Liver Of Pups Research Articles

Distribution and metabolism of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in female rats and their pups at dietary doses.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mammary carcinogen in female rats and is present in a wide variety of cooked meats. We address here the excretion of PhIP and its metabolites into the breast-milk of lactating rats and the ability of chlorophyllin, a food product derivative with chemopreventive properties, to affect these levels at low PhIP doses. Lactating female F344 rats with suckling pups were orally administered 50, 500 and 1000 ng [14C]PhIP/kg body weight. The excretion of the [14C]PhIP into milk and its distribution among the mammary tissue, liver and blood of the dam, as well as among stomach contents and liver of their suckling pups was measured using accelerator mass spectrometry (AMS). PhIP, PhIP-4'-sulfate, 4'-hydroxy-PhIP, and N2-hydroxy-PhIP-N3-glucuronide were found in the milk at all doses. The chlorophyllin (500 microg/kg) co-administration with PhIP (500 ng/kg) caused increased levels of [14C]PhIP in the milk (32%) and stomach contents (35%) of the pups relative to the animals not receiving chlorophyllin at these low PhIP doses. In contrast, lower [14C]PhIP levels in the chlorophyllin treated animals were observed in the blood (47%) and mammary tissue (68%) of the dam, as well as the pup's liver tissue (37%) compared to the animals receiving only PhIP. Chlorophyllin co-administration resulted in an increased amount of N2-hydroxy-PhIP-N3-glucuronide (42%), increased PhIP (79%) and decreased levels of PhIP-4'-sulphate (77%) relative to the animals not receiving chlorophyllin. These results suggest that PhIP and PhIP metabolites are present in the breast-milk of lactating rats at human dietary PhIP exposures and that PhIP is absorbed by the newborn. Furthermore, these results suggest that other dietary components can affect the dosimetry of PhIP in breast-feeding offspring.

Mercury Pollution and the Saimaa Ringed Seal (Phoca hispida saimensis)

Mercury concentrations in the hair and various tissues of the Saimaa ringed seal were monitored from 1980 to 1995. In the liver, muscle and kidney of weaned pups mercury concentrations dropped in the middle of the 1980s. In the natal hair and liver of young pups, however, no clear decrease was seen. In the natal hair and main fish prey species of the seals mercury concentration were highest in areas of humic water. Mercury concentration in the liver of adults has not changed significantly since 1981. Age of the seal is clearly correlated with mercury concentration in the liver. Shortage of selenium is assumed to be one reason for high concentrations of mercury in muscle. The mercury concentration in hair decreased markedly in an adult seal in captivity, after giving selenium. Based on these findings, one reason for the decrease in population density of the Saimaa seal in this century may have been mercury pollution.

Mercury pollution and the Saimaa ringed seal ( phoca hispida saimensis)

Mercury concentrations in the hair and various tissues of the Saimaa ringed seal were monitored from 1980 to 1995. In the liver, muscle and kidney of weaned pups mercury concentrations dropped in the middle of the 1980s. In the natal hair and liver of young pups, however, no clear decrease was seen. In the natal hair and main fish prey species of the seals mercury concentration were highest in areas of humic water. Mercury concentration in the liver of adults has not changed significantly since 1981. Age of the seal is clearly correlated with mercury concentration in the liver. Shortage of selenium is assumed to be one reason for high concentrations of mercury in muscle. The mercury concentration in hair decreased markedly in an adult seal in captivity, after giving selenium. Based on these findings, one reason for the decrease in population density of the Saimaa seal in this century may have been mercury pollution.

Increasing dietary linoleic acid in young rats increases and then decreases docosahexaenoic acid in retina but not in brain.

The accumulation of fatty acids in retina, brain, liver, and plasma of 30-day-old rat pups consuming various levels of linoleic acid (LA, 18:2n-6) and constant alpha-linolenic acid (ALA, 18:3n-3) is reported. Dams were fed graded levels of LA during gestation and lactation, and the pups were maintained on the diet of their dams until the end of the brain growth spurt at 30 d of life. Milk, and pup brain, retina, liver, and plasma were analyzed quantitatively for fatty acid profile. The percentage of docosahexaenoic acid (DHA, 22:6n-3) in retina increased from an LA-deficient dietary level, peaked at the 9:1 (LA/ALA) level, then fell for the 41:1 and 69:1 levels. In contrast, the brain DHA percentage was unaffected by dietary LA levels. Retinal unsaturated fatty acid levels paralleled liver and plasma levels. The milk fatty acid composition mirrored the diets. These data show that the retinal fatty acid composition responds sensitively to dietary fatty acid composition, similar to liver and plasma, while the brain unsaturate composition is nearly independent of dietary composition.

