Hepatic Steatosis, Carbohydrate Intake, and Food Quotient in Patients with NAFLD

Abstract

Is steatosis related to the spontaneous carbohydrate intake in patients with NAFLD? We performed dietary records for 24 patients with NAFLD, 3 months after their liver biopsy was performed and before the deliverance of a dietary advice. The food quotient, indicator of the proportion of calories from carbohydrates, was calculated as (1.00×% calories from carbohydrates/100) + (0.70×% calories from lipids/100) + (0.81×% calories from proteins/100). The associations between diet variables and steatosis% on the hepatic biopsies were tested by regression analysis, and diet variables were compared according to the presence of fibrosis. The subjects displayed a large range of steatosis, 50.5% ± 25.5 [10–90], correlated with their energy intake (1993 ± 597 kcal/d, r = 0.41, P < 0.05) and food quotient (0.85 ± 0.02, r = 0.42, P < 0.05), which remained significant with both variables by a multivariate regression analysis (r = 0.51, P < 0.05). For the 17/24 patients with a hepatic fibrosis, the energy intake was lower (fibrosis: 1863 ± 503 versus others: 2382 ± 733 kcal/d, P < 0.05), and their food quotients did not differ from patients without fibrosis. Hepatic steatosis was related to the energy and carbohydrate intakes in our patients; the role of dietary carbohydrates was detectable in the range of usual carbohydrate intake: 32% to 58% calories.

Dose–response association between physical activity and non-alcoholic fatty liver disease: a case–control study in a Chinese population

“…Other known risk factors of NAFLD are energy intake and BMI. Several previous studies have found that patients with NAFLD tend to have higher energy intake, and a energy-restricted diet was found to have great benefits for weight loss and improving BMI 38–41. However, few studies have considered sedentary time and energy intake at the same time when investigating the association between physical activity and NAFLD.…”

Phyllanthus Niruri Standardized Extract Alleviates the Progression of Non-Alcoholic Fatty Liver Disease and Decreases Atherosclerotic Risk in Sprague–Dawley Rats

“…Since high rates of carbohydrate and fat consumption increase insulin resistance and oxidative stress [ 70 ], improving insulin signalling can be achieved by decreasing the intake of carbohydrates and lipids, and attenuating the postprandial hyperlipidemia. This might contribute by decreasing the hepatic cholesterol and FFAs pool required for the de novo lipogenesis process in the liver [ 71 , 72 , 73 ]. The same mechanism was also suggested for acarbose, orlistat and ezetimibe as a prospective treatment for lipid metabolic disorders such as obesity and other insulin resistance complications including NAFLD and diabetes [ 59 , 74 , 75 ].…”

Effects of Unbalanced Polyunsaturated Fatty Acid Intake on Obesity-related Metabolic and Hepatic Dysfunctions

“…The current opinion is that hypercaloric foods with a high glycemic index induce IR and initialize the steps of liver damage (6,14). However, not only carbohydrates, but all inadequate nutrient intakes may play an important role in the onset and progression of hepatic and metabolic disorders [7,15]. The carbohydrate energy intake could not be considered excessive because it only slightly (17%) exceeded the RDA.…”