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K L Fritsche

Publications and source records attributed to K L Fritsche.

29 records · Page 2Linked to original sources

Alteration in mouse splenic phospholipid fatty acid composition and lymphoid cell populations by dietary fat.

The fatty acid composition of diacyl- and alkylacylglycerophosphocholine (PC), phosphatidylinositol (PI), phosphatidylserine (PS), alkenylacyl-glycerophosphoethanolamine (aPE), and diacyl- and alkylacyl-glycerophosphoethanolamine (dPE) was assessed in isolated splenocytes from C3H/Hen mice fed one of four purified isocaloric diets for six weeks. Diets contained 20% by weight of either a high-linoleate sunflower oil (Hi 18:2), a high-oleate sunflower oil (Hi 18:1), a mixture of 17% menhaden fish oil and 3% high-linoleate sunflower oil (Hi n-3), or a mixture of 17% coconut oil and 3% high-linoleate sunflower oil (Hi SFA). Spleen weight and immune cell yield were significantly higher (P less than 0.05) in mice fed the Hi 18:1 or the Hi n-3 diets compared with those fed the Hi 18:2 and Hi SFA diets. Distinctive patterns of fatty acids were observed for each phospholipid in response to dietary fatty acids. Dietary fat significantly affected (P less than 0.05) total polyunsaturated fatty acids (PUFA) in PC and dPE, total saturated fatty acids (SFA) in PC, total monounsaturated fatty acids (MUFA), and n-3 PUFA in all phospholipid classes examined. In mice fed the Hi n-3 diet, n-3 PUFA were significantly elevated, whereas n-6 PUFA decreased in all of the phospholipids. In these mice, eicosapentaenoic acid (EPA) was the predominant n-3 PUFA in PC and PI, whereas docosahexaenoic acid (DHA) was the major n-3 PUFA in aPE and PS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Dietary (n-3) fatty acid and vitamin E interactions in rats: effects on vitamin E status, immune cell prostaglandin E production and primary antibody response.

To examine the interaction between dietary fat and vitamin E at the level of the rat immune system, a 2 x 3 factorial study was designed. Weanling female Sprague Dawley rats were fed for 8-9 wk diets that contained either corn oil (CO diet) or fish oil (FO diet) and one of three levels (30, 300, 900 mg/kg) of all-rac-alpha-tocopheryl acetate. At the lowest level of dietary vitamin E, alpha-tocopherol content of splenocytes from FO-fed rats was approximately 40% lower (P less than 0.05) than in those from CO-fed rats. Supplementation with all-rac-alpha-tocopheryl acetate elevated alpha-tocopherol in splenocytes from FO-fed rats but not in those from CO-fed rats, and reduced the relative proportion of arachidonic acid and eicosapentaenoic acid in the serum of CO-fed and FO-fed rats, respectively. Prostaglandin E production by isolated immune cells was not affected by all-rac-alpha-tocopheryl acetate supplementation. However, feeding the FO diet consistently reduced prostaglandin E synthesis by 70-80% as compared with the CO diet. Antibody production against sheep RBC was highest in rats fed the FO diet supplemented with 900 mg all-rac-alpha-tocopheryl acetate/kg of diet. However, antibody response was not directly correlated to diet-induced changes in immune cell prostaglandin E production or alpha-tocopherol content. Our data suggest that there are significant interactions between vitamin E and (n-3) fatty acids that affect the immune system and that further research in this area is warranted.

Animals↗

Dietary fat influences Ia antigen expression and immune cell populations in the murine peritoneum and spleen.

Peritoneal cells (PEC) and splenocytes were obtained from Listeria monocytogene (LM)-infected or noninfected mice fed a 20% fat diet rich in either (n-3) polyunsaturated fatty acids [(n-3) PUFA diet], linoleate [(n-6) PUFA diet], oleate (MONO diet), or saturated fatty acids (SAT diet) for 6 wk and were assessed for T cells, B cells, macrophages and Ia expression by flow cytometric analysis. In the peritoneum of noninfected mice, dietary fat did not affect total cell yield or the percentage of B cells, macrophages or Ia+ cells, but the (n-3) PUFA-fed group had a greater percentage of T cells than did the other groups. Among the LM-infected mice, the (n-3) PUFA-fed group generally had the highest percentage of B cells and the lowest percentages of T cells, macrophages and Ia+ cells in the peritoneum. Listeria monocytogene infection elevated peritoneal T cell numbers in all mice except the (n-3) PUFA-fed group. The density of Ia molecules on PEC was 40% lower in mice fed the (n-3) PUFA diet. In the spleen, dietary fat also influenced the immune cell populations and Ia+ cells. Two-color staining of spleen cells revealed that Ia+ splenocytes were predominately B cells. These data demonstrate that dietary fats influence Ia expression and immune cell populations and that the effects observed in one immune tissue or cell type may not be readily extrapolated to others.