Induction of hepatic and renal P4502E1 of neonatal rats exposed translactationally to ethanol

The effect of maternal ethanol intake during lactation on neonatal cytochrome P4502E1 was investigated in Sprague-Dawley rats. Dams were exposed to 15% (v/v) ethanol in drinking water from day 1 of lactation to 4, 7 or 14 days postpartum. Significant ( P < 0.01) enhancement of both hepatic and renal N-nitrosodimethylamine (NDMA) demethylase, an activity of P4502E1, was observed in lactating mothers given ethanol in drinking water. Demethylase activity also significantly increased ( P < 0.01) in the 7- and 14-day livers of both female and male pups and in the 7- and 14-day female and 14-day male kidneys exposed to ethanol through the transmammary route. Cytochrome P4502E1 protein content, assayed by immunoblotting, increased in the maternal liver and kidney of all groups consuming ethanol. Neonatal P4502E1 protein content increased in the 7- and 14-day livers of both sexes and 14-day female kidneys exposed translactationally to ethanol. No effect of ethanol on enzyme activity or protein content of P4502E1 was observed in the liver or kidney of 4-day-old neonates. These results demonstrate the translactational effect of ethanol on neonatal P4502E1 enzyme, which is involved in the metabolism of many low molecular weight xenobiotics, and indicate the possibility of alterations occurring in the kinetics of neonatal drug and xenobiotic metabolism and also in processes connected with perinatal carcinogenesis.

Role of peritoneal macrophages in the effect of natural metabolites in toxic hepatitis

It is demonstrated that under the action of CCl4 cytosol of rat pup liver activates peritoneal macrophages with various enzyme activity. The immunomodulating effect of liver cytosol manifests itself in normalization of cellular and humoral parameters of natural resistance.

Transplacental and Lactational Exposure to Mercury in Hamster Pups after Maternal Administration of Methyl Mercury in Late Gestation

Pregnant Syrian golden hamsters were given a single oral dose of 203Hg-labelled methyl mercury (MeHg), 1.6 mumol/kg body weight, on day 12 of gestation. The uptake, retention and tissue distribution of 203Hg in the dams and pups was studied by gamma-counting during the following three weeks. The average transplacental transfer of 203Hg was 1.1% of the administered dose per pup, corresponding to 11% of the administered dose to a whole litter. This was considerably more than in our previous studies when the dams were treated on gestational day 2 (1.3%) or 9 (4.6%). The amount of 203Hg transferred to each pup in utero was independent of the litter size. The average additional transfer of 203Hg to a litter via milk was 1.7% of the administered dose. In the pups, the content of 203Hg in the liver and brain decreased, while the content in the kidneys and pelt increased during the second and third week. The highest amount of 203Hg was generally found in the pelt, which indicated that unweaned hamster pups primarily excrete MeHg by binding to hair. The chemical form of mercury in the liver and kidneys of the pups was determined by ion-exchange separation of inorganic Hg and MeHg followed by gamma-counting. The amount of inorganic Hg in the liver of the pups remained constant throughout the experiment, while it increased in the kidneys after one week due to the demethylation of MeHg. The inorganic Hg in the liver of newborn pups was probably due to maternal demethylation of MeHg and transplacental transfer of inorganic Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphofunctional aspects of liver regeneration in experimental correction of toxic hepatitis

It is demonstrated that cytoplasmic extract of rat pup liver stimulates cellular and intracellular regeneration of hepatocytes exposed to the toxic agent CCl4. Injection of liver cytosol stabilizes lysosomal membranes, increases the coefficient of energy efficiency of mitochondria, and activates proliferation of polyploid hepatocytes.

