Effect of pasteurization on selected immune components of donated human breast milk.

OBJECTIVE: Pasteurized, donated milk is increasingly provided to preterm infants in the absence of mother's own milk. The aim of this study was to determine the effect of pasteurization on the concentration of selected components in donated human breast milk. STUDY DESIGN: Donated milk from 34 mothers was pooled into 17 distinct batches (4 mothers per batch). Aliquots of each batch were then Holder pasteurized (62.5 °C for 30 min). Interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), IL-2, IL-4, IL-5, IL-8, IL-10, IL-12p70 and IL-13 were measured in a multiplex enzyme-linked immunosorbent assay (ELISA). Granulocyte colony-stimulating factor (G-CSF), heparin-binding epidermal-like growth factor (HB-EGF) and hepatocyte growth factor (HGF) were measured by ELISA. Lipids were assessed by gas chromatography and gangliosides by the resorcinol-HCl reaction. RESULT: IFN-γ, TNF-α, IL-1ß, IL-10 and HGF were significantly reduced by pasteurization (P<0.05). Gangliosides were not affected, but the proportion of medium-chain saturated fats was increased (P<0.05) with a trend towards a decreased proportion of oleic acid (P=0.057). CONCLUSION: Pasteurization significantly reduced the concentration of several immunoactive compounds present in breast milk, but did not have an impact on others.

Loss of adipose tissue and plasma phospholipids: relationship to survival in advanced cancer patients.

BACKGROUND & AIMS: Extensive loss of adipose tissue is a key feature of cancer cachexia. Advanced cancer patients also exhibit low plasma phospholipids. It is not known whether these processes coincide across the cancer trajectory nor has their relationship with survival been defined. Changes in adipose tissue mass and plasma phospholipids were characterized within 500days prior to death and prognostic significance assessed. METHODS: Adipose tissue rate of change was determined in a retrospective cohort of patients who died of colorectal and lung cancers (n=108) and who underwent >2 computed tomography scans in the last 500days of life. Plasma phospholipid fatty acids were measured prospectively in a similar cohort of patients with metastatic cancer (n=72). RESULTS: Accelerated loss of adipose tissue begins at 7months from death reaching an average loss of 29% of total AT 2months from death. Plasma phospholipid fatty acids were 35% lower in patients closest to death versus those surviving >8months. Losses of phospholipid fatty acids and adipose tissue occur in tandem and are predictive of survival. CONCLUSIONS: Depletion of plasma phospholipids likely indicates a deficit of essential fatty acids in the periphery which may contribute to loss of adipose tissue.

Ganglioside composition of differentiated Caco-2 cells resembles human colostrum and neonatal rat intestine.

Gangliosides are glycosphingolipids found in cell membranes and human milk with important roles in cell proliferation, differentiation, growth, adhesion, migration, signalling and apoptosis. Similar changes in ganglioside composition occur during embryonic development, lactation and cancer cell differentiation. It is not known, however, whether ganglioside compositional changes that occur in differentiating colon cancer cells reflect changes that occur during intestinal development. The Caco-2 cell line is commonly used to study physiological and pathophysiological processes in the small intestine and colon. Therefore, to examine this question, undifferentiated and differentiated Caco-2 cells were grown and total lipid was extracted from cell supernatant fractions using the Folch method. The upper aqueous phase containing gangliosides was collected and purified. Total gangliosides were measured as ganglioside-bound N-acetyl neuraminic acid, while individual ganglioside content was quantified via a colorimetric assay for sialic acid and scanning densitometry. The total ganglioside content of differentiated Caco-2 cells was 2.5 times higher compared with undifferentiated cells. Differentiated Caco-2 cells had significantly more (N-acetylneuraminyl) 2-galactosylglucosyl ceramide (GD3) and polar gangliosides, and a lower N-acetylneuraminylgalactosylglucosylceramide (GM3):GD3 ratio than undifferentiated cells. The present study demonstrates that the total ganglioside content and individual ganglioside composition of differentiated Caco-2 cells are similar to those of human colostrum and neonatal rat intestine. Differentiated Caco-2 cells may therefore be an alternative model for studying physiological and pathological processes in the small intestine and colon, and may help to elucidate possible functions for specific gangliosides in development and differentiation. Further research using more sensitive techniques of ganglioside analysis is needed to confirm these findings.