Animals↗

Dietary n-3 fatty acids reduce antibody-dependent cell cytotoxicity and alter eicosanoid release by chicken immune cells.

The overall goal of the present study was to determine whether the incorporation of n-3 fatty acids into poultry rations would alter the immune response of broiler chickens. Female broiler chicks were fed a corn and soybean meal-based diet to which one of four dietary fats were added: lard (LA), corn oil (CO), flaxseed oil (SO), or menhaden fish oil (FO). The latter two fat sources are rich in n-3 polyunsaturated fatty acids (PUFA). Enriching the diet with n-3 PUFA did not alter the primary or secondary antibody response of broiler chickens to sheep red blood cells. Dietary fat source had no effect on antibody-dependent cell cytotoxicity (ADCC) by peripheral blood leukocytes, but ADCC by splenocytes was 50% lower in chickens fed SO and FO compared with LA and CO (P less than .005). As expected, the fatty acid profile of the isolated immune cells reflected the fatty acid composition of the dietary fats fed. Basal release and calcium ionophore (A23187)-stimulated (10 microM) release of thromboxane B were significantly lower (P less than .05) in the SO and FO groups compared with the LA and CO groups. Total leukotriene B release was not significantly altered by dietary fat source. In conclusion, feeding broiler chickens diets rich in n-3 PUFA reduced ADCC of splenocytes and altered eicosanoid production by isolated immune cells.

Animals↗

Essential fatty acid sufficiency does not preclude fat-soluble-vitamin deficiency in short-bowel syndrome.

Patients with extensive small-bowel resection may experience malabsorption and nutrient deficiencies. We evaluated the ability to absorb fat and fat-soluble vitamins in a short-gut patient. For 18 wk after stopping intravenous lipid, while consuming a low-lactose, low-fat diet, he exhibited no clinical manifestations of essential fatty acid deficiency (EFAD). Serum 20:4n-6 (20:4 omega-6) and 18:2n-6 fatty acid concentrations were normal, whereas the concentration of 20:3n-9 remained less than or equal to 0.1% of total serum fatty acids. Although serum vitamin A was normal, beta-carotene was undetectable despite oral supplementation. Prothrombin time was elevated until parenteral vitamin K was given. This patient has fat absorption adequate to prevent EFAD but inadequate absorption of fat-soluble vitamins. In patients with short bowel, the requirements for parenteral lipids and fat-soluble vitamins should be determined independently.

Absorption↗

Effect of dietary fat source on antibody production and lymphocyte proliferation in chickens.

The purpose of the present study was to assess the effect of fat source on the immune response of chickens. One-day-old pullets were fed corn and soybean meal-based diets containing 7% by weight one of the following fat sources: lard, corn oil, canola oil, linseed oil (LO), or fish oil (FO). After being fed experimental diets for 3 wk, humoral and cellular immune responses were assessed. Chicks were injected with SRBC and antibody titers were measured, 7 days later, by hemagglutination. Concanavalin A (Con A), pokeweed mitogen (PWM), or lipopolysaccharide (LPS)-stimulated proliferation of splenocytes was assessed by [3H]thymidine incorporation. Results demonstrated that antibody titers in FO-fed chicks were higher (P less than .005) compared with titers in chicks fed the other fat sources. The proliferative response to Con A and PWM were 30 to 50% lower (P less than .13 and P less than .05, respectively) in chicks fed the oils rich in omega-3 fatty acids, LO and FO. The response to LPS was poor. The effect of dietary fats source on lymphocyte proliferation was completely abrogated when autologous chicken serum was excluded from the culture medium. Fat source also seemed to affect growth and feed intake of the chickens. In conclusion, dietary fat source has a significant impact on the immune response of chickens.

Animal Feed↗

Effect of dietary fats on the fatty acid compositions of serum and immune tissues in chickens.

