Equally rapid activation of lipogenesis in nibbling and gorging mice

Minimal average rates of exogenous glucose-C-conversion to whole body, total lipid fatty acids were measured in nibbling and gorging mice. Gorgers trained to eat 1 meal/day (8-10 am) were fasted 22-24 hr and given [14C]glucose with pure glucose, 30% glucose in water, or a 58% glucose, fat-free diet. Conversion of glucose-C to total lipid fatty acids increased from 0.6 (fasted) to approximately 20 mug/min/20 g body weight during 40 min after glucose feeding using each test meal. Dietary amino acids were not required for activation of lipogenesis in gorgers. Exogenous glucose-C was incorporated into fatty acids as fast in nibbling mice as in gorgers. This was true after varying all of the following conditions: training period, number of meals gorged, previous fasting time, and diet composition. The total rate of fatty acid synthesis from body glucose-C during absorption of a glucose load was also estimated in absorption of a glucose load was also estimated in previously fasted nibbling and gorging mice. These estimates were based on composite, serial measurement of both plasma glucose specific activities and 14C-labeled fatty acids. The total rate of fatty acid synthesis from both exogenous and endogenous glucose-C was only 15% higher than the rate from exogenous glucose-C between 10 and 40 min. No significant differences between nibblers and gorgers were found.     

Fatty acyl desaturation in isolated hepatocytes from Atlantic salmon (Salmo salar): stimulation by dietary borage oil containing gamma-linolenic acid

The effects of different dietary oils on the fatty acid compositions of liver phospholipids and the desaturation and elongation or [1-14C]18:3n-3 and [1-14C]18:2n-6 were investigated in isolated hepatocytes from Atlantic salmon. Atlantic salmon smolts were fed diets containing either a standard fish oil (FO) as a control diet, a 1:1 blend of Southern Hemisphere marine oil and tuna orbital oil (MO/TO), sunflower oil (SO), borage oil (BO), or olive oil (OO) for 12 wk. The SO and BO diets significantly increased the percentages of 18:2n-6, 18:3n-6, 20:2n-6, 20:3n-6, and total n-6 polyunsaturated fatty acids (PUFA) in salmon liver lipids in comparison with the FO diet. The BO diet also increased the percentage of 20:4n-6. Both the SO and BO diets significantly reduced the percentages of all n-3 PUFA in comparison with the FO diet. The OO diet significantly increased the percentages of 18:1n-3, 18:2n-6, total monoenes, and total n-6 PUFA in liver lipids compared to the FO diet, and the percentages of all n-3 PUFA were significantly reduced. With [1-14C]18:3n-3, the recovery of radioactivity in the products of delta 6 desaturation was significantly greater in the hepatocytes from salmon fed SO, BO, and OO in comparison with the FO diet. The BO diet also increased the recovery of radioactivity in the products of delta 5 desaturation. Only the BO diet significantly affected the desaturation of [1-14C]18:2n-6, increasing recovery of radioactivity in both delta 6- and delta 5-desaturation products. In conclusion, dietary BO, enriched in gamma-linolenic acid (18:3n-6), significantly increased the proportions of both 20:3n-6 and 20:4n-6 in salmon liver phospholipids and also significantly increased the desaturation of both 18:2n-6 and 18:3n-3 in salmon hepatocytes. The possible relationships between dietary fatty acid composition, tissue phospholipid fatty acid composition, and desaturation/elongation activities are discussed.     

