Table 1.

Experimental studies examining the effect of different diets on measures of liver fat in healthy normal weight or overweight populations

Study	Participants baseline characteristics	Method of liver fat assessment	Dietary intervention	Duration diet	Key findings
Bortolotti et al. (2009)30 Randomized Crossover	10 Healthy, but sedentary men Mean age: 24 ± 1 years Mean BMI: 22.4 ± 0.6 kg/m2 Non‐smokers No family history of diabetes	H‐MRS	In randomized order, a balanced isocaloric control diet or high‐fat (HF) or high‐fat high‐protein (HFHP) diet. All three diets designed to provide same total carbohydrate intake, and the HF and HFHP diets designed to provide same fat intake	4 days	HF diet nearly doubled intrahepatocellular lipids (IHCL) by 90 ± 26% (P < 0.02) HFHP diet increased the IHCLs to a lesser extent. The increase in IHCL was 22 ± 32% (P < 0.02) less in the HFHP diet compared with the HF diet AST and ALT were not altered by either diet, except for a 28 ± 15% increase in ALT with the HFHP diet (P < 0.02) No change in insulin sensitivity
van der Meer et al. (2008)31	15 Healthy men who undertook regular moderate intensity exercise Mean ± SD age: 25 ± 6.6 years Mean ± SD BMI: 23.4 ± 2.5 kg/m2	H‐MRS	Reference diet (mean TE intake approximately 2100 kcal/day with 40% carbohydrates, 35% fat, and 25% protein. Experimental high‐fat, high‐energy (HFHE) diet consisting of the reference diet, plus 800 mL cream daily (an extra 2632 kcal/day). TE intake approximately 4732 kcal/day with 20% carbohydrates, 69% fat, and 11% protein	3 days	After HFHE, hepatic triglyceride content increased more than twofold compared with baseline from 2.01 ± 1.79 to 4.26 ± 2.78% (P = 0.001)No change in mean BMI
Lammert et al. (2000)32	10 Pairs of healthy men High‐carbohydrate diet group Mean ± SE age: 22.3 ± 1.7 years Mean ± SE weight: 76.4 ± 8.8 kg HF diet group Mean ± SE age: 22.4 ± 1.9 years Mean ± SE weight: 73.4 ± 6.7 kg	Fractional hepatic DNL using mass isotopomer distribution analysis	Energy intake increased by 5 MJ/day with either a carbohydrate‐rich (HC) or fat‐rich diet (HF) over and above each individual's usual habitual diet Each individual in a pair was randomly assigned to the HC diet or the HF diet	21 days	Overall, both groups gained 1.5 kg body weight HC group gained 1.35 ± 0.42 kg (P = 0.01) and HF group gained 1.58 ± 0.41 kg (P = 0.006). There was no difference between the groups
Heilbronn et al. (2013)33	40 Sedentary non‐smoking non‐diabetic men (n = 20) and women (n = 20) Mean ± SE age: 37 ± 2 years Mean ± SE BMI: 25.6 ± 0.6 kg/m2 Mean (SE) weight 75.3 ± 1.9 kg	CT	For 3 days prior to experimental diet, all foods were provided at baseline energy requirements with a nutrient composition of 30% fat, 15% protein, and 55% carbohydrates Then, overfed 1250 kcal/day with nutrient composition 45% fat, 15% protein, and 40% carbohydrates	28 days	Liver density increased from 55 ± 2 to 53 ± 2 HU (P < 0.001) Weight increased by 2.8 to 78.1 ± 1.9 kg (P < 0.001) BMI increased by 1.0 to 26.6 ± 0.6 kg/m2 (P < 0.001) Fasting serum glucose, insulin, and HOMA‐IR increased independent of gender
