Nutritional assessments of patients with non-alcoholic fatty liver disease.
ABSTRACT Obesity is not only associated with nonalcoholic fatty liver disease (NAFLD) but it also adversely affects the progression of other liver diseases. There are limited data regarding the dietary habits of patients with chronic liver disease.
Nutrition surveys containing 13 different food groups were mailed. Nutrition scores were calculated based on weekly servings. Foods were also divided into USDA food pyramid categories with conversion of each group into calories expended. Clinico-demographic data were available. NAFLD patients were compared to patients with chronic viral hepatitis.
A total of 233 subjects were included: age 52.5 +/- 10.0 years, Body mass index (BMI) 28.1 +/- 6.5, MS 24.2%, 31.8% NAFLD, 48.1% hepatitis C virus (HCV), and 20.2% hepatitis B virus (HBV). Six nutrition indices were different among the groups. NAFLD and HCV consumed more low-nutrient food (p = 0.0037 and 0.0011) and more high-sodium food than HBV (p = 0.0052 and 0.0161). Multivariate analysis showed that NAFLD and HCV consumed more high-fat sources of meat/protein than HBV (p = 0.0887 and 0.0626). NAFLD patients consumed less calories from fruits compared to HCV and HBV patients (p = 0.0273 and 0.0023). Nine nutrition indices differed according to BMI. Univariate analysis showed that obese/overweight patients consumed more high-fat sources of meat/protein (p = 0.0078 and 0.0149) and more high-sodium foods (p = 0.0089 and 0.0062) compared to the normal-weight patients. In multivariate analysis, normal-weight patients consumed more fruits than obese (p = 0.0307). Overweight patients also consumed more calories of meat and oil than normal-weight patients (p = 0.0185 and 0.0287).
NAFLD and HCV patients have similar dietary habits. Patients with HBV have the healthiest dietary habits. Specific dietary interventions should focus on decreasing intake of low-nutrient and high-sodium food, as well as high-fat sources of meat/protein.
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ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is now recognized as one of the most important causes of chronic liver disease in Western Countries, and is the hepatic manifestation of metabolic syndrome. The prevalence of NAFLD has increased with the global epidemic of obesity and type 2 diabetes mellitus. The pathophysiological hallmark of NAFLD is insulin resistance, associated with mediators of oxidative stress and inflammatory cytokines. Although simple steatosis by itself is generally benign, patients with histologically proven non-alcoholic steatohepatitis (NASH) can progress to cirrhosis. Hepatitis C (HCV) is another common cause of liver disease with some potential for progression to cirrhosis. Steatosis is present in almost 50% of patients infected by HCV. Hepatic steatosis in the setting of another liver disease (such as HCV) is associated liver disease progression. In particular, significant fibrosis is observed in patients with HCV whose liver biopsies show significant steatosis or superimposed NASH. This article reviews the host and viral factors potentially involved in the interaction between NAFLD and HCV. These factors include mediators of metabolic syndrome such as adipokines, inflammatory cytokines, factors associated with oxidative stress, lipid peroxidation products, as well as apoptosis and hepatic stellate cell activation with the resultant deposition of extracellular matrix. In addition to the mediators of metabolic syndrome (host factors), hepatic steatosis can be influenced by viral factors. The most important viral factor is HCV genotype 3, which has been independently associated with hepatic steatosis. Finally, superimposed NAFLD and visceral fat are associated with lower response rates to antiviral therapy in non-genotype 3 patients. Furthermore, viral clearance is associated with the resolution of hepatic steatosis in HCV genotype 3 but not other HCV genotypes. In these genotypes, hepatic steatosis and its impact on response to therapy are related to metabolic syndrome. Thus, the management of obesity and metabolic syndrome in patients with chronic hepatitis C may be important for reducing the risk of progression as well as improving the efficacy of antiviral therapy.Minerva gastroenterologica e dietologica 07/2006; 52(2):135-43.
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ABSTRACT: Nonalcoholic fatty liver disease is frequently associated with type 2 diabetes mellitus, obesity, and dyslipidemia, but some patients have normal glucose tolerance or normal weight. We tested the hypothesis that there is an association between nonalcoholic fatty liver disease and insulin resistance that is independent of diabetes and obesity. We measured anthropometric and metabolic variables in 46 patients with chronically elevated serum aminotransferase levels, "bright liver" on ultrasound scan, and normal glucose tolerance. Indexes of insulin resistance and secretion were determined using the homeostasis model assessment method. They were compared with 92 normal subjects who were matched for age and sex. Patients with nonalcoholic fatty liver disease were characterized by fasting and glucose-induced hyperinsulinemia, insulin resistance, postload hypoglycemia, and hypertriglyceridemia. Insulin resistance [odds ratio (OR) = 15 per percent increase, 95% confidence interval (CI): 3.0 to 70], fasting triglyceride level (OR = 3.1 per mmol/liter increase, 95% CI: 1.1 to 8.9), 180-minute blood glucose level (OR = 4.3 per mmol/ liter decrease, 95% CI: 1.6 to 12), and average insulin concentration in response to oral glucose (OR = 3.0 per 100 pmol/liter increase, 95% CI: 1.5 to 6.2) were independently associated with nonalcoholic fatty liver disease. The exclusion of overweight and obese subjects did not change the results. Nonalcoholic fatty liver disease is associated with insulin resistance and hyperinsulinemia even in lean subjects with normal glucose tolerance. Genetic factors that reduce insulin sensitivity and increase serum triglyceride levels may be responsible for its development.The American Journal of Medicine 12/1999; 107(5):450-5. · 4.77 Impact Factor
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ABSTRACT: The results of previous studies suggest that de novo lipogenesis may play an important role in the etiology of obesity, particularly during overconsumption of different carbohydrates. We hypothesized that de novo lipogenesis would increase during overfeeding, would vary depending on the type of carbohydrate consumed, and would be greater in obese than in lean women. De novo lipogenesis was measured during 96 h of overfeeding by 50% with either sucrose or glucose and during an energy balance treatment (control) in 8 lean and 5 obese women. De novo lipogenesis was determined by measuring the amount of deuterium incorporation into plasma triacylglycerols. Fat and carbohydrate balance were measured simultaneously by continuous whole-body calorimetry. De novo lipogenesis did not differ significantly between lean and obese subjects, except with the control treatment, for which de novo lipogenesis was greater in the obese subjects. De novo lipogenesis was 2- to 3-fold higher after overfeeding by 50% than after the control treatment in all subjects. The type of carbohydrate overfeeding (sucrose or glucose) had no significant effect on de novo lipogenesis in either subject group. Estimated amounts of absolute VLDL production ranged from a minimum of 2 g/d (control) to a maximum of 10 g/d after overfeeding. This compares with a mean fat balance of approximately 275 g after 96 h of overfeeding. Individual subjects showed characteristic amounts of de novo lipogenesis, suggesting constitutive (possibly genetic) differences. De novo lipogenesis increases after overfeeding with glucose and sucrose to the same extent in lean and obese women but does not contribute greatly to total fat balance.American Journal of Clinical Nutrition 01/2002; 74(6):737-46. · 6.50 Impact Factor