Evidence for high gene flow, nonrandom mating, and genetic bottlenecks of Ganoderma boninense infecting oil palm (Elaeis guineensis Jacq.) plantations in Malaysia and Indonesia.

Ganoderma boninense, the causal agent of basal stem rot (BSR) disease, has been recognized as a major economic threat to commercial plantings of oil palm (Elaeis guineensis Jacq.) in Southeast Asia, which supplies 86% of the world's palm oil. High genetic diversity and gene flow among regional populations of 417 G. boninense isolates collected from Sabah, Sarawak, and Peninsular Malaysia (Malaysia) and Sumatra (Indonesia) were demonstrated using 16 microsatellite loci. Three genetic clusters and different admixed populations of G. boninense across regions were detected, and they appeared to follow the spread of the fungus from the oldest (Peninsular Malaysia and Sumatra) to younger generations of oil palm plantings (Sabah and Sarawak). Low spatial genetic differentiation of G. boninense (FST = 0.05) among the sampling regions revealed geographically nonrestricted gene dispersal, but isolation by distance was still evident. Analysis of molecular variance (AMOVA) confirmed the little to no genetic differentiation among the pathogen populations and the three genetic clusters defined by STRUCTURE and minimum spanning network. Despite G. boninense being highly outcrossing and spread by sexual spores, linkage disequilibrium was detected in 7 of the 14 populations. Linkage disequilibrium indicated that the reproduction of the fungus was not entirely by random mating and genetic drift could be an important structuring factor. Furthermore, evidence of population bottleneck was indicated in the oldest oil palm plantations as detected in genetic clusters 2 and 3, which consisted mainly of Peninsular Malaysia and Sumatra isolates. The population bottleneck or founding event could have arisen from either new planting or replanting after the removal of large number of palm hosts. The present study also demonstrated that migration and nonrandom mating of G. boninense could be important for survival and adaptation to new palm hosts.

Genetic diversity and gene flow amongst admixed populations of Ganoderma boninense, causal agent of basal stem rot in African oil palm (Elaeis guineensis Jacq.) in Sarawak (Malaysia), Peninsular Malaysia, and Sumatra (Indonesia).

In 1911 and 1917, the first commercial plantings of African oil palm (Elaeis guineensis Jacq.) were made in Indonesia and Malaysia in Southeast Asia. In less than 15 years, basal stem rot (BSR) was reported in Malaysia. It took nearly another seven decades to identify the main causal agent of BSR as the fungus, Ganoderma boninense. Since then, research efforts have focused on understanding G. boninense disease epidemiology, biology, and etiology, but limited progress was made to characterize pathogen genetic diversity, spatial structure, pathogenicity, and virulence. This study describes pathogen variability, gene flow, population differentiation, and genetic structure of G. boninense in Sarawak (Malaysia), Peninsular Malaysia, and Sumatra (Indonesia) inferred by 16 highly polymorphic cDNA-SSR (simple sequence repeat) markers. Marker-inferred genotypic diversity indicated a high level of pathogen variability among individuals within a population and among different populations. This genetic variability is clearly the result of outcrossing between basidiospores to produce recombinant genotypes. Although our results indicated high gene flow among the populations, there was no significant genetic differentiation among G. boninense populations on a regional scale. It suggested that G. boninense genetic makeup is similar across a wide region. Furthermore, our results revealed the existence of three admixed genetic clusters of G. boninense associated with BSR-diseased oil palms sampled throughout Sarawak, Peninsular Malaysia, and Sumatra. We postulate that the population structure is likely a reflection of the high genetic variability of G. boninense populations. This, in turn, could be explained by highly successful outcrossing between basidiospores of G. boninense from Southeast Asia and introduced genetic sources from various regions of the world, as well as regional adaptation of various pathogen genotypes to different palm hosts. Pathogen variability and population structure could be employed to deduce the epidemiology of G. boninense, as well as the implications of plantation cultural practices on BSR disease control in different regions.

