The effects of dietary fats, consisting of different fatty acids, on body fat accumulation and uncoupling protein (UCP) in interscapular brown adipose tissue were studied in rats. Metabolisable energy in experimental diets based on safflower oil, soybean oil or beef tallow was measured strictly (experiment 1). Male Wistar rats were then meal-fed an isoenergetic diet for 8 weeks (experiment 2). Each group of rats showed the same weight gain during the 8-week experimental period. Carcass fat content was greater in rats fed the beef tallow diet than in those fed the with the safflower or soybean oil diets, whereas the weight of abdominal adipose tissue was the same for all three dietary groups. Gene expression of UCP1 and the UCP content of the interscapular brown adipose tissue was lower in the beef tallow diet group than in the other dietary groups. A negative correlation was observed between carcass fat content and n-6 unsaturated fatty acid content in dietary fats. These results suggest that the greater body fat accumulation in rats fed the beef tallow diet results from lower expression of UCP1 mRNA and lower UCP content in brown adipose tissue. n-6 Polyunsaturated fatty acids may be the most effective fatty acids in limiting body fat.
This study examined the effects of a tocotrienol-rich fraction (TRF) obtained from palm oil on the healing of aspirin-induced gastric mucosal lesions. Thirty-six male SpragueDawley rats (200250 g) were randomly divided into three groups. Group I was fed a vitamin E-deficient diet (control), Group II was fed a vitamin E deficient diet supplemented with tocopherol (300 mg/kg food) and Group III was fed a vitamin E-deficient diet supplemented with TRF (300 mg/kg food). After eight weeks, the control and treated groups received a single intragastric dose of 400 mg/kg body weight aspirin. The rats were killed 24 h after exposure to aspirin. Assessment of gastric lesions showed a lower gastric lesion index in the TRF (P = 0.0005) and tocopherol groups (P = 0.0008) compared to the control. The gastric malondialdehyde (MDA) content was also lower in the TRF (P = 0.025) and tocopherol groups (P = 0.025) compared to control. There were, however, no significant differences in the gastric lesion index and gastric MDA content between the TRF and tocopherol-fed groups. There were no significant differences in the adherent gastric mucous concentration and gastric acid concentration among all groups. We conclude that the TRF and tocopherol are equally effective in preventing aspirin-induced gastric lesions. The most probable mechanism is through their ability to limit lipid peroxidation, which is involved in aspirin-induced gastric lesions.
Our previous study demonstrated that curcumin, an active compound of Curcuma xanthorrhiza and C. domestica, produces a positive cholekinetic effect. A 20 mg amount of curcumin is capable of contracting the gall bladder by up to 29% within an observation time of 2 h. The aim of the current study was to define the dosage of curcumin capable of producing a 50% contraction of the gall bladder, and to determine if there is a linear relationship between doubling the curcumin dosage and the doubling of gall bladder contraction. A randomised, single-blind, three-phase, crossover-designed examination was carried out on 12 healthy volunteers. Ultrasonography was carried out serially to measure the gall bladder volume. The data obtained was analysed by analysis of variance (anova). The fasting volumes of gall bladders were similar (P > 0.50), with 17.28 ± 5.47 mL for 20 mg curcumin, 18.34 ± 3.75 mL for 40 mg and 18.24 ± 3.72 mL for 80 mg. The percentage decrease in gall bladder volume 2 h after administration of 20, 40 and 80 mg was 34.10 ± 10.16, 51.15 ± 8.08 and 72.25 ± 8.22, respectively, which was significantly different (P < 0.01). On the basis of the present findings, it appears that the dosage of curcumin capable of producing a 50% contraction of the gall bladder was 40 mg. This study did not show any linear relationship between doubling curcumin dosage and the doubling of gall bladder contraction.
