In non-obese NAFLD patients: 1) although visceral fat was increased, insulin resistance and/or dysregulated secretion of adipocytokines was not necessarily shown; 2) intakes of total energy and carbohydrates were not excessive, although dietary cholesterol was superabundant and dietary PUFAs were significantly lower compared with those in obese patients; and 3) characteristic fat intake may be associated with the formation of NAFLD.
Nonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of health problems in Western (industrialized) countries. Moreover, the incidence of infantile NAFLD is increasing, with some of these patients progressing to nonalcoholic steatohepatitis. These trends depend on dietary habits and life-style. In particular, overeating and its associated obesity affect the development of NAFLD. Nutritional problems in patients with NAFLD include excess intake of energy, carbohydrates, and lipids, and shortages of polyunsaturated fatty acids, vitamins, and minerals. Although nutritional therapeutic approaches are required for prophylaxis and treatment of NAFLD, continuous nutrition therapy is difficult for many patients because of their dietary habits and lifestyle, and because the motivation for treatment differs among patients. Thus, it is necessary to assess the nutritional background and to identify nutritional problems in each patient with NAFLD. When assessing dietary habits, it is important to individually evaluate those that are consumed excessively or insufficiently, as well as inappropriate eating behaviors. Successful nutrition therapy requires patient education, based on assessments of individual nutrients, and continuing the treatment. In this article, we update knowledge about NAFLD, review the important aspects of nutritional assessment targeting treatment success, and present some concrete nutritional care plans which can be applied generally.
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease that ranges in severity from simple steatosis to cirrhosis. NAFLD is considered to be associated with hepatic metabolic disorders, resulting in overaccumulation of fatty acids/triglycerides and cholesterol. The pathogenesis and progression of NAFLD are generally explained by the “two-hit theory.” Most studies of lipid metabolism in the NAFLD liver have focused on the metabolism of fatty acids/triglycerides; therefore, the impact of cholesterol metabolism is still ambiguous. In this paper, we review recent studies on NAFLD from the viewpoint of hepatic lipid metabolism-associated factors and discuss the impact of disordered cholesterol metabolism in the etiology of NAFLD. The clinical significance of managing cholesterol metabolism, an option for the treatment of NAFLD, is also discussed.
These results suggest that, in HCV-infected liver, the cholesterol load increases and cholesterol uptake is controlled, while de novo cholesterol synthesis is upregulated compared with the normal physiological state. The positive correlations in the expression levels of some cholesterol metabolism-associated genes indicate that not all of the metabolic pathways are dysregulated in HCV-infected liver.
Water chestnut is an annual aquatic plant that grows in Asia and Europe. Although water chestnut has been used as food and herbal medicine, its physiological functions and active ingredients are unknown. Here, we extracted polyphenols from the husk of the Japanese water chestnut (Trapa japonica) and assessed their effects on blood glucose levels. Three hydrolysable polyphenolics (WCPs), eugeniin, 1,2,3,6-tetra-O-galloyl-β-d-glucopyranose, and trapain, were predominant with dry-weight contents of 2.3 ± 0.0, 2.7 ± 0.1, and 1.2 ± 0.1g/100g, respectively. These WCPs exhibited inhibitory activity against α-amylase and α-glucosidase. Whereas (-)-epigallocatechin gallate does not inhibit α-amylase, WCPs exhibited high inhibitory activity (>80% at 0.15 mg/mL). In mice, administration of WCPs (40 mg/kg) significantly reduced blood glucose and serum insulin levels as assessed by the carbohydrate tolerance test.
Self-monitoring of urinary salt excretion helps to improve 24 h urinary Na:K, salt check sheet scores and stage of eating behaviour. Thus, usage of self-monitoring tools has an educational potential in salt intake reduction.
The objective was to investigate the validity of a self-monitoring device that estimates 24-h urinary salt excretion from overnight urine samples as a tool for education regarding salt restriction. Twenty healthy volunteers consumed test meals for 14 days, with salt content as follows: 10 g (days 1-5); 5 g (days 6-8, 12 and 14); and 13 g (days 9-11 and 13). On days 2-15, urinary salt excretion was estimated from overnight urine samples by a self-monitoring device. Twenty-four-hour urine samples were collected on days 5 and 8 to measure salt excretion directly. Blood pressure was measured in the morning and during sleep on days 1-15. Estimated urinary salt excretion measured by the device showed a correlation with salt intake, and the ratio of estimated urinary salt excretion to salt intake was 0.84±0.10 (days 2-6), 1.27±0.28 (days 7-9), 0.70±0.11 (days 10-12), 1.37±0.22 (day 13), 0.68±0.13 (day 14) and 1.33±0.19 (day 15). The correlation between estimated urinary salt excretion measured by a device and directly measured 24-h urinary salt excretion was significant (r=0.65, P<0.05) during the period of 10 g salt intake, but not during 5 g salt intake. Blood pressure in the morning was not influenced by the change in salt intake, but systolic pressure during sleep showed a significant increase or decrease according to the levels of salt intake. In conclusion, a self-monitoring device, which can estimate 24-h urinary salt excretion from overnight urine samples, is considered to be a practical tool for education regarding salt restriction, although a similar future investigation is needed in older and/or hypertensive subjects.
Abstract. This study aimed to examine the usefulness of the self-monitoring of urinary salt excretion for educating individuals about the risk of excessive dietary salt intake. The subjects were 30 volunteers (15 men and 15 women) not consuming anti-hypertensive medication. The subjects measured urinary salt excretion at home for 4 weeks using a self-monitoring device. Blood pressure (BP), anthropometric variables and nutritional variables (by a dietary-habits questionnaire) were measured before and after the measurement of urinary salt excretion. Statistical analyses were performed, including paired t-tests, Chi-square test, Pearson's product moment correlation coefficient and multiple linear regression analysis. In all subjects, the average urinary salt excretion over 4 weeks was 8.05±1.61 g/day and the range (maximum-minimum value) was 5.58±2.15 g/day. Salt excretion decreased significantly in weeks 3 and 4 (P<0.05 and P<0.01, respectively). Diastolic BP decreased from 77.7±14.3 (at baseline) to 74.3±13.3 after 4 weeks (P<0.05), while systolic BP and anthropometric variables remained unchanged. Nutrition surveys indicated that energy intake was correlated with salt intake both before and after the measurements; changes in both variables during the observation period were correlated (r=0.40, P<0.05). The percentage of subjects who were aware of the restriction in dietary salt intake increased from 47 to 90%. In conclusion, daily monitoring of the amount of urinary salt excretion using a selfmonitoring device appears to be an effective educational tool for improving the quality of life of healthy adults.
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