Kechagias et al. (2008)34	18 Healthy men (n = 12) and women (n = 6) and 18 matched controls Cases (intervention group): Mean ± SD age: 27 ± 6.6 years Mean ± SD BMI: 21.9 ± 1.9 kg/m2 Controls: Mean ± SD age: 25 ± 3.5 years Mean ± SD BMI: 22.2 ± 2.1 kg/m2	H‐MRS	Hyperalimentation diet: an extra two fast food‐based meals per day with the goal to double their regular caloric intake to achieve a body weight increase of 5–15% in combination with the adoption of a sedentary lifestyle	4 weeks, or earlier if reached 15% weight gain goal	Controls maintained their body weight with BMI remaining the same 17 of the 18 intervention groups met the goal of a 5–15% body weight increase. They gained 6.4 kg and BMI significantly increased to 23.9 ± 2.2 kg/m2 (P < 0.001) Liver fat content increased from 1.1 ± 1.9 to 2.8 ± 4.8% over the diet period in cases (P = 0.003)
Sevastianova et al. (2012)35	16 Non‐diabetic men (n = 5) and women (n = 11) Median age: 54 years (25th–75th percentile: 40–59 years) Mean ± SE BMI: 30.6 ± 1.2 kg/m2	H‐MRS	High‐carbohydrate hypercaloric (HCHC) diet: participant's normal diet plus extra 1000 kcal/day with 98% of energy from carbohydrates	3 weeks	Weight increased by 2% from 88.7 ± 4.1 to 90.5 ± 4.1 kg (P < 0.0001), BMI by 3% from 30.6 ± 1.2 to 31.2 ± 1.3 kg/m2 (P < 0.0005) and liver fat by 27% from 9.2 ± 1.9 to 11.7 ± 1.9% (P = 0.005) with the HCHC diet With the weight loss diet, weight decreased by 4% from 90.5 ± 4.1 to 87.3 ± 4.1 kg (P < 0.0001), BMI from 31.2 ± 1.3 to 30.0 ± 1.3 kg/m2 (P < 0.0005) and liver fat by 25% from 11.7 ± 1.9 to 8.8 ± 1.8% (P < 0.05)
			Dietitian‐guided weight loss diet	6 months
Koopman et al. (2014)37 RCT	36 Healthy men randomized to a control group or one of the four experimental diets Mean ± SD age for five groups ranged from 21.5 ± 1.9 to 23.0 ± 3.1 years Mean ± SD BMI for five groups ranged from 21.7 ± 1.1 to 22 ± 2.3 kg/m2	H‐MRS	All four diets 40% caloric surplus in addition to normal diet: high‐fat high‐sugar diet with extra calories eaten either with meals (HFHS‐S) or as a snack 2–3 h after meals (HFHS‐F) High sugar only diet with extra calories eaten either with meals (HS‐S) or 2–3 h after meals (HS‐F)	6 weeks	No change in weight or IHTG in control group Overall, diet groups gained 2.5 ± 1.7 kg with no differences between the four diet groups IHTG significantly increased in the HFHS‐F (0.98 ± 0.91% vs 1.38 ± 1.26%; P = 0.018) and the HS‐F (1.49 ± 0.95% vs 3.10 ± 2.16%; P = 0.043) groups, and was higher in the HS‐F group (P = 0.043) No change in IHTG in the two groups with increased meal size (HFHS‐S and HS‐S) Overall, effect of increased meal size versus increased frequency eating (P = 0.03, F = 5.435) but not of HFHS versus HS (P = 0.13, F = 2.418)
Westerbacka et al. (2005)38 Randomized crossover	10 Women Mean ± SD age: 43 ± 5 years Mean ± SD BMI: 33 ± 4 kg/m2 (range: 27–38 kg/m2)	H‐MRS	Two isocaloric diets consumed successively: a low fat (LF) 16% TE, and an HF 56% TE	2 weeks	Body weight was unchanged during LF and HF diets Mean ± SD liver fat at baseline 10 ± 7%. Liver fat decreased by 20 ± 9% during the LF diet and increased by 35 ± 21% during the HF diet (P < 0.014 for liver fat after LF vs HF diets; P < 0.042 for change in liver fat by the LF vs HF diet)
