Patients with liver cirrhosis are in a state of protein and energy malnutrition (PEM), and this can lead to patients' poor prognosis and quality of life. Metabolic abnormalities such as hypermetabolism or decreased glucose level and increased fat oxidation, as measured by indirect calorimetry, might trigger and/or worsen PEM. Supplementation with branched-chain amino acids (BCAA) improves hepatic encephalopathy and protein malnutrition (e.g., increasing the serum albumin level and improving the nitrogen balance), and subsequently improves patients' prognosis and quality of life. Late evening snack (LES) shortens the starvation period during the night in cirrhosis. Decreased respiratory quotient, suggesting patients' poor prognosis, was recovered to almost normal by LES. This might help to prevent the reduction of muscle volume and fat tissue, improving energy malnutrition in cirrhosis. Preservation of muscle volume is a critical issue for the patients whose muscle strength is weakened, which contributes to poor quality of life. In future studies, the mechanism of the clinical effects of BCAA and LES should be elucidated for the improvement of PEM in patients with cirrhosis.
The calcium intake should be adequate to prevent osteoporosis. The Japanese often eat fish, and small fish whose bones can be eaten are an important source of calcium. However, there have been only a few studies on fish bones, and fish bones are not efficiently used in the diet at present. To enable more efficient use of fish bones, we immersed the bones of horse mackerel in an acetic acid solution and evaluated changes in the crystallinity of bone apatite and in the inorganic components. Raw or steamed horse mackerel bones were immersed in a4% acetic acid solution for 120h. The crystal structure of bone apatite was measured by an X-ray diffraction analysis and the inorganic components were measured by ICP-AES. The crystallinity of fish bones immersed in the acetic acid solution showed a negligible change after 4h, but the amorphous part increased after 24h. Among the inorganic components, calcium, phosphorus, magnesium, and manganese rapidly decreased early after immersion. This decrease in such inorganic components as calcium, despite a negligible change in the crystallinity of bone apatite in the early stage of immersion, suggests the presence of calcium phosphate other than apatite in horse mackerel bones. When the fish bones were heated before immersion, the crystallinity of apatite was improved. Even after immersing the heated bones in the acetic acid solution, the amorphous part increased, while the apatite structure remained and inorganic components were difficult to elute. The softening of fish bones after their immersion in the acetic acid solution may be due to the elution of calcium phosphate that did not crystallize as apatite, with subsequent disintegration and elution of the crystalline apatite. Therefore, the vinegar solution used for immersing the bones contained inorganic substances eluted from the bone, and its use as a source of calcium would be suitable for increasing calcium intake.
Changes in intestinal epithelial integrity have been postulated to explain the association between vitamin A status and diarrhoeal disease in children living in areas where vitamin A deficiency is a major public health problem. Fatty acids are an integral component of normal enterocyte structure, and changes to their profile in the intestinal mucosa may impact on the efficacy of the mucosal barrier. The aim of this study therefore was to determine the effect of vitamin A deficiency on intestinal mucosal fatty acid profile. Weanling male specific pathogen free rats were maintained on a vitamin A deficient diet for either 40-42 (subclinical deficiency) or 60-63 days (clinical deficiency), and compared with rats pair fed or allowed free access to the same diet, but supplemented with vitamin A (vitamin A sufficient). Fatty acid profile of jejunal mucosal homogenates was determined using gas chromatography. While subclinically vitamin A deficient rats had only minor differences in fatty acid profile as compared with pair fed and vitamin A sufficient rats, there were marked differences in a number of fatty acids in the clinically vitamin A deficient rats. Clinically vitamin A deficient rats had more arachidonic acid (C20: 4n-6) than pair fed rats, and less linoleic acid (C18: 2n-6) than both pair fed and vitamin A sufficient rats. These findings suggest that vitamin A deficiency modifies intestinal mucosal fatty acid composition such that there is an increase in proinflammatory eicosanoid precursors. This may contribute towards our understanding of a biological mechanism of the epidemiological association between vitamin A status and diarrhoeal disease.