Reduced growth and integrin expression of prostate cells cultured with lycopene, vitamin E and fish oil in vitro.

Integrins are transmembrane proteins that facilitate the interaction of cells with the extracellular environment. They have also been implicated in cancer progression. The effects of nutrients thought to be involved in the prevention of prostate cancer on integrin expression have not been determined. Prostate cancer cell lines representing a range of malignancy from normal (RWPE-1) to highly invasive phenotypes (22Rv1 < LNCaP < PC-3) were cultured with or without lycopene (10 nM), vitamin E (5 microm) or fish oil (100 microm) for 48 h. Growth and integrin (alpha2beta1, alphavbeta3 and alphavbeta5) expression were assessed using Trypan Blue exclusion and monoclonal antibodies combined with flow cytometry. Vitamin E enhanced (P < 0.001) whereas fish oil reduced the growth of all the cell lines tested (P < 0.001). Lycopene had no effect on growth. All the malignant cell lines exhibited lower expression of alpha2beta1 with the addition of lycopene to culture media. Supplemental fish oil reduced alpha2beta1 in most invasive cell lines (LNCaP and PC-3). Each nutrient at physiological levels reduced integrins alphavbeta3 and alphavbeta5 in most invasive cell lines (PC-3). The results suggest that integrins may represent an additional target of bioactive nutrients and that the effects of nutrients may be dependent on the type of cell line used.

Long-chain polyunsaturated fat supplementation in children with low docosahexaenoic acid intakes alters immune phenotypes compared with placebo.

OBJECTIVES: The objectives of this study were to assess the effects of long-term supplementation with arachidonic acid (AA; 20:4n-6) and docosahexaenoic acid (DHA; 22:6n-3) on cell phenotypes and cytokine production in children. PATIENTS AND METHODS: This randomized, double-blind, placebo-controlled trial provided children, (ages 5-7 years; n = 37) who had low intakes of DHA, with a dietary supplement containing AA (20-30 mg daily) and DHA (14-21 mg daily) or a placebo supplement for 7 months. After the supplementation period, a series of stimulants (pokeweed mitogen, phytohemagluttinin, lipopolysaccharide, beta-lactoglobulin, and ibuprofen) was used to stimulate peripheral blood mononuclear cells ex vivo. Antigen expression on T cells (CD25 and CD80), B cells, and macrophages (CD54), as well as cytokine production (interleukin [IL]-4, IL-10, tumor necrosis factor, IL-2, IL-6, and interferon-gamma), were measured using flow cytometry, monoclonal antibodies, and cytometric bead array, respectively. RESULTS: Mononuclear cells from children provided long-chain polyunsaturated fatty acids (LCPUFAs) had fewer CD8+ cells expressing CD25 and CD80 compared with placebo after exposure to each mitogen. The LCPUFA group also exhibited lower proportions of CD14+ cells after stimulation with beta-lactoglobulin and ibuprofen. The proportion of CD54+ cells was 2-fold higher for the LCPUFA group compared with placebo after exposure to ibuprofen and beta-lactoglobulin (P < 0.05). Each of these immune effects related to the amount of AA and/or DHA in the plasma and erythrocyte phospholipids. CONCLUSIONS: Alterations in cell phenotypes were evident when children were supplemented with AA and DHA. The results of this study have important implications for immune development and sensitivity to antigens in children.

Fatty acids in blood and intestine following docosahexaenoic acid supplementation in adults with cystic fibrosis.