An innovative brilliant blue FCF method for fluorescent staining of fungi and bacteria.

Most natural and synthetic dyes currently used for microbial fluorescent staining are toxic or carcinogenic and are harmful to animals, humans and the environment. A food dye for microbial staining, brilliant blue FCF, was used as an alternative to lactofuchsin and lactophenol blue. Brilliant blue FCF shows pronounced microbial cell fluorescence staining of an array of pathogenic/toxigenic (Fusarium granunearum 3- and 15-acetyldeoxynivalenol chemotypes, and Escherichia coli O157:H7) and beneficial fungi and bacteria (Trichoderma harzianum and Bacillus subtilis). Brilliant blue FCF has no toxic effects on the microbes tested and is inexpensive.

Assessment of alcohol percentage test for fungal surface hydrophobicity measurement.

AIM: To determine whether assessing the penetration of solutions with different concentrations of ethanol (alcohol percentage test: APT) on fungal surfaces is effective in characterization of hydrophobicity on fungal surfaces. METHODS AND RESULTS: APT and contact angle (CA) measurements were conducted on nine hydrophobic and two hydrophilic fungal strains from the phyla of Ascomycota, Basidiomycota and Zygomycota. There was a strong positive correlation (R(2) = 0.95) between the APT and CA measurements from eight of the nine hydrophobic stains (four pathogenic and mycotoxigenic Fusarium taxa, one melanosporaceous biotrophic taxon, Alternaria sp, Penicillium aurantiogriseum and Cladosporium cladosporioides). Hydrophilic control strains, Mortierella hyalina and Laccaria laccata, had CAs <90 degrees and no measurable degree of hydrophobicity using the APT method. CONCLUSIONS: The APT method was effective in measuring the degree of hydrophobicity and can be conducted on different zones of fungal growth. SIGNIFICANCE AND IMPACT OF THE STUDY: Characterization of fungal surface hydrophobicity is important for understanding of its particular role and function in fungal morphogenesis and pathogenesis. APT is a simple method that can be utilized for fungal hydrophobicity measurements when CA cannot be measured because of obscured view from aerial mycelia growth.

Synthesis of specific fatty acids contributes to VLDL-triacylglycerol composition in humans with and without type 2 diabetes.

AIMS/HYPOTHESIS: It is recommended that patients with diabetes reduce their intake of saturated fat and increase their intake of monounsaturated fat or carbohydrate. However, high-carbohydrate diets may result in higher saturated fatty acids in VLDL-triacylglycerol. This is attributed to de novo lipogenesis, although synthesis of specific fatty acids is rarely measured. The objective of this study was to examine the contribution of de novo fatty acid synthesis to VLDL-triacylglycerol composition. It was hypothesised that levels of total and de novo synthesised fatty acids would increase with increased carbohydrate intake in diabetic participants. METHODS: Seven individuals with type 2 diabetes mellitus and seven matched non-diabetic controls consumed two diets differing in fat energy (lower fat <25%, higher fat >35%) for 3 days in a randomised crossover design. Blood samples were drawn before and 24 h after the ingestion of (2)H-labelled water. RESULTS: In the control participants, the higher-fat diet resulted in a 40% reduction in VLDL-triacylglycerol fatty acids because of decreases in myristic, palmitic, palmitoleic and linoleic acids, but the opposite trend occurred in participants with diabetes. The lower-fat diet increased the fractional synthesis rate by 35% and 25% in the control and diabetes participants, respectively (range: 0-33%). Palmitate accounted for 71% of fatty acids synthesised (range: 44-84% total de novo synthesised fatty acids). CONCLUSIONS/INTERPRETATION: (2)H incorporation was used for the first time in humans showing variability in the synthesis rate of specific fatty acids, even palmitic acid. A lower-fat diet stimulated saturated fatty acid synthesis at high rates, but no net stimulation of synthesis of any fatty acid occurred in the diabetes group. The implications of this finding for our understanding of lipid metabolism in diabetes require further investigation.