The effects of essential fatty acid (EFA) deficiency were studied on male Wistar rats membrane lipid composition, enzyme activities and proliferation of liver peroxisome by feeding the animals, during 4 weeks, with fat free diets supplemented or not with a peroxisome proliferator, clofibrate (CLO). In deficient (E) goup, peroxisomal membrane was characterized by higher level of total de novo synthesized unsaturated (n-9 and n-7 series) fatty acids and lower content of EFA (n-6 and n-3 series) and exhibited cholesterol (CHOL) to phospholipids (PLs) ratio diminution compared with that of control (C) group. Co-administration of CLO with the fat-free diet (EC group) enhanced the membrane uptake of n-9 fatty acids. Slight increase of membrane dihydroxyacetone-phosphate acyl-transferase (DHAP-AT) and decrease of palmitoyl-CoA synthetase activities were found in E group which featured normal-shaped peroxisomes. In EC group, enzyme inductions of peroxisomal pamitoyl-CoA oxidase and palmitoyl-CoA synthetase were slightly higher and significantly lower respectively compared with those of C group treated with CLO (CC group) whereas activity of DHAP-AT was stable. Identical marked proliferation of peroxisomes were observed in both groups. It is inferred that, despite the parallel alterations of membrane lipid composition and of enzyme activities of peroxisomes upon 4 weeks of EFA deficientdiet, the biogenesis and proliferation of the organelles were independently processed at a normal level. The possibility of homeostatic regulation and its physiological importance were discussed.
A study was conducted to determine whether the catabolism of an intravenously injected fat emulsion could be correlated with lipoprotein lipase (LPL) mass and activity in postheparin plasma. We observed the relationship between the fractional removal rate (K2) of an intravenously injected fat emulsion (Intralipid®) and LPL mass and activity in postheparin plasma of 20 normolipidemic and 21 hypertriglyceridemic subjects. The K2 level was determined by the intravenous fat emulsion tolerance test. LPL mass was measured by a sandwich enzyme immunoassay system. K2 was significantly correlated with the LPL mass in total group of subjects (r=0.51, p<0.001), as well as in normolipidemic (r=0.72, p<0.001) and hypertriglyceridemic (r=0.43, p<0.05) subgroups. K2 was also significantly correlated with LPL activity in the total group (r=0.40, p<0.05), as well as in the normolipidemic subjects (r=0.55, p<0.05). Kinetics following an intravenous injection of a fat emulsion reflect LPL mass and activity in postheparin plasma.
Membrane lipid composition influences a number of immune functions including those of neutrophils, an important defense against infection after burn injury that has also been implicated in causing damage to host tissues. This study investigates compositional changes in phospholipid (PL) fatty acids and functional alterations of neutrophils immediately following and during recovery from burn injury. Ten patients with>10% total body surface area burn had blood drawn at specific times (0 days to>50 days) following burn injury. Neutrophil lipids were extracted, major PL classes separated by thin layer chromatography, and fatty acid composition determined using gas liquid chromatography. Neutrophil granularity and oxidative burst were measured in whole blood before and after stimulation with phorbol myristate acetate using flow cytometry. Neutrophils were less granular and had a greater oxidative burst early (<20 days) vs. later (>50 days) after burn injury. The arachidonic acid (20: 4n-6) content in all PL fractions was significantly reduced following burn injury and increased with recovery (p<0.05). The total n-6 fatty acid content of PS and PI increased with recovery (p<0.05). In conclusion, reduced 20: 4n-6 in neutrophil PL is suggestive of increased release or reduced synthesis of 20: 4n-6 early after burn. Lower granularity and higher oxidative burst immediately post-injury normalized with increases in 20: 4n-6. Compositional changes in neutrophil membranes early after burn may impact effector functions of neutrophils. Further work is needed to develop nutritional intervention strategies designed to modulate fatty acid composition of neutrophils to reduce the harmful effects of the oxidative burst while maintaining important infection defense mechanisms following burn injury.
Oxygen radical-mediated lipid peroxidation is involved in the tissue injury of inflammatory bowel disease. The present study investigated the effects of a novel water-soluble vitamin E derivative, 2-(α-D-glucopyranosyl) methyl-2, 5, 7, 8-tetramethylchroman-6-ol (TMG), on dextran sulfate sodium-induced olonic inflammation in mice. Acute colitis was induced in female mice by giving 8% dextran sulfate sodium orally in drinking water for 7 days. Animals were randomized to different concentrations of TMG (1, 10, and 100mg/kg) or physiologic saline (vehicle) by daily intraperitoneal injection. After days of dextran sulfate sodium administration, mice had severe colonic nflammation characterized by significant decreases in total colon length, increases in luminal hemoglobin content and colonic myeloperoxidase activity. TMG at doses of 10 and 100mg/kg reduced colonic injury and inflammation. The contents of thiobarbituric acid-reactive substances were significantly increased by dextran sulfate sodium administration, and this increase was reduced by TMG. These results indicate that the protective effect of TMG against colonic injury induced by dextran sulfate sodium may result, in part, from its inhibitory action toward lipid peroxidation, as well as from reducedneutrophil recruitment into the inflammatory site.