UNLABELLED: The objective of this study was to investigate the effect of docosahexaenoic acid (DHA) supplementation on blood and intestinal DHA levels and lung function in mild/moderately affected adult CF patients with the DeltaF508 genotype. BACKGROUND: Cystic Fibrosis (CF) patients often present with plasma fatty acid levels indicating low levels of linoleic (18:2n-6) and docosahexaenoic (22:6n-3) acids and an increased level of arachidonic acid (20:4n-6). Improved dietary fat intake or reducing fat malabsorption with pancreatic enzymes has failed to normalize this biochemical deficiency of DHA. METHODS: Five CF patients, aged 18-43, received 70 mg of DHA/kg body weight/d for six weeks. At baseline and at six weeks a physical exam, lung function, 3-day dietary intake, duodenal mucosal biopsy and blood sample were assessed. The blood was analyzed for plasma vitamin A, D and E levels, liver function tests, clinical chemistry (CBC, differential and electrolytes). Plasma and red blood cell fatty acid levels were also analyzed. At three weeks, assessment included a physical exam, lung function test and fasting blood sample (vitamin levels, liver function and clinical chemistry only). RESULTS: Pre- and post-measurements were compared for the four subjects who completed the study. An increase in DHA content (% w/w) was observed in all phospholipid fractions of plasma, red blood cell and mucosal samples. No significant differences in vitamin levels, liver function or lung function were observed. CONCLUSIONS: The study proves the concept that an increase in tissue DHA levels in CF patients can be achieved by supplementing for six weeks with 70 mg/kg/d DHA.

Dietary lipids containing gangliosides reduce Giardia muris infection in vivo and survival of Giardia lamblia trophozoites in vitro.

We examined whether a ganglioside supplemented diet affected the course of Giardia muris infection in mice and survival of Giardia lamblia trophozoites in vitro. Female CD-1 mice were fed 1 of 5 experimental diets: standard lab chow as a control diet; semi-synthetic diets containing 20% (w/w) triglyceride based on the fat composition of a conventional infant formula; triglyceride diet; triglyceride diet containing a low level of ganglioside (0.1% w/w); and triglyceride diet containing a high level of ganglioside (1.0% w/w of diet). After 2 weeks of feeding, mice were inoculated with G. muris by gastric intubation and fed the experimental diets during the course of the infection. Cysts released in the faeces and trophozoites present in the small intestine were enumerated at various times post-infection. The average cyst output and the number of trophozoites during the course of the infection in mice fed ganglioside-containing diet were found to be significantly lower (3-log10 reduction) compared to animals fed control diets. The results of in vitro growth studies indicated that gangliosides may be directly toxic to the parasites. Thus, gangliosides have a protective effect against G. muris infection in vivo and affect the survival of G. lamblia trophozoites in vitro.

Adaptation following intestinal resection: mechanisms and signals.

The intestine has an inherent ability to adapt morphologically and functionally in response to internal and external environmental changes. The functional adaptations encompass modifications of the brush border membrane fluidity and permeability, as well as up- or down-regulation of carrier-mediated transport. Intestinal adaptation improves the nutritional status following the loss of a major portion of the small intestine, following chronic ingestion of ethanol, following sublethal doses of abdominal irradiation, in diabetes, in pregnancy and lactation, with ageing, and with fasting and malnutrition. Following intestinal resection, morphological and functional changes occur depending upon the extent of the intestine removed, the site studied, and the lipid content of the diet. Therefore, intestinal adaptation has important implications in the survival potential and welfare of the host. An understanding of the mechanisms of, and signals for, intestinal adaptation in the experimental setting forms the basis for the use of management strategies in humans with the short-bowel syndrome.

Feeding a polyunsaturated fatty acid diet prevents the age-associated decline in glucose uptake observed in rats fed a saturated diet.