Cholesterolaemic influence of palmitic acid in the sn-1, 3 v. the sn-2 position with high or low dietary linoleic acid in healthy young men.

Healthy young men were fed four diets for 2 weeks each providing natural fats containing palmitic acid (16 : 0) predominantly in the sn-1, 3 position of dietary TAG or containing 16 : 0 predominantly in the sn-2 position with low or high levels of linoleic acid (18 : 2n-6). Two treatments supplied 16 : 0 in the sn-1, 3 positions from palmstearin with low (3 % energy) or high (>7 % energy) 18 : 2n-6 and two treatments supplied 16 : 0 in the sn-2 position from lard with high or low levels of 18 : 2n-6. Diets contained 30-35 % energy as fat, 7-11 % energy as 16 : 0 and moderate levels of cholesterol. Fasting serum cholesterol and lipoprotein concentrations were measured. Cholesterol fractional synthesis rate (FSR) was determined by 2H incorporation. Diets providing 16 : 0 in the sn-2 position resulted in lower fasting serum total cholesterol (TC) and a lower TC:HDL ratio than diets providing 16 : 0 in the sn-1, 3 positions. Diets with high levels of 18 : 2n-6 significantly decreased the TC:HDL ratio, reaffirming the well-known cholesterol-reducing effect of 18 : 2n-6. A lower non-esterified cholesterol FSR was observed with low dietary levels of 18 : 2n-6. No differences between dietary treatments were found for serum HDL-cholesterol, LDL-cholesterol or TAG. It is concluded that dietary fats containing 16 : 0 in the sn-2 position may result in slightly lower fasting TC than diets providing 16 : 0 in the sn-1, 3 positions, while the level of n-6 polyunsaturated fat influences endogenous cholesterol synthesis.

The effect of palmitic acid on lipoprotein cholesterol levels and endogenous cholesterol synthesis in hyperlipidemic subjects.

The present study assesses the effect of high vs. low palmitic acid intakes on plasma lipoprotein cholesterol levels and on rates for endogenous synthesis of cholesterol in healthy and hyperlipidemic subjects. Four diets were formulated to provide combinations of 16:0 at two levels of 18:2n-6. Subjects received each diet treatment for 21 d, followed by washout periods of 21 d. On day 21 of each diet treatment, a fasting blood sample was drawn for lipoprotein determination and to provide a measure of the background level of deuterium. A priming dose of deuterium was consumed and a second blood sample obtained 24 h after the first sample. Isotope ratio mass spectrometry was used to determine the incorporation of deuterium into the newly synthesized cholesterol molecule, and fractional synthetic rates were calculated. Serum total cholesterol and low density lipoprotein-cholesterol was not significantly affected by the high level of 16:0 when diets also contained a high level of 18:2n-6. There was no effect of dietary 16:0 on high density liproprotein-cholesterol at either the high or low levels of intake. The results indicate that 16:0 has no effect on serum lipoprotein profiles in the presence of recommended intakes for 18:2n-6.

Use of deuterium oxide to measure de novo fatty acid synthesis in normal subjects consuming different dietary fatty acid composition1.

The effect of dietary linoleic (C18:2n-6) and palmitic acids (C16:0) on rate of hepatic de novo fatty acid synthesis was assessed in normal subjects. The diet was formulated to provide combinations of high and low levels of C18:2n-6 and C16:0. After 21 days of diet treatment, plasma triacylglycerol level and incorporation of deuterium into the plasma very low density lipoprotein triacylglycerol (VLDL-TG) pool over 24 hours was measured. Plasma triacylglycerol levels were within the normal range. Increasing dietary intake of linoleic acid decreased plasma triacylglycerol level when subjects consumed a low level of dietary palmitic acid. The relative and net amount of de novo synthesized fatty acid in the plasma VLDL-TG pool was not influenced by the diet treatments. A relationship between plasma triacylglycerol level and rate of hepatic de novo fatty acid synthesis was observed.