Changes in subcellular and zonal distribution of glucokinase in rat liver during postnatal development

Subcellular and zonal distribution of glucokinase in rat liver during postnatal development was examined immunohistochemically. Before day 11 after birth, only some hepatocytes were immunostained, and a positive immunostaining was found in the cytoplasm but not in the nucleus. No zonal distribution of glucokinase was observed in livers of such pups. From day 15, at which time a dietary change from milk to laboratory chow begins to take place, glucokinase immunoreactivity increased; this increase was associated with increases in glucokinase activity and in glucokinase protein, and also the immunostaining was observed mainly in the nuclei. At day 21, the glucokinase immunoreactivity was found almost exclusively in the perivenous zone. At day 30, an intense immunostaining was seen both in the perivenous zone and in the periportal zone, being slightly predominant in the former. The present results indicate that dramatic changes in the distribution of glucokinase in developing rat liver may be related to dietary change.

仔ラットの肝臓と大脳皮質脂質および脂肪酸組成に及ぼす泌乳期ラットのドコサヘキサエン酸エチルエステル摂取の影響

仔ラットの肝臓と大脳皮質脂質および脂肪酸組成に及ぼす泌乳期ラットのドコサヘキサエン酸エチルエステル摂取の影響

Effects of porcine growth hormone on pregnancy and fetal/neonatal development in the rat.

Porcine growth hormone was given subcutaneously twice daily to two groups of 20 females at dose levels of 0.5 and 2.5 IU/kg (1 and 5 IU/kg/day). A control group of 20 females was similarly treated with vehicle. The females were given either vehicle or porcine growth hormone from gestation day (GD) 6 through GD 21, for 10 females that were cesarean sectioned, or through lactation day (LD) 21, for 10 females scheduled for natural delivery. There were no deaths, abortions, or drug-related physical signs in any treatment group. Drug-related effects during gestation were limited to significant (p < or = 0.05) pharmacologically mediated increases in F0 maternal body weight gain during GD 6-20 in the 2.5-IU/kg group, approximately 24% above controls. During LD 0-21, there were significant (p < or = 0.05) dose-related increases in average maternal body weight gain in the 0.5- and 2.5IU/kg groups (72 and 200% above controls, respectively). Consistent with these findings, there were dose-dependent increases in maternal serum growth hormone and IGF-1 levels noted on GD 21 and LD 21 in both drug-treated groups. There were no drug-related effects on embryonal/fetal survival, GD 21 fetal body weight, placental weight, fetal femur length and width, or fetal morphology as determined by external, visceral, and skeletal examinations. There were no drug-related effects on F1 pup mortality, physical signs, body weight, biparietal diameter, liver weight, and femur length or width. These data suggest that subcutaneous administration of growth hormone to pregnant and lactating rats, at a dose that produces significant (p < or = 0.05) increases in maternal body weight gain and serum IGF-1 levels, has no apparent effect on embryonal/fetal development or preweaning growth.

Metabolism of the food-derived carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine by lactating Fischer 344 rats and their nursing pups.

An important class of dietary mutagens and carcinogens are the heterocyclic arylamine compounds that have been identified in a variety of cooked, protein-containing foods. Among these heterocyclic amines, 2-amino-1-methyl-6-phenylimidazo[4,5-b]-pyridine (PhIP) is potentially the most important carcinogen for human cancer risk. We have recently observed that PhIP-derived radioactivity is excreted into the breast milk of lactating rats administered [3H]PhIP. To better assess the significance of breast milk as a route of exposure of the newborn to dietary heterocyclic amines, we examined the metabolites of PhIP in breast milk and in urine of nursing pups. Lactating Fischer 344 rats with 5-day-old pups were given a single oral dose of 10 mg/kg of [3H]PhIP. We collected milk from the dams and urine from the pups and then analyzed the samples for metabolites of PhIP, using high-pressure liquid chromatography (HPLC). PhIP-DNA adduct levels in the tissues of the pups were determined by 32P-postlabeling analysis. Three radioactive peaks were observed by HPLC separation of milk samples: an unidentified early eluting peak, 4'-hydroxy-PhIP, and PhIP. Four metabolites and the parent compound were found in urine of the pups nursed by dams given radiolabeled PhIP: PhIP-4'-O-glucuronide, PhIP-4'-sulfate, 4'-hydroxy-PhIP, and N2-hydroxy-PhIP-N3-glucuronide. 4'-Hydroxy-PhIP and its conjugates contributed approximately 60% of the radioactivity found in the urine. By 32P-postlabeling analysis, PhIP-DNA adducts were detected in spleen, lung, heart, kidney, liver, and stomach of pups at mean levels ranging from 0.06 to 0.55 adducts/10(7) nucleotides. The large percentage of 4-hydroxy-PhIP and its conjugates in the urine indicates that 5-day-old pups detoxify PhIP and further metabolize 4'-hydroxy-PhIP obtained from the breast milk. The presence of the glucuronide conjugate of N-hydroxy-PhIP in the urine of pups and the lack of detectable conjugate or N-hydroxylamine itself in breast milk suggest that PhIP from breast milk undergoes metabolic activation via N-hydroxylation in 5-day-old rat pups. This conclusion was further supported by the observation that hepatic S9 fractions from the pups activated PhIP to a mutagen in the Ames Salmonella mutagenicity assay and by the presence of PhIP-DNA adducts in the tissues of the pups. The findings reported here may have carcinogenic and toxicologic implications for the offspring of women who breast-feed and consume a diet rich in cooked meat.

