NAFLD
Conditions
Brief summary
The major adverse health consequences of obesity occur only when non-alcoholic fatty liver disease (NAFLD) also develops. NAFLD is characterized by abnormal hepatic accumulation of triglycerides and other lipids. The first-line approach to NAFLD management is caloric restriction and weight loss, but these remain difficult to achieve. Little attention has been given to dietary carbohydrate restriction, despite recent reports showing that hepatic de novo lipogenesis, a process that converts dietary carbohydrates into fatty acids in the postprandial state, accounts for approximately 25% of liver triglyceride content in hyperinsulinemic subjects with NAFLD. For comparison, only 15% of the liver triglycerides were derived from dietary fatty acids in patients with NAFLD who had consumed a standardized 30% fat diet for four days before being assessed.
Detailed description
To establish the time-course of hepatic fat loss in NAFLD subjects on a carbohydrate-restricted diet (\<20 g/day), a serial assessments of liver fat during two week diet will be performed. Also, markers of lipid and insulin metabolism, liver function test and changes in gut microbiota during rapid metabolic improvement will be assessed. The overall aim is to exploit this unique set of human material to determine the specific cellular and molecular pathways that are modified in the early stages of metabolic improvement and fatty liver regression.
Interventions
OTHERLow carbohydrate diet
Isocaloric, carbohydrate restricted diet 14 days
Sponsors
Sahlgrenska University Hospital
Göteborg University
Helsinki University Central Hospital
Study design
Allocation
NA
Intervention model
SINGLE_GROUP
Primary purpose
TREATMENT
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
20 Years to 70 Years
Healthy volunteers
Yes
Inclusion criteria
* increased liver fat above 5 % in magnetic resonance spectroscopy * body mass index 27-39.9 kg/m2
Exclusion criteria
* liver cirrhosis * portal hypertension * chronic liver disease other than NAFLD * diabetes mellitus or other significant endocrine disease * any medication acting on nuclear hormone receptors or inducing liver enzymes or self-administration of supplements other than calcium or vitamins/trace elements * any significant cardiovascular co-morbidity * history of non-compliance * genotype (PNPLA3-MM and TM6SF2-TT) promoting liver fat accumulation
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Liver fat percent by nuclear magnetic resonance imaging | 14 days | Liver fat percent measured by nuclear magnetic resonance imaging |
Secondary
| Measure | Time frame |
|---|---|
| De novo lipogenesis measured as Incorporation of new fatty acids (%) to very-low density lipoprotein triglycerides | 14 days |
| Gut microbiota measured as change in microbiome profile from baseline | 14 days |
Countries
Finland, Sweden
Outcome results
None listed