First Report of Erwinia carotovora subsp. carotovora Causing Bacterial Root Rot of Sweetpotato (Ipomoea batatas) in Louisiana.

Bacterial root and stem rot of sweetpotato (Ipomoea batatas (L.) Lam.) was first fully characterized in the U.S. in 1977 (2). It was thought to be caused exclusively by Erwinia chrysanthemi. Although a previous report described sweetpotato as a host for E. carotovora subsp. carotovora, based on artificial inoculations, others have reported that neither E. carotovora subsp. carotovora nor E. carotovora subsp. atroseptica decay sweetpotato storage roots (1). In October 1995, storage roots of sweetpotato cv. Beauregard were received from St. Landry Parish, LA, that displayed typical bacterial root rot. Isolations from these roots yielded bacteria that showed a similarity of 0.945 to E. carotovora subsp. carotovora with the Biolog GN Bacterial Identification System (version 3.50). This isolate (Ecc-LH) also differed from isolates of E. chrysanthemi (Ech) from sweetpotato and other hosts in that it was insensitive to erythromycin, did not produce phosphatase or lecithinase, and did not produce gas from glucose. Ecc-LH differed from known strains of E. carotovora subsp. atroseptica in that it did not produce reducing substances from sucrose or acid from palatinose. When Beauregard storage roots were inoculated by inserting micropipette tips containing 50 µl of 1.0 × 108 CFU/ml, both Ecc-LH and Ech-48 produced typical bacterial root rot symptoms. However, when they were compared by infectivity titrations at 28 to 32°C, Ecc-LH was less virulent than Ech-48. Ecc-LH had an ED50 of approximately 1.0 × 106 CFU/ml and did not cause appreciable disease below inoculum concentrations of 1.0 × 105, whereas Ech-48 had an ED50 of approximately 1.0 × 108 and caused soft rot at the lowest concentration tested, 1.0 × 103. Similar disease incidence was observed in infectivity titrations at 22 to 24°C, but Ech-48 caused less severe soft rot. E. carotovora subsp. carotovora was reisolated from inoculated storage roots and its identity was reconfirmed by Biolog. When terminal vine cuttings of Beauregard were dipped in 1.0 × 108 CFU/ml and planted in a greenhouse, bacterial stem rot symptoms developed on plants inoculated with Ech-48 at about 4 weeks postinoculation, or when new growth began. However, no symptoms developed on plants inoculated with Ecc-LH. This is the first report of natural occurrence of E. carotovora subsp. carotovora causing bacterial root rot of sweetpotato in Louisiana. E. chrysanthemi remains the most important pathogen causing bacterial soft rot in sweetpotato since it is widely associated with sweetpotato, is more virulent on storage roots and also causes a stem rot. E. carotovora subsp. carotovora can cause root rot, but has been isolated in only one location to date, is less virulent on storage roots, and apparently does not cause stem rot on the predominant cultivar in U.S. sweetpotato production, Beauregard. References: (1) C. A. Clark and J. W. Moyer. 1988. Compendium of Sweet Potato Diseases. American Phytopathological Society, St. Paul, MN. (2) N. W. Schaad and D. Brenner. Phytopathology 67:302, 1977.

During neuronal and glial cell development diet n-6 to n-3 fatty acid ratio alters the fatty acid composition of phosphatidylinositol and phosphatidylserine.

Brain development was examined in the neonatal rat in response to feeding increased levels of 18:3n - 3, 20:4n - 6 or 22:6n - 3 at levels proposed for infant formula. Diets varying in n - 6 to n - 3 fatty acid ratio, with or without 20:4n - 6 and 22:6n - 3 alone or in combination, were fed to nursing dams at parturition and subsequently to weaned pups until six weeks of age. Neuronal and glial cells were isolated from the frontal, cerebellar and hippocampal brain regions of rat pups at birth, one, two, three and six weeks of age. Fatty acid analysis of inositol- and serine- phosphoglycerides indicated that small changes in dietary n - 6 to n - 3 fatty acid ratio significantly affect neuronal and glial cell membrane composition. Fatty acid composition of phosphatidylinositol and phosphatidylserine was distinct and exhibited change with age. Individual brain regions and cell types varied in amount and rate of 20:4n - 6 and 22:6n - 3 accretion. Alteration of brain fatty acid composition reflected the fatty acid composition of the diet fed. If analogous changes occur during human brain development, feeding infants 20:4n - 6 and 22:6n - 3 or a reduced 18:2n - 6 to 18:3n - 3 ratio may alter fatty acid profiles of brain cells.