Translactational exposure of F 1 mouse pups to selenium

In an investigation of the modulation of certain neonatal xenobiotic-metabolizing enzymes in liver of mouse pups postnatally exposed to selenium through the transmammary route, sodium selenite was administered in drinking water to lactating dams at the dose levels of 1 or 5 ppm from day 1 of lactation and continued daily for 14 or 21 days. The higher dose of selenium was found to increase the hepatic acid-soluble sulfhydryl content significantly after 21 days of treatment in dams, their pups ( P < 0.01) and in the 14-day-old male pups ( P < 0.05). Cytochrome b 5 content decreased in the livers of dams that received 5 ppm selenium ( P < 0.01) and in the F 1 pups ( P < 0.01) translactationally exposed to selenium for 14 days. Cytochrome P-450 content decreased in dams and pups exposed to 5 ppm selenium for 14 days and either dose for 21 days ( P < 0.01). Hepatic glutathione S-transferase decreased in the dam that had received 5 ppm selenium for 14 days ( P < 0.05) and in the 14-day-old pups ( P < 0.01). Glutathione reductase and glutathione peroxidase activities decreased in both dams and pups ( P < 0.01). The overall suppression of neonatal hepatic detoxification enzymes demonstrates that selenium may have far-reaching consequences on neonatal growth, development and drug pharmacokinetics.

Transmammary modulation of xenobiotic metabolizing enzymes in liver of mouse pups by mace ( Myristica fragrans Houtt.)

The present study examines the possible transfer of the active principle(s) of mace (aril of the plant Myristica fragrans) through the transmammary route and its ability to modulate hepatic xenobiotic metabolizing enzymes in the F 1 progeny of mice. An aqueous suspension of mace at the dose levels of 0.025 or 0.1 g/animal/day was administered by oral gavage to dams from day 1 of lactation and continued daily for 14 or 21 days. Dams receiving mace treatment and their F 1 pups showed significantly elevated hepatic sulfhydryl content, glutathione S-transferase and glutathione reductase activities and cytochrome b 5 content. Hepatic cytochrome P450 content decreased in dams ( P < 0.05) receiving the lower mace dose for 21 days and the F 1 pups ( P < 0.001), but increased in dams receiving the higher dose for both time periods (P < 0.001) and the lower dose for 14 days ( P < 0.05). Only the 14-day-old pups of dams receiving either mace dose showed significantly elevated ( P < 0.001) levels of hepatic glutathione peroxidase.

Dose-dependent milk transfer and tissue distribution of the food mutagen PhIP in rats and their suckling pups.