Lipoprotein lipase activity and its relationship to high milk fat transfer during lactation in grey seals

Lipoprotein lipase regulates the hydrolysis of circulating triglyceride and the uptake of fatty acids by most tissues, including the mammary gland and adipose tissue. Thus, lipoprotein lipase is critical for the uptake and secretion of the long-chain fatty acids in milk and for the assimilation of a high-fat milk diet by suckling young. In the lactating female, lipoprotein lipase appears to be regulated such that levels in adipose tissue are almost completely depressed while those in the mammary gland are high. Thus, circulating fatty acids are directed to the mammary gland for milk fat production. Phocid seals serve as excellent models in the study of lipoprotein lipase and fat transfer during lactation because mothers may fast completely while secreting large quantities of high fat milks and pups deposit large amounts of fat as blubber. We measured pup body composition and milk fat intake by isotope (deuterium oxide) dilution and plasma post-heparin lipoprotein lipase activity in six grey seal (Halichoerus grypus) mother-pup pairs at birth and again late in the 16-day lactation period. Maternal post-heparin lipoprotein lipase activity increased by an average of four-fold by late lactation (P = 0.027), which paralleled an increase in milk fat concentration (from 38 to 56%; P = 0.043). Increasing lipoprotein lipase activity was correlated with increasing milk fat output (1.3-2.1 kg fat per day) over lactation (P = 0.019). Maternal plasma triglyceride (during fasting) was inversely correlated to lipoprotein lipase activity (P = 0.027) and may be associated with the direct incorporation of long-chain fatty acids from blubber into milk. In pups, post-heparin lipoprotein lipase activity was already high at birth and increased as total body fat content (P = 0.028) and the ratio of body fat: protein increased (P = 0.036) during lactation. Although pup plasma triglyceride increased with increasing daily milk fat intake (P = 0.023), pups effectively cleared lipid from the circulation and deposited 70% of milk fat consumed throughout lactation. Lipoprotein lipase may play an important role in the mechanisms involved with the extraordinary rates of fat transfer in phocid seals.     

Depression of lipogenesis in swine adipose tissue by specific dietary fatty acids

The objective of this study was to document the influence of specific dietary fatty acids on rates of lipid synthesis and sensitivity to insulin in porcine adipose tissue. Weanling pigs were assigned to one of six groups, and each group was fed diets containing 10 g/100 g of added cornstarch or 10 g/100 g of added fatty acid. The fatty acid-enriched diets contained either a combination of 14:1 plus 16:1 (14:1/16:1 diet), 16:0, 18:0, 18:1, or 18:2 (n-6). With the exception of the cornstarch diet, all diets contained approximately 35% 14:0. Subcutaneous adipose tissue samples were collected at slaughter from the area overlying the first cranial vertebra. Fresh samples were incubated for 2 h in 20 mM glucose and 0, 10, 100 or 1,000 microU/mL of porcine insulin. The smallest adipocytes were observed in adipose tissue from pigs fed the 16:0 or 18:2 diets. Glucose incorporation into lipids was greater (P < .05) in adipose tissue from cornstarch-fed pigs than in adipose tissue from the other treatment groups. Lipogenesis was 67, 53, 35, 32, and 20% lower (P < .05) in adipose tissue from 16:0-, 14:1/16:1-, 18:0-, 18:2-, and 18:1-fed pigs, respectively, than in adipose tissue from the cornstarch-fed pigs. Insulin increased lipogenesis by 19% (P < .05) in adipose tissue from the cornstarch-fed pigs and by 15 to 40% (P < .05) in adipose tissue from the 14:1/16:1-fed pigs. Insulin did not stimulate lipogenesis (P > .4) in adipose tissue from pigs fed the 16:0, 18:0, or 18:1 diets. The data suggest that fatty acid chain length and unsaturation are determinants in the effects of dietary fat and insulin on de novo lipogenesis.     