Omega-3 fatty acid intake results in a relationship between the fatty acid composition of LDL cholesterol ester and LDL cholesterol content in humans.

The relationship between the fatty acid composition of the low density lipoprotein (LDL) cholesterol ester and LDL cholesterol content was assessed in 26 free-living, normal subjects. Dietary intakes of 14:0, 16:0, 18:0, 18:1, 18:2omega6, 18:3omega3, 20:4omega6, 20:5omega3, 22:6omega3 were calculated from seven-day food records kept by each subject at baseline and after three months of supplementation with olive, flaxseed or fish oil, respectively. A randomized cross-over design was used. The fatty acid content of specific foods was calculated. Fasting blood samples, taken at the beginning and end of each supplementation period, were analyzed for the fatty acid content present in individual lipoproteins. There was a significant correlation between 20:5omega3 and 22:6omega3 intake and the content of these fatty acids in the LDL cholesterol ester fraction. During the fish oil treatment period the 16:0 and 18:0 content of the LDL cholesterol ester was highly predictive of LDL cholesterol content. This relationship was not observed during the baseline or placebo (olive oil) supplement period.

Small changes of dietary (n-6) and (n-3)/fatty acid content ration alter phosphatidylethanolamine and phosphatidylcholine fatty acid composition during development of neuronal and glial cells in rats.

It has been suggested that the fat composition of infant formula should provide arachidonic acid [20:4(n-6)] and docosahexaenoic acid [22:6(n-3)] or increased alpha-linolenic acid [18:3(n-3)] to optimize the (n-3) and (n-6) fatty acid content of brain during infant development. This experiment examined the effects of feeding increased levels of 18:3(n-3), 20:4(n-6) and 22:6(n-3) on brain development in neonatal rats. Diets varying in (n-6) and (n-3) fatty acid content with or without 20:4(n-6) or 22:6(n-3), at levels proposed for infant formula, were fed to nursing dams from parturition and subsequently to weaned pups until 6 wk of age. Neuronal and glial cells were isolated from the frontal region, cerebellum and hippocampus of the brain. Fatty acid analyses of ethanolamine- and choline-phosphoglycerides indicated that small changes in the dietary (n-6)/(n-3) ratio significantly altered neuronal and glial membrane fatty acid composition. Brain regions and cell types varied in amount and rate of 20:4(n-6) and 22:6(n-3) accretion. Fatty acid composition of individual phosphoglycerides was distinct and exhibited changes with age. Inclusion of both 20:4(n-6) and 22:6(n-3) in the diet resulted in alteration of brain fatty acid composition reflecting the fatty acid composition of the diet. If analogous developmental changes occur in human brain, then these results imply that addition of 20:4(n-6) and 22:6(n-3) or a reduced 18:2(n-6):18:3(n-3) ratio in infant formula may result in fatty acid profiles of neuronal and glial cells in formula-fed infants similar to those observed in breast-fed infants.

Effect of omega 3 fatty acid on plasma lipids, cholesterol and lipoprotein fatty acid content in NIDDM patients.