The ability of the intestine to adapt to changes in environmental stimuli may be compromised with aging. Young animals fed saturated fatty acids (SFA) versus polyunsaturated fatty acids (PUFA) have an increased intestinal uptake of glucose. The objectives of this study were to determine (1) the effects of age on glucose uptake in rats; (2) the influence of feeding SFA versus PUFA; and (3) the mechanisms of these age- and diet-associated changes. Male Fischer 344 rats aged 1, 9 and 24 months received semi-purified isocaloric diets enriched with either SFA or PUFA. The uptake of 14C-labelled D-glucose was determined in vitro using the intestinal sheet method. Northern blotting, Western blotting and immunohistochemistry were used to determine the effects of age and diet on SGLT1, GLUT2 and Na(+)K(+)-ATPase. The mucosal surface area of the jejunum was reduced in 9 and 24 as compared with 1-month-old rats fed SFA. PUFA delayed this age-associated reduction in surface area. In SFA, the ileal uptake of glucose fell with age when expressed on the basis of intestinal or mucosal weight. Feeding PUFA prevented this decline. Alterations in glucose uptake were not paralleled by the changes in SGLT1, GLUT2 or Na(+)K(+)-ATPase abundance.

The locally acting glucocorticosteroid budesonide enhances intestinal sugar uptake following intestinal resection in rats.

BACKGROUND AND AIMS: Locally and systemically acting corticosteroids alter the morphology and transport function of the intestine. This study was undertaken to assess the effect of budesonide, prednisone, and dexamethasone on sugar uptake. METHODS: Adult male Sprague Dawley rats underwent transection or resection of 50% of the middle portion of the small intestine, and in vitro uptake of sugars was measured. RESULTS: The 50% enterectomy did not alter jejunal or ileal uptake of glucose or fructose. Prednisone had no effect on the uptake of glucose or fructose in resected animals. In contrast, in resected rats budesonide increased by over 120% the value of the jejunal maximal transport rate for the uptake of glucose, and increased by over 150% ileal uptake of fructose. Protein abundance and mRNA expression of the sodium dependent glucose transporter in brush border membrane (SGLT1), sodium independent fructose transporter in the brush border membrane (GLUT5), sodium independent glucose and fructose transporter in the basolateral and brush border membranes (GLUT2), and Na(+)/K(+) ATPase alpha1 and beta1 did not explain the enhancing effect of budesonide on glucose or fructose uptake. Budesonide, prednisone, and dexamethasone reduced jejunal expression of the early response gene c-jun. In resected animals, expression of the mRNA of ornithine decarboxylase (ODC) in the jejunum was reduced, and corticosteroids reduced jejunal expression of the mRNA of proglucagon. CONCLUSIONS: These data suggest that the influence of corticosteroids on sugar uptake in resected animals may be achieved by post translational processes involving signalling with c-jun, ODC, and proglucagon, or other as yet unknown signals. It remains to be determined whether budesonide may be useful to stimulate the absorption of sugars following intestinal resection in humans.

Plasma and neutrophil fatty acid composition in advanced cancer patients and response to fish oil supplementation.

Metabolic demand and altered supply of essential nutrients is poorly characterised in patients with advanced cancer. A possible imbalance or deficiency of essential fatty acids is suggested by reported beneficial effects of fish oil supplementation. To assess fatty acid status (composition of plasma and neutrophil phospholipids) in advanced cancer patients before and after 14 days of supplementation (12+/-1 g day(-1)) with fish (eicosapentaenoic acid, and docosahexaenoic acid) or placebo (olive) oil. Blood was drawn from cancer patients experiencing weight loss of >5% body weight (n=23). Fatty acid composition of plasma phospholipids and the major phospholipid classes of isolated neutrophils were determined using gas liquid chromatography. At baseline, patients with advanced cancer exhibited low levels (<30% of normal values) of plasma phospholipids and constituent fatty acids and elevated 20 : 4 n-6 content in neutrophil phospholipids. High n-6/n-3 fatty acid ratios in neutrophil and plasma phospholipids were inversely related to body mass index. Fish oil supplementation raised eicosapentaenoic acid and docosahexaenoic acid content in plasma but not neutrophil phospholipids. 20 : 4 n-6 content was reduced in neutrophil PI following supplementation with fish oil. Change in body weight during the supplementation period related directly to increases in eicosapentaenoic acid in plasma. Advanced cancer patients have alterations in lipid metabolism potentially due to nutritional status and/or chemotherapy. Potential obstacles in fatty acid utilisation must be addressed in future trials aiming to improve outcomes using nutritional intervention with fish oils.