The transfer of the neonatal carcinogen and food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) into milk of lactating Sprague-Dawley rats and the uptake in 10 day old suckling pups were investigated. PhIP was quantified by HPLC. In dams given a single i.v. injection of PhIP (0.5 mg/kg body wt) and milked 1 h later, 0.04-0.16% of the dose per ml milk was excreted. In dams dosed i.v. with PhIP (0, 0.05, 0.5 and 5.0 mg/kg body wt) and killed 4 h later a linear dose-dependent milk excretion and uptake of PhIP in the tissues were observed (y = 76.1 chi + 1.0; r = 0.94; P < 0.001). In addition, a linear correlation was found between PhIP levels in dam's liver and milk (y = 0.61 chi + 37.4; r = 0.97; P < 0.001). Following administration of PhIP at doses of 0.05 and 0.5 mg/kg body wt, the highest level of PhIP was observed in the milk samples. Following injection of 5.0 mg PhIP/kg body wt, the highest level of PhIP was observed in the mammary gland and liver. The milk/plasma ratio was 9.3 +/- 6.8 at the highest dose at 4 h. High levels of unmetabolized PhIP were also detected in liver and blood of pups allowed to suck the PhIP-dosed dams for 3 h. Autoradiography of pups injected i.p. with [2-14C]PhIP (4.8 mg/kg body wt) showed that only a low level of radioactivity was irreversibly bound in the liver, and high levels of radioactivity were found in stomach milk, intestinal contents and in the urine, 1 h and 4 h following injection. In addition, radioactivity was present in the skin, liver and kidney. Since milk is the major dietary source for nursing infants, the milk transfer of PhIP is of great concern.

Modulation of hepatic glutathione system of enzymes in suckling mouse pups exposed translactationally to malathion.

The present study examines the transmammary modulation of the glutathione system of enzymes in the F1 generation of mouse pups postnatally exposed to malathion. Lactating Swiss albino mice received either 30 or 100 mg malathion kg-1 body wt. (98% pure) for 14 or 21 days postpartum. The acid-soluble sulphydryl content was significantly increased (P < 0.001) in the liver of 14-day-old pups of dams that had received the higher malathion dose. A similar significant increase was seen in the 21-day-old male pups of dams that had received 30 mg (P < 0.05) or 100 mg (P < 0.01) malathion kg-1 body wt. Dams showed an enhanced hepatic glutathione S-transferase activity following treatment with 100 mg malathion kg-1 body wt. for 14 days (P < 0.02) and 21 days (P < 0.001). Pups of either age groups also showed enhanced hepatic glutathione S-transferase activity (P < 0.001). A significant enhancement in glutathione reductase activity was observed with malathion treatment in livers of dams and pups (P < 0.001). However, dams that had received 30 mg malathion kg-1 body wt. daily for 21 days or 100 mg malathion kg-1 body wt. for either 14 or 21 days showed significantly reduced hepatic glutathione peroxidase activity (P < 0.01, P < 0.001). A significant decrease in glutathione peroxidase activity was also observed in the liver of the 21-day-old male (P < 0.01) and female (P < 0.02) pups of dams that were treated with the higher dose of malathion.

Postnatal modulation of xenobiotic metabolizing enzymes in liver of mouse pups following translactational exposure to sandalwood oil

Transmammary exposure of suckling mouse pups to the oil from the tree, Santalum album, Linn. and its ability to modulate hepatic neonatal xenobiotic metabolizing enzymes was examined. Sandalwood oil, at the dose levels of 5 ul and 10 ul per animal per day, was fed by oral gavage to lactating Swiss albino mice from day 1 of lactation. Treatment continued for 14 and 21 days, at the end of which, dams and pups were sacrificed. The oil was able to significantly increase (P<0.01) the acid soluble sulfhydryl content in the liver of dams receiving the oil as well as in the liver of their F 1 progeny. Hepatic glutathione S-transferase, glutathione reductase and glutathione peroxidase activities were significantly enhanced (P<0.01) in the F 1 progeny of dams who received 5 ul sandalwood oil/day for 21 days and those who received 10 ul sandalwood oil/day for 14 and 21 days. Cytochrome P-450 content decreased (P<0.05) in liver of the dam on the higher dose of oil for 21 days and her pups. Hepatic cytochrome b 5 content increased (P<0.01) in all the groups. The observed changes in hepatic enzyme levels suggest that sandalwood oil its constituents or its metabolites pass via mother's milk and modify the hepatic detoxifying machinery.

Brain phospholipids as dietary source of (n-3) polyunsaturated fatty acids for nervous tissue in the rat.