This study was conducted to examine the effect of omega 3 fatty acid supplementation on plasma lipid, cholesterol and lipoprotein fatty acid content of non-insulin-dependent diabetic individuals consuming a higher (0.65, n = 10) or lower (0.44, n = 18) ratio of dietary polyunsaturated to saturated fatty acid (P/S). The participants were initially given an olive oil supplement (placebo) equivalent to 35 mg of 18:1. kg body weight-1.day-1 for 3 months. This was followed by two omega 3 supplement periods in a randomized crossover. In these 3-month periods, participants were given a linseed oil supplement equivalent to 35 mg of 18:3 omega 3.kg body weight-1.day-1 or a fish oil supplement equivalent to 35 mg of 20:5 omega 3 + 22:6 omega 3.kg body weight-1. day-1. At the end of each supplement period, a blood sample was drawn from each participant for lipid, lipoprotein, insulin, glucagon and C-peptide analyses. At the end of each 3-month period a 7-day dietary record was completed to calculate dietary fat intake and P/S ratio. Results indicate that fish oil significantly reduced plasma triacylglycerol level (p < 0.05) and increased 20:5 omega 3 and 22:6 omega 3 content of all lipoprotein lipid classes. Linolenic acid supplementation had no effect on plasma triacylglycerol level, but it increased 18:3 omega 3 content of lipoprotein cholesterol ester fractions (p < 0.05). A slight increase in 20:5 omega 3, but not 22:6 omega 3, content was noted in lipoprotein lipid classes as a result of 18:3 omega 3 supplementation. LDL and HDL cholesterol, insulin, glucagon and C-peptide levels were not affected by either omega 3 supplement. It is concluded that a modest intake of omega 3 fatty acids, such as could be obtained from consuming fish regularly, will reduce plasma triglyceride level without affecting LDL or HDL cholesterol levels.

Palmitic acid effect on lipoprotein profiles and endogenous cholesterol synthesis or clearance in humans.

The effect of palmitic acid (C16:0) on serum lipoprotein cholesterol levels is debatable. If C16:0 is hypercholesterolaemic, then it may increase the endogenous synthesis or decrease clearance of cholesterol. Four diets were formulated to provide combinations of two levels of C16:0 in relation to two levels of PUFA. Healthy male subjects received each of the four diet treatments for 21 days, followed by washout periods of 21 days. On day 21 of each diet treatment, a fasting blood sample was drawn for lipoprotein determination and to provide a measure of the background level of deuterium. A priming dose of deuterium was consumed and a second blood sample obtained 24 hours after the first sample. Isotope Ratio Mass Spectrometry was used to determine the incorporation of deuterium into the newly synthesised cholesterol molecule, and fractional synthetic rates calculated. Serum total cholesterol and LDL-cholesterol was not significantly affected by the high level of C16:0 when diets also contained the high level of PUFA. There was no effect of C16:0 on HDL-cholesterol at either the high or low levels of intake. The fractional synthetic rates of cholesterol observed for each of the diet treatments did not significantly differ from one another, suggesting no relationship between the endogenous synthesis of cholesterol and diet C16:0 content. These results indicate that C16:0 had no effect on serum lipoprotein profiles in the presence of recommended intakes for PUFA, nor did it increase rates of cholesterol synthesis in healthy males.

Normal subjects consuming physiological levels of 18:3(n-3) and 20:5(n-3) from flaxseed or fish oils have characteristic differences in plasma lipid and lipoprotein fatty acid levels.