Carry-over effects of dietary crude protein and triiodothyronine (T3) in broiler chickens

Indian River male broiler chickens growing from 7 to 30 d of age were fed on diets containing crude protein levels ranging from 120 to 300 g/kg plus 0 or 1 mg triiodothyronine (T3)/kg diet. The purpose of this study was to examine the effects of these treatments on lipogenesis after a common diet was fed (180 g crude protein/kg diet from 30 to 56 d of age). Dietary treatment groups were sampled at 30 and 56 d. In vitro lipogenesis was determined by incubating liver explants for 2 h at 37 degrees in Hanks' salts containing 25 mM-HEPES and 10 mM-[2-14C]acetate and then measuring acetate incorporation into total lipid. Growth and feed consumption from 7 to 30 d increased (P < 0.01) as dietary protein increased from 120 to 210 g/kg diet. Both measurements decreased as crude protein increased from 210 to 300 g/kg diet. T3 decreased (P < 0.01) growth and feed intake during this period. Low-protein (< 180 g/kg) diets increased (P < 0.05) and T3 decreased lipogenesis in 30-d-old chickens. Although birds given T3 from 7 to 30 d grew at the greatest rate from 30 to 56 d of age, the final body weight was still less than controls. In vitro lipogenesis at 56 d of age was not affected by either of the two dietary treatments. In contrast, the relative size of the abdominal fat pad (g/kg body weight) at 56 d was decreased by feeding T3 from 7 to 30 d. Any changes in metabolism elicited by either dietary protein levels or hormone treatments may be specific to the particular dosing interval and are not sustained when a common diet is fed during a repletion period.     

The influence of gastric juice acidity on the occurrence of esophageal reflux]

Protective properties of n-3 and n-6 polyunsaturated, monosaturated and saturated fatty acids (respectively, n-3 PUFA, n-6 PUFA, MUFA and SFA) against ethanol induced hemorrhagic gastric mucosal lesions were compared. Female Wistar rats (90-100 g) were fed to four weeks semisyntethic diets containing 9% butter (SFA-diet), 6% butter and 3% olive oil (MUFA-diet), 6% butter and 3% sunflower oil (n-6 PUFA-diet) or 6% butter and 3% concentrate of n-3 PUFA ethyl esters (n-3 PUFA-diet). One group of rats received a non-lipid diet. Under all types of lipid containing diets, development of ethanol-induced hemorrhagic gastric mucosal lesions was reduced in compared with non-lipid diet. Cytoprotective effect of n-3 PUFA-E was greater than MUFA and SFA, but smaller than n-6 PUFA.     

Our experience with caustic substance ingestion in children

Several formulas for preterm infants contain medium-chain triglycerides (MCT) to enhance fat absorption. Although fat absorption with MCT was slightly higher in several studies in preterm infants, a beneficial effect on growth has only been reported in one publication. We hypothesized that when part of the fat blend of preterm formula is substituted by MCT oil, this might lead to a different metabolic pattern in which, due to the preferential oxidation of MCT, an increase in lipogenesis from glucose could lead to an increase in metabolic rate. To study the impact of MCT on glucose metabolism, 18 preterm infants were randomized to receive either an MCT or an LCT formula containing 38- and 6%-by-weight medium-chain fatty acids, respectively, in their fat blend. At 4 wk of age, the metabolic rate, substrate utilization, glucose kinetics, and oxidation were measured by indirect respiratory calorimetry in combination with a constant-rate oral infusion of [U-13C]glucose. The "true" rate of appearance of glucose (Ra "true") was measured from the dilution of the uniformly labeled (m + 6) species of infused tracer, whereas "apparent" rate of appearance of glucose (Ra "apparent") was measured from the dilution of infused tracer C (carbon). The latter was measured by an on-line combustion method using a gas chromatograph-isotope ratio mass spectrometer. At a carbohydrate intake of 8.4 mg.kg-1.min-1, total utilization of carbohydrate was equal in both groups at 7.6 mg.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Significance of lipid consumption during lactation

Human milk lipids are the main source of energy to support optimum growth of the breast-fed infant. The content and composition of milk lipids come from three main sources of fatty acids: the diet, mobilization of body fat stores and fatty acid synthesis de novo by the mammary gland. On account of these, the consumption and composition of the lipids from the diet and also the nutritional state, specifically the body fat percentage of the lactating woman, are elements that maintain a close relation with the content and composition of milk lipids which translates into the energy content given to the baby. The evidence suggests that the body fat stores significantly provide the demand imposed by lactation, and under suboptimal nutritional conditions where body fat stores are depleted, dietary lipid consumption is essential. It is necessary to elucidate the physiological regulatory mechanisms involved in the utilization of dietary lipids on milk synthesis. This information will be of great practical value, since it may allow the development of optimum diets for lactating women.     

