. Stansbie D., Brownsey R. W., Crettaz M., Denton R. M. Acute effects in vivo of anti-insulin serum on rates of fatty acid synthesis and activities of acetyl-coenzyme A carboxylase and pyruvate dehydrogenase in liver and epididymal adipose tissue of fed rats. Biochem. J. 1976;160:413-416[Medline]
29. Tead W.W.C., Lutz P., Tashjia A. Human milk lipids. A study in four ethnic groups. Am. J. Clin. Nutr. 1965;17:180-183[Abstract]
30. Warman N. L., Rasmussen K. M. Effects of malnutrition during the reproductive cycle on nutritional status and lactation performance of rat dams. Nutr. Res. 1983;3:527-545
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