The study assessed the effect of low doses of fatty acids from fish or flaxseed oil on plasma lipid concentrations in normal humans consuming diets with either high (0.87, n = 11) or low (0.48, n = 15) dietary polyunsaturated/saturated fatty acid (P/S) ratios. The dose of (n-3) fatty acids reflected an (n-3) intake that could easily be attained by selection of foods in a normal diet. The individuals were initially supplemented with olive oil [35 mg 18:1/(kg body weight.d)], and then were randomly assigned to either flaxseed or fish oil [35 mg 18:3(n-3) or 35 mg 20:5(n-3) + 22:6(n-3)/(kg body weight.d), respectively] treatments. Participants consumed each oil supplement for 3 mo. Blood samples were drawn for analysis at the end of each 3-mo period. Plasma triacylglycerol, total, LDL and HDL cholesterol concentrations, and lipoprotein fatty acid concentrations are shown. Fish oil reduced plasma triacylglycerol and increased lipoprotein levels of 20:5(n-3) and 22:6(n-3). The flaxseed oil did not alter plasma triacylglycerol level and produced small changes in 20:5(n-3) and 22:6(n-3) concentrations. Total, LDL and HDL cholesterol levels were not affected by either (n-3) fatty acid. Significant differences in plasma triacylglycerol concentrations and total and LDL cholesterol levels were found between the two dietary P/S groups after all oil treatment periods. Levels of 18:3(n-3), 20:4(n-6), 20:5(n-3), and 22:6(n-3) in LDL were also different in high vs. low dietary P/S groups for all oil treatments and in the VLDL for the olive oil and fish oil supplementation. This study indicates that low intake of purified fish oil induces changes in plasma triacylglycerol, 20:5(n-3) levels in VLDL, LDL, and HDL, and 22:6(n-3) levels in LDL and HDL that are apparent after 3 mo and which might influence atherogenicity of lipoprotein particles in normal free-living individuals.

Fatty acid pool size in plasma lipoprotein fractions of cystic fibrosis patients.

The objective of this study was to quantitatively measure the essential fatty acid pools in lipid fractions of plasma lipoproteins and the alteration of these pool sizes after consumption of a physiologic intake of fish oil. Twenty-three cystic fibrosis (CF) patients and 21 normal subjects were supplemented with fish oil, providing 35 mg n-3 fatty acids/kg body wt for 4 wk. Blood was collected pre- and postsupplementation and was quantitatively analyzed to determine the fatty acid pool size in each lipid class of low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and very-low-density lipoproteins. Two 7-d food records were collected to determine total fat and fatty acid intakes. Intakes of protein, carbohydrate, and fat as a percentage of energy and the ratio of polyunsaturated to saturated fats was similar for the CF and control groups. Energy intake was greater for CF subjects. Smaller lipoprotein essential fatty acid pools were observed in CF patients than in control subjects. Healthy subjects had larger essential fatty acid pool sizes in cholesterol ester fractions of HDLs and LDLs than CF subjects. Cholesterol ester and phosphatidylcholine pools transported the majority of essential fatty acids in both CF and control subjects.

Increasing the dietary polyunsaturated fat content alters whole-body utilization of 16:0 and 10:0.

Six healthy adult males were fed four different diets to determine the effects of the quantity of fat (30% or 40% of energy as fat) and type of fat (polyunsaturated or saturated) on utilization of fatty acids. Each diet was fed for 15 d. The ratio of dietary polyunsaturated to saturated fat (P:S) was formulated at either 0.2 or 1.0 at both fat intakes. Subjects provided breath tests to measure background 13C and response to [1-13C]10:0 and [1-13C]16:0 fed with a test meal. Increasing the P:S increased whole-body oxidation of labeled 10:0 by 30% after consumption of both low- and high-fat diets. When labeled 16:0 was fed, the amount of 13C excreted in breath increased by a factor of 2.4 after the low-fat diet with a high P:S compared with the diet with a low P:S. The results suggest that the amount and type of fat in the diet affect utilization of individual fatty acids in normal subjects.

Chain shortening of palmitic acid in human subjects.

Chain shortening of palmitic acid was examined in vivo by comparing oxidation rates of [1-13C]palmitate vs [16-13C]palmitate fed to four male subjects consuming a high-fat diet. For 9 d subjects were fed a diet of normal foods providing an energy intake equal to their estimated requirements. The diet provided (as energy) approximately 14% protein, 46% carbohydrate, and 40% fat at a P:S ratio of 0.25. Analysis of breath 13CO2 enrichment on day 3 permitted analysis of background 13C contribution from the test diet alone. On days 4 and 7 either [1-13C]palmitic acid or [16-13C]palmitic acid (9-13.5 mg/kg body wt) was fed with the breakfast meal. The whole-body rate of oxidation of [1-13C]palmitic acid was significantly greater than that observed for [16-13C]palmitic acid. These results suggest that up to 34% of dietary palmitic acid consumed may be subjected to extramitochondrial chain shortening.