Abdominal hysterectomy practice patterns in the United States

Diets rich in polyunsaturated fatty acids (PUFA) are well known to suppress hepatic lipogenic enzymes compared to fat-free diets or diets rich in saturated fatty acids. However, the mechanism underlying suppression of lipogenic enzymes is not quite clear. The present study was undertaken to investigate whether lipid peroxidation products are involved in suppression of lipogenic enzymes. Therefore, an experiment with growing male rats assigned to six groups over a period of 40 d was carried out. Rats received semisynthetic diets containing 9.5% coconut oil and 0.5% fresh soybean oil (coconut oil diet, peroxide value 5.1 meq O2/kg oil), 10% fresh soybean oil (fresh soybean oil diet, peroxide value 9.5 meq O2/kg oil), or 10% thermally treated soybean oil (oxidized soybean oil diet, peroxide value 74 meq O2/kg oil). To modify the antioxidant state of the rats, we varied the vitamin E supply (11 and 511 mg alpha-tocopherol equivalents per kg of diet) according to a bi-factorial design. Food intake and body weight gain were not influenced by dietary fat and vitamin E supply. Activities of hepatic lipogenic enzymes were markedly influenced by the dietary fat. Feeding either fresh or oxidized soybean oil diets markedly reduced activities of fatty acid synthase, (FAS), acetyl CoA-carboxylase, (AcCX), glucose-6-phosphate dehydrogenase, (G6PDH), 6-phosphogluconate dehydrogenase, and ATP citrate lyase (ACL) relative to feeding the coconut oil diet. Moreover, feeding oxidized soybean oil slightly, but significantly, lowered activities of FAS, AcCX, and ACL compared to feeding fresh soybean oil. Activities of hepatic lipogenic enzymes were reflected by concentrations of triglycerides in liver and plasma. Rats fed the coconut oil diet had markedly higher triglyceride concentrations in liver and plasma than rats consuming fresh or oxidized soybean oil diets, and rats fed oxidized soybean oil had lower concentrations than rats fed fresh soybean oil. The vitamin E supply of the rats markedly influenced concentrations of thiobarbituric acid-reactive substances in liver, but it did not influence activities of hepatic lipogenic enzymes. Because the vitamin E supply had no effect, and ingestion of an oxidized oil had only a minor effect, on activities of hepatic lipogenic enzymes, it is strongly suggested that neither exogenous nor endogenous lipid peroxidation products play a significant role in the suppression of hepatic lipogenic enzymes by diets rich in PUFA. Therefore, we assumed that dietary PUFA themselves are involved in regulation of hepatic lipogenic enzymes. Nevertheless, the study shows that ingestion of oxidized oils, regardless of the vitamin E supply, also affects hepatic lipogenesis, and hence influences triglyceride levels in liver and plasma.     

Effects of variations in the proportions of saturated, monounsaturated and polyunsaturated fatty acids in the rat diet on spleen lymphocyte functions

To obtain further information about the immunomodulatory effects of specific dietary fatty acids, weanling male rats were fed for 6 weeks on high-fat (178 g/kg) diets which differed according to the principal fatty acids present. The nine diets used differed in their contents of palmitic, oleic, linoleic and alpha-linolenic acids; as a result the total polyunsaturated fatty acid (PUFA) content and the PUFA:saturated fatty acid ratio varied (from 17.8 to 58.5 g/100 g fatty acids and from 0.28 to 5.56 respectively). The n-6 PUFA:n-3 PUFA ratio was kept constant in all diets at approximately 7.0. The fatty acid composition of the serum and of spleen lymphocytes were significantly influenced by that of the diet fed. The ex vivo proliferation of spleen lymphocytes decreased as the level of oleic acid in the diet increased. Spleen natural killer cell activity decreased as the oleic acid content of the diet increased and increased as the palmitic acid content of the diet increased. The extent of the effects of these fatty acids on lymphocyte functions was modified by the nature of the background fatty acid composition of the diet.     

Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16:0, oleate 18:1, or linoleate 18:2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18:2 addition to the basal diet did result in a significant (P less than 0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18:2 or linolenate 18:3 significantly (P less than 0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18:1 caused no depression in hepatic FAS activity but did result in a significant (P less than 0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18:2- or +18:3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18:3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18:2 and 18:3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis.     

Effects of medium-chain triglyceride ingestion on fuel metabolism and cycling performance

On three occasions separated by 10 days, six endurance-trained cyclists rode for 2 h at 60% of peak O2 uptake and then performed a simulated 40-km time trial (T-trial). During the rides, the subjects ingested a total of 2 liters of a [U-14C]glucose-labeled beverage containing a random order of either 10% glucose [carbohydrate (CHO)], 4.3% medium-chain triglycerides (MCTs); or 10% glucose + 4.3% MCTs (CHO+MCT). Although replacing CHO with MCTs slowed the T-trials from 66.8 +/- 0.4 (SE) to 72.1 +/- 0.6 min (P < 0.001), adding MCTs to CHO improved the T-trials from 66.8 +/- 0.4 to 65.1 +/- 0.5 min (P < 0.05). Faster T-trials in the CHO+MCT trial than in the CHO trial were associated with increased final circulating concentrations of free fatty acids (0.58 +/- 0.09 vs. 0.36 +/- 0.06 mmol/l; P < 0.05) and ketones (1.51 +/- 0.25 vs. 0.51 +/- 0.07 mmol/l; P < 0.01) and decreased final circulating concentrations of glucose (5.2 +/- 0.2 vs. 6.3 +/- 0.3 mmol/l; P < 0.01) and lactate (1.9 +/- 0.4 vs. 3.7 +/- 0.5 mmol/l; P < 0.05). Adding MCTs to ingested CHO reduced total CHO oxidation rates from 14 +/- 1 to 10 +/- 1 mmol/min at 2 h and from 17 +/- 1 to 14 +/- 1 mmol/min in the T-trial (P < 0.01), without affecting the corresponding approximately 5 and approximately 7 mmol/min rates of [14C]glucose oxidation. These data suggest that MCT oxidation decreased the direct and/or indirect (via lactate) oxidation of muscle glycogen. A reduced reliance on CHO oxidation at a given O2 uptake is similar to an endurance-training effect, and that may explain the improved T-trial performances.     

A comparison of the effects of feeding concentrate diets, based on either maize or barley, or dried grass on adipose tissue lipogenesis in sheep

1. Three groups of 4 sheep were penned individually and provided with diets composed of either dried grass, 80% ground maize/20% soyabean meal or 80% ground barley/20% soyabean meal. 2. The diets were fed ad libitum for 3 weeks before s.c. adipose tissue biopsy samples were taken from the rump region. 3. Although the rate of lipogenesis was significantly increased by concentrate feeding the order of utilization of the various substrates was always acetate greater than glucose greater than lactate. Throughout this work lactate was always of minor significance as a lipogenic substrate. 4. The diet-induced differences in lipogenesis were reflected in significant increases in the specific activities of the fatty acid synthetase system, glucose-6-phosphate dehydrogenase and phosphogluconate dehydrogenase in concentrate fed animals. 5. No differences were observed in in vitro lipogenesis from any of the substrates or enzyme specific activity between the 80% barley diet and the 80% maize diet. 6. These results are discussed in relation to the effect of concentrate and roughage feeding on the entry of alpha-linked glucose polymer into the small intestine of sheep.     