Intestinal resection- and steroid-associated alterations in gene expression were not accompanied by changes in lipid uptake.

BACKGROUND/AIMS: Glucocorticosteroids alter the morphology and transport function of the intestine of adult rats. This study was undertaken to assess the possible effect on intestinal lipid uptake of the locally acting steroid budesonide, or the systemically active prednisone or dexamethasone. METHODS: Sprague-Dawley rats underwent intestinal transection or 50% intestinal resection. Budesonide, prednisone, dexamethasone, or control vehicle was given for 2 weeks from the time of surgery. Uptake was measured using ring uptake technique. RESULTS: Resection had no effect on the mRNA expression for the early response genes, for proglucagon, or for the ileal lipid binding protein (ILBP), but was associated with reduced jejunal ornithine decarboxylase (ODC) mRNA and with reduced jejunal mRNA for the liver fatty acid binding protein (L-FABP). All three steroids reduced jejunal mRNA for proglucagon and c-jun, and did not affect the mRNA for L-FABP or for ILBP. These resection- and steroid-associated changes in gene expression were not associated with alterations in the intestinal uptake of long chain fatty acids or cholesterol. CONCLUSIONS: The resection-associated alterations in the RNA expression of ODC and L-FABP and the steroid-associated changes in mRNA expression of c-jun and proglucagon were not accompanied by variations in lipid uptake.

Locally and systemically active glucocorticosteroids modify intestinal absorption of lipids in rats.

Orally administered systemically active steroids enhance the digestive and absorptive functions of the intestine, but their effect on lipid uptake is unknown. The effect of the locally acting steroid budesonide on intestinal absorptive function also is unknown. Accordingly, this study was undertaken to assess the influence of 4 wk of treatment of weaning male rats with a daily oral gavage of budesonide (BUD), prednisone (PRED), or control vehicle on the jejunal and ileal uptake of fatty acids and cholesterol. BUD enhanced jejunal uptake of oleic acid and ileal uptake of linoleic acid. PRED increased jejunal uptake of cholesterol and ileal uptake of lauric, palmitic, linoleic, and linolenic acids. Higher doses of BUD (up to 1 mg/kg) given to adult rats for 2 wk further increased the uptake of some lipids. The changes in the uptake of lipids were not due to variations in the weight of the intestinal mucosa or in the animals' food intake. Ileal ornithine decarboxylase mRNA expression was increased with PRED, but there were no steroid-associated changes in the expression of the mRNA of the early response genes c-myc, c-jun, or c-fos or of proglucagon, the liver fatty acid-binding protein (FABP), the ileal lipid-binding protein, tumor necrosis factor alpha, interleukin 2 (IL-2), IL-6, or IL-10. In summary, treatment of weanling rats with BUD and PRED enhances the uptake of some lipids by a process that is independent of the effects of early response genes and genes encoding cytokines, proglucagon, and FABP.

R3230AC rat mammary tumor and dietary long-chain (n-3) fatty acids change immune cell composition and function during mitogen activation.

Because anticancer immunity declines progressively with tumor growth, a major focus of current research in tumor immunology is the development of means to stimulate the host immune system. This study determined the effects of dietary long-chain (n-3) fatty acids and tumor burden on immune cell phospholipid composition and membrane-mediated immune defense in rats implanted with the R3230AC mammary adenocarcinoma. Fischer 344 rats (145 +/- 2 g) were fed one of two semipurified diets (20 g/100 g fat) for 21 d before and 17 d after tumor implantation. Diets provided long-chain (n-3) fatty acids at 0 or 50 g/kg of total fat. Mammary tumor growth was 31% lower (P = 0.1) in rats fed long-chain (n-3) fatty acids. Dietary long-chain (n-3) fatty acids had beneficial effects on several host immune defenses, including activation of CD8(+) T cells and type-1 cytokine (interferon-gamma and tumor necrosis factor-alpha) production (P < 0.05). Upregulated immune function in tumor-bearing rats fed the high (n-3) diet occurred concurrently with specific changes in the major membrane phospholipids phosphatidylcholine and phosphatidylethanolamine in high (n-3)-fed rats. Because membrane composition plays a critical role in immune function, additional work is needed to determine the relationship between alterations in the phospholipid composition of immune cells during cancer and subsequent upregulation of host defense in the tumor-bearing state.