Influence of genotype on the phospholipid fatty acid composition of splenic T and B lymphocytes in MRL/MpJ-lpr/lpr mice.

The MRL/MpJ-lpr/lpr mice manifest a T cell proliferative and autoimmune disorder. Similar changes occur much later in the life of MRL/MpJ-+/+ mice. MRL/MpJ-lpr/lpr (lpr/lpr) and MRL/MpJ-+/+ (+/+) mice were fed for six weeks nutritionally adequate semipurified diets containing 20% (w/w) fat, but differing in linoleic acid content. The phospholipid fatty acid composition of T and B cells was found to be dependent on genetic background of mice and level of linoleic acid in the diet. Changes in the levels of specific fatty acids like 16:0, 18:2 omega 6, 22:5 omega 3 and 22:6 omega 3 in some of the phospholipid components were observed in the MRL/MpJ-lpr/lpr strain in both the B and T cell types as compared with their normal +/+ counterpart strain. T cells of lpr/lpr mice exhibited significantly higher levels of 20:4 omega 6 than did T cells of other strain. High levels of dietary linoleic acid significantly increased incorporation of 18:2 omega 6 in T and B cells, while the effect on other fatty acids of the two types of cells varied with the phospholipid classes and fatty acids when compared with the low linoleic acid fed-group. Differences observed in the phospholipid fatty acid composition of the T and B cells of the congenic mice might contribute to differences in rate of progression of age-related changes suggesting that the autoimmune disorder might be mitigated by dietary manipulation.

Rate of passage of corn-canola meal and corn-soybean meal diets through the gastrointestinal tract of broiler and White Leghorn chickens.

The effect of corn-canola meal and corn-soybean meal diets on the form and function of the gastrointestinal tract of broiler (meat-type) and White Leghorn (egg-type) cockerels was measured from 14 to 44 and 14 to 86 days of age or 203 to 1,844 and 115 to 1,777 g of body weight, respectively. Dry weights of the empty crop (P less than .01), gizzard (P less than .001), and ceca (P less than .001) relative to live body weight (g/kg) were lighter in broilers than in Leghorns. Canola meal at 370 g/kg diet was associated with increased (P less than .001) dry weight of the gizzard and jejunum relative to body weight. Soybean meal at 370 g/kg diet was associated with increased (P less than .001) dry weight of the ceca relative to body weight. The lengths, relative to a power of body weight of the duodenum (cm/g.187) and jejunum plus ileum (cm/g.240), were longer (P less than .001) in broilers than in Leghorns. The canola meal diet was associated with an increase (P less than .001) in length of the jejunum plus ileum (cm/g.240) relative to a power of body weight. Mean retention time (MRT) of a particle marker, 103ruthenium phenanthroline, increased with body weight in the entire gastrointestinal tract (P less than .001) and in each of its segments except in the proventriculus, where it was not affected by body weight (P greater than .05), and in the gizzard, where it decreased (P less than .05) with body weight. The MRT, adjusted for body weight in the entire gastrointestinal tract of broilers (338.0 +/- 10.8 min) and Leghorns (359.9 +/- 10.8 min), was similar (P greater than .05) but varied significantly in segments of the gut for both type of chicken and diet. Adjusted MRT was shorter in the crop (P less than .001) and gizzard (P less than .001) and longer in the duodenum (P less than .001) and ileum (P less than .01) of broilers than Leghorns. The soybean meal diet was retained for 2.3 min longer in the duodenum (P less than .001) and 84.2 min longer in the ceca (P less than .001) than the canola meal diet, which accounted for the longer (P less than .001) retention of the soybean meal diet in the entire gastrointestinal tract (388.0 +/- 10.6 vs. 309.8 +/- 10.8 min). Segments of the gastrointestinal tract vary in length, weight, and MRT of digesta with dietary composition and type and body weight of chicken.