Lipid-depleted diet perturbs membrane composition and intracellular transport in lactating mammary cells

When rats were fed a control or a lipid-depleted diet for five generations, reproduction was not disturbed but pup growth was affected. The membrane organization and the secretory activity of mammary epithelial cells from these lactating rats were investigated. This diet induced a large decrease in the level of polyunsaturated fatty acids of membrane phospholipids (26.6% versus 44.0%). The level of 20:4 (n-6) was strongly decreased, mainly in phosphatidylethanolamine. Annexin VI, which interacts preferentially with this phospholipid, accumulated at the periphery of the cell and was largely associated to the hydrophobic region of the bilayer as compared to control membranes. Casein synthesis and casein secretion measured in incubated explants, after pulse-chase metabolic labeling, were both reduced by about 60% in lipid-deprived cells. The secretory ratio (radioactive secreted caseins in %) was not modified, suggesting that the mechanism of basal secretion was not mainly affected. On the contrary, the secretagogue effect of prolactin disappeared. The intracellular transport of the hormone was considerably slowed down by the diet and prolactin did not reach the lumen of the acini after 1 h of chase, in contrast to what occurred in control cells. Addition of 20:4 (n-6), in vitro, to mammary fragments from lipid-deprived rats restored the localization of annexin VI, increased synthesis and secretion of caseins as well as intracellular transport of PRI. Together, these data underline the importance of the level of 20:4 (n-6) in membrane phospholipids for exocytic and endocytic transport in lactating mammary epithelial cells.     

Postprandial effects of an oleic acid-rich oil compared with butter on clotting factor VII and fibrinolysis in healthy men

BACKGROUND: Factor VII coagulant activity (FVII:c) is associated with an increased risk of fatal ischemic heart disease, is correlated with plasma triacylglycerol concentration, and increases after a meal rich in long-chain fatty acids. OBJECTIVE: We planned to compare effects of meals rich in oleate and butter fat with those of a low-fat meal on FVII:c and fibrinolytic activity. DESIGN: A crossover design was used to compare the postprandial effects on coagulant and fibrinolytic activities in 12 men of 3 high-fat (95 g) meals--high oleate, butter, and oleate + medium-chain triacylglycerols (oleate+MCT)--with an isoenergetic low-fat meal (18 g MCT). The oleate+MCT blend was used to mimic the ratio of long-chain to shorter-chain fatty acids in butter. RESULTS: Neither the amount nor type of fat consumed influenced plasminogen activator inhibitor 1 or t-plasminogen activator activities or D-dimer concentration. FVII:c increased by 12.5% (95% CI: 4.6%, 20.5%) after the high-fat meals at 3 h and by 6.7% (95% CI: 1.6%, 11.7%) at 7 h and changed 7 h after the low-fat meal by -14.3% (95% CI: -3.3%, -25.4%). The responses to the high-fat meals did not differ. Measurements of activated FVII (FVIIa), FVII zymogen, and activated FXII (FXIIa) concentrations made after the low-fat and high-oleate meals showed a significant increase in FVIIa only after the high-oleate meal. CONCLUSIONS: The results of this study confirm that FVII:c falls after a low-fat meal and suggests that postprandial activation of FVII occurs rapidly after a fat-rich meal without involving an increase in FXIIa.     

Proliferation, development and DNA adduct levels in the mammary gland of rats given 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine and a high fat diet

