Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in Western countries and is strongly associated with obesity and insulin resistance-related comorbidities. Moreover, there is some evidence of a relationship between NAFLD and depression. The aim of this study was to compare the effect of two personalized energy-restricted diets on liver fat and depressive symptoms in overweight or obese subjects with NAFLD after a 6-month follow-up.

Ninety-eight overweight or obese adults with NAFLD were enrolled and randomized to follow one of two different personalized energy-restricted diets (American Heart Association vs. FLiO diet) accompanied by healthy lifestyle advice. Study registered as FLiO: Fatty Liver in Obesity; NCT03183193. Anthropometry, body composition, biochemical features and liver status were assessed at baseline and after a 6-month follow-up. Liver fat was evaluated by Magnetic Resonance Imaging and depressive symptoms using the Beck's Depression Inventory-II (BDI-II).

Participants of both groups showed significant reductions in body weight, total fat mass, glucose, insulin and alanine aminotransferase (p < 0.001 for all these parameters in both groups). A significant decrease in liver fat (p < 0.001 in both groups) and depressive symptoms (p < 0.01 in both groups) was observed after the follow-up. The effects of the intervention in the evaluated variables did not differ when both diets were compared. Consequently, the two groups were considered together as one sample for the further analyses. Correlation analyses evidenced a positive association between the decrease in depressive symptoms and the reduction in body weight (r = 0.241; p = 0.044) and liver fat (r = 0.251; p = 0.046).

Previous studies have reported that the prevalence of depression in patients with chronic liver disease (including NAFLD) is higher than in the general population and that major depressive disorder is associated with more severe hepatic steatosis and with worse outcomes in the treatment of NAFLD subjects. In our study, both healthy personalized energy-restricted diets were able to improve metabolic parameters, liver fat content and depressive symptoms in overweight and obese participants with NAFLD. To our knowledge, this is the first study to report an association between the changes in depressive symptoms and the decrease in liver fat after a dietary randomized controlled trial. Further investigation is needed to clarify the relationship between depression and the development and treatment of NAFLD.

Dietary components are contributing factors in the development of Nonalcoholic fatty liver disease (NAFLD). The glycaemic index (GI), glycaemic load (GL) and total antioxidant capacity (TAC) have been considered potential dietary tools influencing diet–disease relationships. The aim of this study was to evaluate associations of the dietary GI, GL, TAC and insulin resistance (IR) condition with hepatic fat in NAFLD adults.

Material and methods: 112 overweight/obese adults with NAFLD (age: 50.8 ± 9 years old) were included in the trial. Dietary intake was assessed by a validated 137-item food frequency questionnaire (FFQ). Anthropometric, glycemic and lipid profiles, fatty liver quantification by magnetic resonance imaging (MRI) and IR measured by the Homeostatic Model Assessment of IR (HOMA-IR) were assessed at baseline. This study was registered as FLiO: Fatty Liver in Obesity study; NCT03183193.

Results: The median of liver fat content by MRI was 6.4 (3.8–10.9) in the recruited population. Participants with higher liver fat content showed significantly increased values of glucose, insulin, HbA1c and HOMA-IR than those with lower liver fat content (p < 0.05). Correlation analyses revealed relevant positive associations of hepatic fat with GI (r = 0.17; p = 0.077) and GL (r = 0.19; p = 0.047). Also, a negative association between liver fat content and TAC (r = -0.22; p = 0.023) was found. Linear regression analyses were used to examine the associations of hepatic fat and dietary quality indicators as well as IR adjusted for potential confounders (sex, age and physical activity). The final models showed that HOMA-IR, GI, GL and TAC were able to explain between 22.4 and 22.8 % (p < 0.001) of the variability of liver fat content.

The pathophysiology of NAFLD is thought to be associated with dietary determinants that contribute to metabolic dysregulation such as IR, ectopic liver fat deposition and hepatic damage. In accordance with other authors, we suggest that monitoring GI, GL and TAC may be useful approaches for the dietary treatment of NAFLD since they are related to hepatic fat. Additionally, it is important to highlight the essential role of IR in NAFLD as a key mediator in the development of NAFLD. Certainly, findings of the present study revealed a significant association of hepatic fat accumulation and IR.

In summary, GI, GL and TAC are potential markers of diet quality, with an impact on susceptible population at hepatic risk.