The purpose of the present study was to measure the effect of dietary fat source on the fatty acid composition of immune cells in chickens. One-day-old female chicks were fed corn and soybean meal-based diets containing 7% of either lard, corn oil, canola oil, linseed oil (LO), or menhaden fish oil (FO). After being fed experimental diets for 3 to 4 wk, samples of serum, thymus glands, bursa of Fabricius glands, and splenocytes were collected. All samples were frozen and stored at -80 C until lipid analysis. Results indicate that the fatty acid composition of the sera and immune tissues of chickens reflected the fat in the diet. The relative content of long-chain polyunsaturated fatty acids varied considerably among immune tissues, with, from greatest to least, spleen, bursa, and thymus. The young chick demonstrated a substantial capacity to elongate and desaturate linoleic (C18:2n-6) and alpha-linolenic acids (C18:3n-3). Feeding chicks fats rich in n-3 fatty acids (e.g., LO or FO) decreased significantly (P less than .05) the level of arachidonic acid (C20:4n-6) present in the serum and immune tissues by 50 to 75%. The levels of eicosapentaenoic acid (EPA, C20:5n-3) and docosahexaenoic acid (DHA, C20:6n-3) were substantially increased (P less than .05) by FO and LO feeding. However, LO, which is rich in C18:3n-3, was generally only one-half to one-quarter as effective as FO in elevating EPA and DHA levels in immune tissues. The implications for these changes in serum and immune tissue fatty acid profiles are discussed briefly.

Animals↗

Effect of dietary alpha-linolenic acid on growth, metastasis, fatty acid profile and prostaglandin production of two murine mammary adenocarcinomas.

The purpose of this study was to determine whether dietary (n-3) fatty acids would affect mammary tumor growth and metastasis. Weanling female BALB/c mice were fed diets that contained 10% corn oil (CO), linseed oil (LO) or a fish oil-corn oil mix (FO) for 3-8 wk prior to receiving subcutaneous injections of one of two syngeneic mammary tumor cell types (410 and 410.4). Tumor growth was assessed by monitoring mean tumor diameter and tumor weight upon removal. Feeding LO, but not FO, reduced the growth (p less than 0.05) of 410.4 mammary tumors compared with growth in those fed CO. Metastasis data paralleled the tumor growth rate. Feeding LO and FO enhanced (p less than 0.005) incorporation of (n-3) fatty acids into tumors. Tumor prostaglandin E (PGE) production was reduced (p less than 0.005) by LO and FO, compared with CO. FO feeding reduced 410.4 tumor PGE synthesis more (p less than 0.05) than LO feeding, yet tumor growth was only inhibited by LO. These data suggest an inhibitory effect of dietary linolenic acid [i.e., 18:3 (n-3)] on mammary tumor growth and metastasis. However, this effect did not directly correlate with diet-induced changes in PGE synthesis.

Adenocarcinoma↗

Modulation of eicosanoid production and cell-mediated cytotoxicity by dietary alpha-linolenic acid in BALB/c mice.

The effects of dietary alpha-linolenic acid (18:3n-3) on fatty acid composition, eicosanoid production, and cell-mediated cytotoxic activity of immune cells before and after challenge with virus or poly I-C from BALB/c mice were studied. Weanling BALB/c mice were fed purified diets containing either 10%-by-weight corn oil or linseed oil providing a ratio of 18:3n-3 to 18:2n-6 of 1/32 or 2/1, respectively, for 6-10 weeks. Fatty acid analysis of splenocyte phospholipids showed an appreciable increase in the percentage of n-3, and a decrease in n-6, fatty acids in splenocytes from mice fed the linseed oil diet. Splenocyte prostaglandin E and peritoneal exudate cell leukotriene C production was significantly lower in the linseed oil-fed mice. In general, cell-mediated cytotoxic activity was similar for immune cells from linseed oil and corn oil-fed mice. However, 6 days after the viral challenge, splenocyte cell-mediated cytotoxic activity was significantly higher in linseed oil mice. This higher activity was associated with nonspecific cytotoxicity rather than that of viral-specific cytotoxic T-lymphocytes. Cell yields from the spleen and peritoneum were frequently significantly higher in linseed oil mice. Interactions between dietary 18:3n-3, eicosanoid production, and immune cell proliferation and/or migration are discussed. In summary, feeding mice a diet rich in 18:3n-3 elevates immune cell n-3 fatty acid content, reduces eicosanoid synthesis and, to a limited extent, enhances the cell-mediated cytotoxic response to a viral challenge.

Animals↗

Rapid autoxidation of fish oil in diets without added antioxidants.

Feeding of purified diets containing fish oil without added antioxidant leads to rapid autoxidation of the oil and the possibility of artifactual results due to the feeding of autoxidation products. Purified diets containing menhaden oil without any added antioxidant deteriorate quickly. Peroxide value of the diet is elevated 5- to 6-fold within 24 h and 12-fold within 48 h when exposed to air at room temperature. Addition of 0.02% t-butylhydroquinone to the fish oil prevents this deterioration for at least 72 h. Determination of fatty acid composition is not a sensitive indicator of diet integrity. Supplementation of fish oil diets with vitamin E to help protect against in vivo peroxidation is discussed.

Antioxidants↗