Small bowel review: diseases of the small intestine.

In the past year there have been many advances in the area of small bowel physiology and pathology and therapy. In preparation for this review, over 1500 papers were assessed. The focus is on presenting clinically useful information for the practicing gastroenterologist. Selected important clinical learning points include the following: (1) glutamine may restore the AIDs-associated increased intestinal permeability to normal; (2) substance P is a major mediator of diarrhea caused by Costridium difficile toxin A, acting by binding to a G-protein-coupled receptor, and represents a possible 2therapeutic target; (3) the serological diagnosis of celiac disease has been greatly enhanced with the use of anti-endomysial antibody testing, and the recent antitransglutaminase; (4) a quarter of patients with celiac disease may have secondary pancreatic insufficiency and require enzyme replacement therapy; (5) in the patient with unexplained elevation in the serum transaminase concentration, consider celiac disease as an obscure possibility; (6) bosentan and endothelin receptor agonist may prove to be useful in reducing gut ischemia in patients with septic shock; and (7) the administration of recombinant human fibroblast growth factor-2 may prove to be useful to prevent radiation damage to the gastrointestinal tract.

Small bowel review: normal physiology part 2.

In the past year there have been many advances in the area of small bowel physiology and pathology and therapy. In preparation for this review, over 1500 papers were assessed. The focus is on presenting clinically useful information for the practising gastroenterologist. Selected important clinical learning points include the following: (1) numerous peptides are being identified which stimulate the proliferation and functional response of the small intestine to disease or resection, and may in time find a clinical use; (2) under usual in vivo conditions, absorption of nutrients has little effect on the paracellular movement of water; (3) the permeability of the intestine is modified by the function of the tight junctions, and measuring intestinal permeability may be useful to reflect the presence of disease; (4) the release of serotonin is influenced by cholinergic, adrenergic, and nonadrenergic, noncholinergic mechanisms, and serotonin agonists and antagonists may play an important future role in the treatment of motility disorders; (5) the use of endothelin receptor antagonists may be useful for the treatment of intestinal anaphylaxis; (6) the alterations in intestinal pH and motility in patients with Crohn's disease may influence the action of pH- or time-dependent release medications; and (7) patients with irritable bowel syndrome may also have abnormalities in gastric and small intestinal motility.

The deltaF508 mutation in the cystic fibrosis transmembrane conductance regulator alters control of essential fatty acid utilization in epithelial cells.

Essential fatty acid (EFA) incorporation into phospholipid is influenced by chloride channels, suggesting that the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) may regulate aspects of EFA metabolism. The objective of this study was to determine whether the DeltaF508 mutation in the CFTR lowers 18:2(n-6) levels in phospholipid. Control cells, CF cells and CF cells transfected with the "normal" CFTR gene or the DeltaF508 CFTR gene were cultured for 3-5 d and used to determine [1-(14)C]18:2(n-6) incorporation into cell lipids. CF cells exhibited low 18:2(n-6) levels in phospholipid, reduced [1-(14)C]18:2(n-6) incorporation into phospholipid (50% of control) and greater [1-(14)C]18:2(n-6) incorporation into the triacylglycerol fraction (400% of control; P: < 0.05). Kinetic modeling of time course data for [1-(14)C]18:2(n-6) incorporation revealed a loss of metabolic control over the intracellular partitioning of 18:2(n-6) between phospholipid and triacylglycerol pools in CF cells. Expression of the normal CFTR gene in transfected CF cells increased chloride efflux and the incorporation of [1-(14)C]18:2(n-6) into phospholipid and triacylglycerol fractions. The increased incorporation of [1-(14)C]18:2(n-6) into phospholipid was attributed to significantly increased incorporation of [1-(14)C]18:2(n-6) into phosphatidylcholine and phosphatidylinositol. In CF cells expressing the defective DeltaF508 CFTR gene, conversion of [1-(14)C]18:2(n-6) to 20:4(n-6) by desaturation-chain elongation was 1.8-fold greater (P: < 0.05) than observed for CF cells transfected with the normal gene. The observations suggest that CF results in a defect in the utilization of 18:2(n-6), which is attributed in part to the defective CFTR.