Increased lipid peroxidation plays a role in the pathology associated with fructose feeding. The present study reports the effects of metformin on the liver lipid peroxidation and antioxidant defence system of rats fed a high-fructose diet. The experimental animals were divided into two batches of 12 animals each. The control batch received a control diet containing 60% starch; the second batch was given a high-fructose diet containing 60% fructose as the sole source of carbohydrate. At the end of second week these were each subdivided into two groups. One was given metformin (50 mg/kg body weight/day in water) by intragastric intubation and the other group was left untreated. The rats were continued on the same dietary regimen for the next two weeks. After the experimental period of four weeks, liver lipid peroxidation and antioxidant status were quantified. Enhanced thiobarbituric acid-reactive substance reactivity and lipid hydroperoxides were observed in high-fructose-fed rats. However, the activities of enzymic antioxidants were lower in this group. Administration of metformin attenuated the rise in lipid peroxidation and improved the antioxidant potential in high-fructose-fed rats. Metformin did not have any effect on the antioxidant status of control rats. Attenuation of lipid peroxidation by metformin could be related to its insulin sensitising action.
The objectives of this study were: (i) to investigate the energy, iron, zinc, calcium and vitamin C intakes of a group of healthy term Caucasian infants resident in Dunedin, New Zealand, prospectively from age 9 months to 2 years; and (ii) to determine the prevalence of iron deficiency anaemia among these infants. A self-selected sample of 74 Caucasian mothers and their infants born in Dunedin, New Zealand, between October 1995 and May 1996 were recruited. Dietary intake was determined using estimated diet records at 9, 12, 18 and 24 months of age. Haemoglobin concentration, mean corpuscular volume and zinc protoporphyrin concentration were determined at the same ages. The infants' zinc, calcium and vitamin C intakes appeared adequate. Their median iron intakes ranged from 4.3 mg (at 12 months) to 7.0 mg (at 9 months) per day and were below estimated requirements at all ages. At 9, 12 and 18 months of age, 7% (n = 4) of the infants had iron deficiency anaemia. None of the infants had iron deficiency anaemia at
24 months. The iron intakes of this group of Caucasian infants and young children appeared inadequate. However, their rate of iron deficiency anaemia was lower than has been reported in previous New Zealand studies.
Nutritional assessment reveals the nutritional status of a patient. It thereby helps identify each patient's need for specific nutritional care and facilitates early intervention. Generally, the common nutrition and nutrition-related problems in hospitalised paediatric patients are: protein energy malnutrition in various degrees; vitamin deficiencies such as A, B1, B2, niacin, folic acid, K and E; mineral deficiencies such as Zn, Fe, Ca, Mg, P, K and Na; essential fatty acid deficiencies; carbohydrate intolerance; maldigestion and malabsorption; and overweight and obesity. However, there is limited information about nutritional status of hospitalised patients in some countries, especially in developing countries. In Thailand, it was found that the prevalence of hospital malnutrition in children aged 115 years in the paediatric ward was similar (5060%) to that of a study conducted 10 years earlier. In another study of micronutrients in 45 paediatric AIDS patients (aged 346 months), high prevalences of malnutrition, anaemia and mineral deficiencies were found. For convenience in clinical practice, body mass index (BMI) values for use as an indicator in the assessment of undernutrition in children whose heights are less than 145 cm have been published. These BMI values have been tested and retested using normal children and patients with various degrees of undernutrition and were found to be reliable and valid. Therefore, nutritional status must be assessed in all hospitalised patients. At the very least, weight and height (length) should be obtained.
A double-blind, placebo, controlled trial was conducted in Banyudono subdistrict, Boyolali regency, Central Java province, Indonesia. The aim of the study was to determine whether adding low-dosage vitamin A and riboflavin can enhance the effect of iron-folate supplementation in anaemic pregnant women. From July to November 2000, 202 pregnant women were screened for anaemia (haemoglobin <11.0 g/dL). One hundred and three pregnant women (51%) were found to be anaemic and were then allocated alternately into four groups. Over a period of 60 days, group IF (n = 29) received iron-folate tablets (200 mg FeSO4 and 250 µg folic acid) + 5 mg glucose; group IFR (n = 22) received iron-folate tablets + 5 mg riboflavin; group IFA (n = 29) received iron-folate tablets + 2.75 mg retinyl palmitate (equal to 5000 IU vitamin A); and group IFRA (n = 23) received iron-folate tablets + 5 mg riboflavin + 2.75 mg retinyl palmitate. At the end of the study 19 pregnant women (18.4%) were excluded from the analysis because of various reasons. Statistical analysis was based on 84 women (81.5%): group IF, n = 25; group IFR, n = 22; group IFA, n = 18; and group IFRA, n = 19. Haemoglobin measurements were carried out using the Technicon H1* (cyanmethaemoglobin method). All groups showed a significant increase in haemoglobin concentration (P < 0.05), except group IFA (P > 0.05), with the highest increment being in group IFR. Multiple comparisons only showed significant differences between group IFR and group IFA (P < 0.05). It can be concluded that iron-folate supplementation can increase haemoglobin concentrations in anaemic pregnant women. Adding riboflavin tends to enhance the effect of iron-folate supplementation, but this is not the case with adding vitamin A.