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a heterocyclic amine derived from cooked meat that is a mammary gland carcinogen in rats. A carcinogenic dose-regimen of PhIP (75 mg/kg, p.o., 10 doses, once per day) was administered to 43-day old female Sprague-Dawley rats, and the rats were then placed on a defined high fat (23.5% corn oil) or low fat (5% corn oil) diet for up to 6 weeks. At various times after carcinogen and diet, and prior to carcinogenesis, we examined the percentage of proliferating cells in terminal end bud (TEB) epithelial structures of the rat mammary gland by proliferating cell nuclear antigen staining, mammary gland architecture by whole mounting, and PhIP-DNA adduct levels in mammary epithelial cells by the 32P-post-labeling assay. Immediately after dosing, the percentage of proliferating epithelial cells in TEBs was significantly higher in PhIP-treated rats than in control rats receiving vehicle only [7.5 +/- 0.9% (n = 99) versus 4.2 +/- 0.6% (n = 127), respectively]. The mammary glands of PhIP-treated rats showed a significantly lower density of alveolar buds (ABs) and a higher density of TEBs than control rats, which suggests that PhIP exposure partially inhibited the normal glandular differentiation of TEBs to ABs. After 6 weeks on the diet, proliferation in TEBs was statistically higher in rats given PhIP plus a high fat diet than in rats given vehicle plus a low fat diet. The mammary glands from rats on a high fat diet also showed a statistically higher density of TEBs when compared with rats on a low fat diet [2.08 +/- 0.34% versus 1.04 +/- 0.20%, respectively (n = 6)]. PhIP-DNA adduct levels were relatively high in mammary epithelial cells of treated rats. At 3 h after the last dose of PhIP, DNA adduct levels [relative adduct labeling (RAL) x 10(7), mean +/- SE] were 10.5 +/- 1.7 (n = 8) and 0.9 +/- 0.2 (n = 7) in epithelial cells isolated from mammary gland and in the liver, respectively. DNA adduct removal rates from the mammary gland were not different between rats on the high fat and low fat diets. Adducts were still detected after 6 weeks on either diet. Thus, events that occurred prior to neoplasia in the mammary glands of PhIP-treated rats include formation of PhIP-DNA adducts at relatively high levels, and enhanced proliferation in TEBs (putative sites of origin of mammary gland carcinomas) and partial inhibition of TEB differentiation. The high fat diet, a promoter of PhIP-induced mammary gland carcinogenesis, appeared to sustain the proliferative effect of PhIP in mammary gland TEBs at a time when PhIP-DNA adducts are still detectable. These early events may contribute to the targeting and carcinogenicity of PhIP to the mammary gland of rats.     

Nutritional aspects of hydrogenated and regular soybean oil added to diets of broiler chickens

The objective of the present study was to evaluate the effect of degree of saturation of fat incorporated into broiler diets on performance and body fatty acid (FA) profile. The various degrees of saturation were achieved by using regular soybean oil (SO) and hydrogenated soybean oil (HSO), mixed at different proportions. The work was carried out on commercial broilers (Experiment 1) and on lines of chickens divergently selected for high (HF) or low (LF) abdominal fat (Experiment 2). Daily BW gain and gain:feed ratio increased and the amount of feed intake decreased as the dietary fat saturation decreased. Digestibility of total fat and of each of the FA was lowest in the HSO group and reached maximal values when 23% or more of the added oil was SO. The AMEn values of the diets were almost parallel to fat digestibility. The performance of the HF and LF chickens was affected by the degree of saturation similarly to that observed for the commercial stock. The degree of dietary fat saturation had very little effect on saturated FA (C16:0 and C18:0) in body lipids, reduced the level of monoenoic FA (C16:1 and C18:1), and raised that of polyunsaturated FA (PUFA) (C18:2, C18:3, and C20:4). Monoenoic FA were higher, whereas PUFA were lower in the HF than in the LF line. The improved AMEn in diets containing unsaturated fat is probably due to higher fat digestibility, direct deposition of PUFA in body lipids, and lower lipogenesis, associated with lower heat production.     

Uptake and metabolism of tryptophan by the isolated perfused guinea-pig mammary gland

Tryptophan uptake by the isolated perfused lactating guinea-pig mammary gland was 46.5+/-4.6 mug/h per g. Results of absorption studies and the use of [methylene-14C]tryptophan suggest that tryptophan is one of the group of amino acids that are transferred almost quantitatively from blood plasma to milk protein.