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. 2020 Mar 7;37(4):1381–1406. doi: 10.1007/s12325-020-01281-6

Table 2.

Dietary intervention studies

Study Participants Proportion of patients with both NAFLD and T2D (% of total participants) Study design Intervention Assessment of liver outcomes Duration Change in body weight Liver outcomes
Lim et al. (2011) [48] 11 M + F with T2D Not reported. Mean IHTAG of cohort was 12.8 ± 8.0% Interventional Hypocaloric diet (~ 600 kcal/day) MRI 8 weeks ~ 15% reduction IHTAG decreased by ~ 70% following the intervention
Taylor et al. (2018) [50] 45 M + F with T2D Not reported. Mean IHTAG of cohort was 16.0 ± 1.3% Subgroup analysis of the DiRECT study [49] Hypocaloric diet (~ 825–853 kcal/day) for 3–5 months, followed by food reintroduction for 2–8 weeks, followed by follow-up support until 12 months MRI 12 months ~ 14.1 kg reduction in responders vs. ~ 9.4 kg reduction in non-responders IHTAG decreased by ~ 14% in responders vs. ~ 10% in non-responders (absolute values). NSD between groups
Petersen et al. (2005) [52] 8 M + F with T2D 100% Interventional Hypocaloric diet (~ 1200 kcal/day) MRS Diet continued until normoglycaemia (~ 3–12 weeks), followed by 4 weeks of weight stabilisation ~ 8% reduction IHTAG decreased by ~ 81% following the intervention
Dasarathy et al. (2015) [55] 37 M + F with T2D 100% RCT PUFA (2160 mg EPA/1440 mg DHA) vs. placebo Biopsy 48 weeks NSD Histological analysis demonstrates improvements in steatosis/NAS and a worsening of lobular inflammation following placebo. NSD were observed following PUFA
Vilar-Gomez et al. (2019) [53] 349 M + F with T2D 90–95% Non-randomised control study Access to remote care team (i.e. personal health coach and clinical professionals) who support adherence to a ketogenic diet vs. standard care Liver enzymes and surrogate indices 12 months ~ 79% of participants in the intervention group reduced by > 5% vs. ~ 19.5% of participants in standard care ALT, AST, and surrogate indices of steatosis and fibrosis reduced following the intervention

Where applicable data are presented as mean ± standard deviation

M male, F female, NAFLD non-alcoholic fatty liver disease, T2D type 2 diabetes, IHTAG intrahepatic triacylglycerol, RCT randomised controlled trial, PUFA polyunsaturated fatty acid, EPA eicosapentaenoic acid, DHA docosahexaenoic acid, MRI magnetic resonance imaging, MRS magnetic resonance spectroscopy, NSD no significant difference, NAS non-alcoholic fatty liver disease activity score, ALT alanine aminotransferase, AST aspartate transaminase