The aim of this study was to investigate the impact of magnesium-enriched, high-calcium milk on serum parathyroid hormone (PTH) and biochemical markers of bone turnover in postmenopausal women. We recruited 50 healthy postmenopausal women to take part in this randomised controlled study. Half of the women consumed two serves of high-calcium skim milk enriched with magnesium (milk group) and half consumed two serves apple drink per day (apple group), each for 4 weeks. The milk provided 1200 mg calcium and an additional 106 mg magnesium. We investigated the responses of serum PTH, as well as the serum and urinary calcium, magnesium and biochemical markers of bone turnover. There was no effect of time or drink on the clinical biochemistry, serum PTH or urine markers of bone resorption (free deoxypyridinoline and Ntelopeptides). Serum C-telopeptides (CTX), another marker of bone resorption, did not change with time in the apple group. However, in the milk group, serum CTX decreased significantly from 0.43 ± 0.04 ng/mL to 0.32 ± 0.02 at 2 weeks (p < 0.0001) and 0.28 ± 0.02 at 4 weeks (p < 0.0001). In the milk group, urinary calcium and magnesium each increased during the night but not during the day. Overall, these data suggest that milk has an antiresorptive effect on bone, but that this is not accompanied by measurable changes in serum PTH.
The correspondence between the dietary fibre contents of 28 breakfast cereals and their faecal bulking efficacies was measured and used to assess criterion values controlling nutrient claims for dietary fibre. A valid, standardised rat assay was used to measure faecal bulking efficacy as the content of wheat bran equivalents for faecal bulk (WBEfb) in the cereals. Regression analysis of WBEfb content against dietary fibre content allowed the adequacy of criterion fibre values for claims of 'source of fibre,''high in fibre' and 'very high in fibre' to be assessed relative to a daily reference requirement of 63 WBEfb, based on human data. Faecal bulking by breakfast cereals was much lower than implied by the dietary fibre claims associated with them. Many more were claimed to be 'high' or 'very high' in dietary fibre (n = 13) than were 'high' or 'very high' in faecal bulking efficacy (n = 4). Conversely, dietary fibre requirements per serving predicted from WBEfb requirements, as necessary to maintain adequate faecal bulk in the current Australian diet, were much higher (4.4 g) than the criterion fibre content (1.5 g) for the most modest claim, 'source of fibre'. After removing four high-bran cereals (>15% dietary fibre) from the analysis, a modest correlation of r = 0.62 between dietary fibre content and faecal bulk was obtained. It is concluded that, with respect to breakfast cereals, fibre values specified for nutrient claims are too low, dietary fibre content is not a reliable guide to faecal bulking efficacy and direct measures of faecal bulking capacity would be more useful than dietary fibre content in describing faecal bulking efficacy for evidence-based food choice.
