Seasonal acclimatization to temperature in cardueline finches

1. Seasonal variation in body constituents and utilization of lipid, protein, and carbohydrate during cold stress in American goldfinches were studied to determine relations of these functions to the pronounced seasonal shift in thermogenic capacity documented in a previous study (Dawson and Carey, 1976).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47119/1/360_2004_Article_BF00686746.pd

The inhibition of T-lymphocyte proliferation by fatty acids is via an eicosanoid-independent mechanism

Eicosanoids, in particular prostaglandin E2 (PGE2), are potent inhibitors of a number of immune responses, including lymphocyte proliferation. We have previously shown that fatty acids, especially polyunsaturated fatty acids (PUFA), inhibit mitogen-stimulated proliferation of lymphocytes. One mechanism by which fatty acids could exert their inhibitory effect is via modulation of eicosanoid synthesis. This possibility was investigated in the present study. PGE2 concentrations in the medium taken from lymphocytes cultured in the presence of a range of different fatty acids did not correlate with the inhibitory effects of the fatty acids upon lymphocyte proliferation. Although PGE2 at concentrations above 10 nM caused inhibition of lymphocyte proliferation, PGE2 at the concentration measured in lymphocyte culture medium (0.3-4 nM) was not inhibitory. PGE3 did not inhibit lymphocyte proliferation, except at high concentrations (greater than 250 nM). The maximal inhibition of proliferation caused by PGE2 or PGE3 was less than the inhibition caused by each of the fatty acids except myristic or palmitic acids. Inclusion of inhibitors of phospholipase A2, cyclo-oxygenase or lipoxygenase in the culture medium did not prevent the fatty acids from exerting their inhibitory effect on lymphocyte proliferation. The eicosanoids present in lymph node cell cultures originate from macrophages rather than lymphocytes. Depletion of macrophages from the cell preparation by adherence did not prevent fatty acids from inhibiting proliferation. Proliferation of thoracic duct lymphocytes, which are devoid of macrophages, is inhibited by fatty acids to a similar extent as proliferation of lymph node lymphocytes. These observations provide convincing evidence that the inhibition of lymphocyte proliferation by fatty acids is independent of the production of eicosanoids. Therefore, other mechanisms must be investigated if the effect of fatty acids upon lymphocyte proliferation is to be understood at a biochemical level

The effect of dietary manipulation on rat lymphocyte subsets and proliferation

Polyunsaturated fatty acids (PUFA) have been shown to suppress immune cell functions in vitro. Dietary studies investigating the effects of PUFA-containing oils on lymphocyte functions have yielded contradictory findings: such studies are difficult to compare as there are many variations in protocols. The present study investigated the effects of diets containing oils rich in saturated fatty acids, monounsaturated fatty acids, n-6 PUFA or n-3 PUFA on rat lymphocyte proliferation and on receptor and surface marker expression. Rats were fed for 10 weeks on a low-fat (LF) diet (approximately 2% fat by weight) or on one of five high-fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Compared with feeding the LF diet, all of the high-fat diets suppressed the proliferation of lymphocytes from the spleen: although there was no significant effect of diet on the proliferation of lymphocytes from the thymus, there was a trend towards decreased proliferation with high-fat feeding. Feeding the OO, EPO or MO diets significantly suppressed proliferation of mesenteric lymph node lymphocytes compared with feeding the LF, HCO or SO diets. Dietary lipid manipulation had no effect on the proportion of T cells, B cells or monocytes/macrophages in the spleen, thymus or lymph nodes. Dietary lipid manipulation also had no significant effect on the proportions of CD4+ or CD8+ lymphocytes in spleen, thymus or lymph nodes, either in freshly prepared cells or in cells cultured in the presence of mitogen. There were no significant effects of dietary lipid manipulation on the expression of IL-2 receptors or transferrin receptors by concanavalin A (Con A)-stimulated lymphocytes. However, there was a trend towards a decrease in transferrin receptor expression by Con A-stimulated lymphocytes from the thymus and lymph nodes of the MO-fed rats and towards a decrease in the expression of IL-2 receptors by lymphocytes from the spleens and thymi of the MO-fed rats. These observations provide evidence that some dietary oils, particularly OO, EPO and MO, possess immunosuppressive properties and so may be useful in the therapy of diseases involving inappropriate lymphocyte activation

Influence of diet on the kinetic behavior of hepatic carnitine palmitoyltransferase I toward different acyl CoA esters

The influence of diet on the kinetics of the overt form of rat liver mitochondrial carnitine palmitoyltransferase (CPT I; EC 2.3.1.21) was studied using rats fed either a low-fat diet (3% w/w fat), or diets which were supplemented with either olive oil (OO), safflower oil (SO) or menhaden (fish) oil (MO) to 20% w/w of fat (high fat diets). When animals were fed each of these four diets for 10 days, the order of the apparent maximal activity (v(max)) of CPT I toward various individual fatty acyl CoA, when measured under a fixed molar ratio of acyl CoA/albumin, was 16:1n-7>18:1n- 9>18:2n-6>16:0>22:6n-3, and was thus not affected by the fat composition of the diet. However, in all but one case, the SO and MO diets elicited a higher v(max) for each substrate than either the LF diet or the high fat OO diet. The apparent K0.5 for the different acyl CoA esters was generally lowest in LF-fed animals, and highest in those fed the high-fat SO diet. Moreover, when compared with the situation of animals fed high-fat diets, the K0.5 values of CPT I in LF-fed animals for palmitoyl CoA and oleoyl CoA were low. This possession by CPT I of a high 'affinity' toward these nonessential fatty acyl CoAs, but a lower 'affinity' toward linoleoyl CoA, the ester of an essential fatty acid, may enable this latter fatty acid to be spared from oxidation when its concentration in the diet is low. The data also emphasize that palmitoleoyl CoA, if available in the diet, is likely to be utilized by CPT I at a high rate