In a previous work, we calculated the dietary alpha-linolenic requirements (from vegetable oil triglycerides) for obtaining and maintaining a physiological level of (n-3) fatty acids in developing animal membranes as determined by the cervonic acid content [22:6(n-3), docosahexaenoic acid]. The aim of the present study was to measure the phospholipid requirement, as these compounds directly provide the very long polyunsaturated fatty acids found in membranes. Two weeks before mating, eight groups of female rats (previously fed peanut oil deficient in alpha-linolenic acid) were fed different semisynthetic diets containing 6% African peanut oil supplemented with different quantities of phospholipids obtained from bovine brain lipid extract, so as to add (n-3) polyunsaturated fatty acids to the diet. An additional group was fed peanut oil with rapeseed oil, and served as control. Pups were fed the same diet as their respective mothers, and were killed at weaning. Forebrain, sciatic nerve, retina, nerve endings, myelin, and liver were analyzed. We conclude that during the combined maternal and perinatal period, the (n-3) fatty acid requirement for adequate deposition of (n-3) polyunsaturated fatty acids in the nervous tissue (and in liver) of pups is lower if animals are fed (n-3) very long chain polyunsaturated fatty acids found in brain phospholipids [this study, approximately 60 mg of (n-3) fatty acids/100 g of diet, i.e., approximately 130 mg/1,000 kcal] rather than alpha-linolenic acid from vegetable oil triglycerides [200 mg of (n-3) fatty acids/100 g of diet, i.e., approximately 440 mg/1,000 kcal].

Excretion of food-derived heterocyclic amine carcinogens into breast milk of lactating rats and formation of DNA adducts in the newborn.

The distribution, DNA adduction and excretion into breast milk of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were examined in lactating female F344 rats with 5 day old pups. Six hours after a single dose (10 mg/kg, p.o.) of radiolabeled IQ, MeIQx or PhIP to lactating dams, radioactivity in the dams was highest in the liver and kidney followed, in descending order, by the mammary gland, omental fat and brain. By 24 h after carcinogen administration, all tissues of the dams showed significantly reduced levels of radioactivity except for omental fat which changed only marginally from 6 to 24 h. 32P-Postlabeling analysis showed that the level of DNA adducts in mammary gland 6 h after dosing was 2.2, 0.7 and 0.2 adducts/10(7) nucleotides for PhIP, IQ and MeIQx respectively. In contrast, in hepatic DNA, the levels of IQ-DNA adducts (5.5 adducts/10(7) nucleotides) were 11-fold higher than those of PhIP or MeIQx. The stomach contents, liver, kidney and urine of pups nursed by dams given radiolabeled IQ, MeIQx or PhIP were radioactive, indicating that these carcinogens (and/or metabolites) were excreted into breast milk and absorbed by the pups. After a 6 h suckling period, the amount of PhIP-derived radioactivity in the stomach contents of the pups was approximately 10-fold higher than that seen with IQ or MeIQx. Urine from pups from the three groups was mutagenic in the Ames assay with Salmonella TA98 in the presence of an S9 activating system. IQ-, MeIQx- and PhIP-DNA adducts, at levels in the range of 0.25-0.46 adducts per 10(8) nucleotides, were detected in the livers of pups using the 32P-postlabeling method under intensification conditions. The results from this study indicate that breast milk is a route of exposure of the newborn to heterocyclic amines. The presence of DNA adducts in the tissues of pups further suggests that this route of exposure may have a carcinogenic consequence to the newborn.

Lipoprotein lipase in developing rat tissues: differences between Wistar and Sprague-Dawley rats.

Lipoprotein lipase in animal tissues is known to be affected by fasting, but contradictory results have been published concerning this effect in particular tissues. For example, we reported that lipoprotein lipase activity expressed in the liver of neonatal rats was either increased or not affected by fasting. To evaluate the influence of the rat strain used as experimental animal model, we studied differences between Wistar and Sprague-Dawley rats in the development and in the effect of fasting on lipoprotein lipase and hepatic lipase activities in tissues of neonatal rats. Beside some minor differences in the development of lipoprotein lipase in some tissues like brown adipose tissue and lungs, we found quite remarkable differences between both strains in the development of lipoprotein lipase and hepatic lipase activities in the liver. In 1-day-old neonates, differences between both strains were also observed in the effect of fasting on lipoprotein lipase activity both in liver and lungs. In the liver of Wistar pups lipoprotein lipase activity was increased by fasting by 350%, but only by 50% in the liver of Sprague-Dawley pups. In contrast, in the lungs of Wistar pups lipoprotein lipase activity was increased by fasting by 280%, but by 580% in lungs of Sprague-Dawley rats. Therefore, our results indicate that quantitative differences exist between Wistar and Sprague-Dawley rats in the regulation of lipoprotein lipase.