The aim of this study was to determine the acute and chronic effects of low doses of long chain (LC) n-3 polyunsaturated fatty acids (PUFA) (<100 mg per day) on plasma LC n-3 PUFA levels using a novel delivery form; bread containing microencapsulated tuna oil (MTO). Six omnivores (three men and three women) participated in the acute study, which involved ingesting a prototype MTO bread containing approximately 80 mg of LC n-3 PUFA/four slices. Plasma triacylglycerol fatty acid compositions were measured after an overnight fast and postprandially at 2 and 4 h. In the chronic study, 10 vegetarian subjects (nine men and one woman) consumed MTO bread at six to eight slices/day (comprising 60 mg of LC n-3 PUFA) as the only dietary source of these PUFA for three weeks. Fasting plasma total and
phospholipid fatty acid compositions were measured at baseline and endpoint. In the acute study, the proportions of 22:6 n-3 and total n-3 PUFA in plasma triacylglycerol were significantly increased (P < 0.05). In the chronic study, the proportions of 20:5 n-3, 22:5 n3, 22:6 n-3, total n-3 PUFA in plasma, and 22:6 n-3 and total n-3 PUFA in plasma phospholipid fractions were significantly increased (P < 0.05) at the endpoint compared with the baseline. This study showed that a low dose of LC n-3 PUFA, consumed as MTO-enriched bread, was bioavailable, as measured by an increase in LC n-3 PUFA levels in the plasma of human subjects.
The purpose of this study was to investigate the effect of green tea catechin on the cyclooxygenase and lipoxygenase pathways in chronic cadmium-poisoned rats. SpragueDawley male rats weighing 100 ± 10 g were randomly assigned to one normal and three cadmium-poisoned groups. The cadmium groups were classified as catechin-free diet group (Cd-0C), 0.25% catechin diet group (Cd-0.25C) and 0.5% catechin diet group (Cd0.5C), in accordance with the level of catechin supplement. The phospholipase A2 activity was remarkably increased 117% in the Cd-0C group and 60% in the Cd-0.25C group compared with the normal group, and the level in the Cd-0.5C group was the same as the normal group. Activity of platelet cyclooxygenase increased 284% in the Cd-0C group, 147% in the Cd-0.25C group and 193% in the Cd-0.5C group. The synthesis of platelet thromboxane A2 (TXA2) increased 157% in the Cd-0C group and 105% in the Cd-0.25C group, compared with the normal group. The Cd-0.5C group showed the same level as the normal group. Prostacyclin (PGI2) formation in the aorta decreased 24% in the Cd-0C group and 18% in the Cd-0.25C group. The ratio of PGI2/TXA2, the thrombocyte synthesis index, decreased 70% in the Cd-0C group and 59% in the Cd-0.25C group. The activity of 5'-lipoxygenase in the polymorphonuclear leukocyte was increased 40% in the Cd-0C group as compared with the normal group. Catechin-supplemented Cd-0.25C and Cd-0.5C groups showed the level of the normal group. In this study, the observed content of leukotriene B4, which induces the inflammatory process, increased 54% in the Cd-0C group, and in catechin-supplemented groups, showed the same level as in the normal group. The serum peroxide value increased 60% in the Cd-0C group compared with the normal group; but in the Cd-0.5C group, it showed the level of the normal group. These results indicate that chronic cadmium poisoning in rats accelerates arachidonic acid metabolism. Inhibition of arachidonic acid metabolism due to catechin supplementation, however, decreases platelet aggregation and inflammatory action. In conclusion, it would appear that green tea catechin supplementation in chronic cadmium-poisoned rats inhibits the arachidonic acid cascade by regulating the activity of phospholipase A2.
Thirty-two commercially available teas consisting of green, oolong and black teas were bought from supermarkets in Christchurch, New Zealand in June 2001. Fifteen herbal teas were also purchased at the same time. The soluble oxalate content of the infusate made from each of the teas was determined using high pressure liquid chromatography. The mean soluble oxalate contents of black tea in tea bags and loose tea leaves were 4.68 and 5.11 mg/g tea, respectively, while green teas and oolong tea had lower oxalate contents, ranging from 0.23 to 1.15 mg/g tea. The soluble oxalate content of the herbal teas ranged from not detected to 3.00 mg/g tea. A regular tea drinker consuming six cups of tea/day would have an intake of between 26.46 and 98.58 mg soluble oxalate/day from loose black tea, 17.88 and 93.66 mg soluble oxalate/day from black tea in tea bags and a maximum of 18.0 mg/day from herbal teas. The oxalate intake from the regular daily consumption of black teas is modest when compared to the amounts of soluble oxalate that can be found in common foods. However, oxalate in black teas has the potential to bind to a significant proportion of calcium in the milk, which is commonly consumed with the black teas.