Ontogeny of intestinal nutrient transport.

Children born prematurely lack the ability to digest and to absorb nutrients at rates compatible with their nutritional needs. As a result, total parenteral nutrition may need to be given. While this nutritional support may be lifesaving, the baby who receives this therapy is exposed to the risks of possible sepsis, catheter dysfunction, and liver disease. The rodent model of postnatal development provides a useful framework to investigate some of the cellular features of human intestinal development. The up-regulation of intestinal gene expression and precocious development of intestinal nutrient absorption can be achieved by providing growth factor(s) or by modifying the composition of the maternal diet during pregnancy and nursing or the weaning diet of the infant. Accelerating the digestive and absorptive functions of the intestine would thereby allow for the maintenance of infant nutrition through oral food intake, and might possibly eliminate the need for, and risks of, total parenteral nutrition. Accordingly, this review was undertaken to focus on the adaptive processes available to the intestine, to identify what might be the signals for and mechanisms of the modified nutrient absorption, and to speculate on approaches that need to be studied as means to possibly accelerate the adaptive processes in ways which would be beneficial to the newborn young.

Dietary fat-induced suppression of lipogenic enzymes in B/B rats during the development of diabetes.

This study was designed to determine the level of inhibition of gene transcription by the reduction in insulin levels upon the onset of diabetes in spontaneously diabetic B/B rats and if reducing the level of polyunsaturated fatty acids (PUFA) in the diet will increase lipogenic enzyme activity. Control (eight animals per group) and spontaneously diabetic B/B male weanling rats (25 animals per group) were fed semipurified diets containing 20% (w/w) fat of either low (0.25) or high (1.0) polyunsaturated to saturated (P/S) fatty acid ratio. Rats were killed at the onset of diabetes [blood glucose level of approximately/= 100 mg/dL (5.55 mM)] and as they became highly diabetic [blood glucose level of approximately/= 400 mg/dL (22.22 mM)]. Total RNA was extracted from liver, and the relative amount of mRNA coding for fatty acid synthase (FAS), acetyl-CoA carboxylase, malic enzyme, pyruvate kinase, and phosphoenolpyruvate carboxykinase was determined. Liver enzyme activities were also measured. The mRNA levels for FAS, acetyl-CoA carboxylase, and malic enzyme decreased compared to control animals. The mRNA level for pyruvate kinase decreased at the onset of diabetes as compared to control animals. Feeding animals the low P/S diet treatment elevated the level of mRNA and lipogenic enzyme activity compared to animals fed the high P/S diet treatment, suggesting that the effect of PUFA on lipogenic enzymes is through a direct effect on gene expression.

Conjugated linoleic acid in canadian dairy and beef products.

Conjugated linoleic acid (CLA) is a dietary fatty acid produced by ruminant animals and exhibits promising beneficial health effects. CLA has been identified as having anticancer, antiatherogenic, and body fat reducing effects. There are no published data on the CLA content of Canadian beef and dairy products. The purpose of this study was to assess the level and type of CLA isomers found in commercial beef and dairy products. Under the present experimental conditions only the Delta9c,11t-18:2 isomer was detected. Other minor isomers, which may be present, were not determined by the method used in this study. Levels of CLA ranged between 1.2 and 6.2 mg/g of fat or 0.001-4.3 mg/g or mg/mL of sample. On the basis of a usual serving size, levels of CLA ranged between 0.03 and 81.0 mg per serving. It is concluded that the Delta9c,11t-18:2 isomer is present in dairy and beef products and levels when expressed per gram of fat are not significantly different among products.