Van Herpen et al. (2011)39 RCT	20 Overweight sedentary healthy men randomized to two groups LF group (n = 10) Mean ± SE age: 54.0 ± 2.3 years Mean ± SE BMI: 29.3 ± 0.6 kg/m2 HF group (n = 10) Mean (SE) age: 56.4 ± 2.5 years Mean (SE) BMI: 28.3 ± 0.5 kg/m2	H‐MRS	LF run‐in diet consisting of 15% protein, 65% carbohydrates, and 20% fat	3 weeks	IHLs decreased by 13% in the LF group and increased by 17% in the HF group (P = 0.047) Insulin sensitivity was unaffected Liver enzymes and body weight were unchanged
			Randomized to continue LF diet or change to isocaloric HF diet consisting of 15% protein, 55% carbohydrates, and 30% fat	6 weeks
Rosqvist et al. (2014)40 RCT	37 Healthy normal weight men randomized to two groups Saturated fat group (13 men, 5 women) Mean ± SD age: 26.7 ± 4.6 years Mean (IQR) BMI: 20.8 (19.5–23.1) Polyunsaturated fat group (13 men, 6 women) Mean ± SD age: 27.1 ± 3.6 years Mean (IQR) BMI: 19.9 (18.9–20.7)	MRI	Addition of one of the two types of muffins to habitual diet to achieve 3% weight gain Muffins high in palm oil saturated fat (SFA diet), or Muffins high in sunflower oil polyunsaturated fat (PUFA diet) Composition of muffins: 5% protein, 44% carbohydrates, and 55% fat Number of muffins eaten per day was adjusted to achieve 3% weight gain. Average 3.1 muffins (or 750 kcal) eaten per person/day	7 weeks	Both groups gained 1.6 kg in weight. Liver fat increased more in the SFA group compared with the PUFA group. The increase in the PUFA group was 0.04 ± 0.24% from 0.75% (IQR: 0.65–1.0%) compared with 0.56 ± 1.0% from 0.96% (IQR 0.79–1.1%) in the SFA group. Mean (95% CI) difference in change was −0.52 (−1.0 to −0.01; P = 0.033)
Bjermo et al. (2012)41 RCT	61 Men (n = 21) and women (n = 40); 15% type 2 diabetes PUFA group (n = 32) Median (IQR) age: 57 (51–63) years Mean ± SD BMI: 30.3 ± 3.7 kg/m2 SFA group (n = 29) Median (IQR) age: 56 (50–64) years Mean ± SD BMI: 31.3 ± 3.9 kg/m2	H‐MRS (and MRI)	Quality of fat in diet changed without altering intakes of total fat, and type and amount of carbohydrates and protein. Randomly assigned to one of the two different diets PUFA diet: isocaloric diet high in vegetable n‐6 PUFA diet (14% of TE (increase of 10%) SFA diet: isocaloric diet high in SFA mainly from butter (20% of TE (increase of 5%)	10 weeks	Nonsignificant weight increase in both groups. Mean ± SD weight gain was 0.4 ± 1.4 kg in PUFA group and 0.8 ± 1.6 kg in SFA group (P = 0.41) Liver fat decreased by 0.9% (95% CI: −1.7 to 0.0; MRS) from 3.2% (95% CI: 1.0 to 6.6) with the PUFA diet, and increased by 0.3% (95% CI: −0.6 to 1.8) from 3.2% (95% CI: 1.3 to 7.7) with the SFA diet. The between‐group difference in relative change from baseline was 34% (P = 0.02)
Lecoultre et al. (2013)43 Non‐randomized	55 Healthy men Mean ± SD age: 22.5 ± 1.6 years Mean ± SD BMI: 22.4 ± 1.6 kg/m2	H‐MRS	All consumed a balanced isocaloric control diet first, then this diet was supplemented with one of the following five overfeeding diets: 1.5 g fructose/kg/day (F1.5) (n = 7), or 3 g fructose/kg/day (F3) (n = 17), or 4 g fructose/kg/day (F4) (n = 10), or 3 g glucose/kg/day (G3) (n = 11), or 30% excess energy as saturated fat (fat30%) (n = 10)	All diets 6–7 days	F3, F4, G3, and fat30% diets all significantly increased intrahepatic lipid content by 113 ± 86% (P < 0.05), 102 ± 115% (P < 0.05), 59 ± 92% (P < 0.05), and 90 ± 74% (P < 0.05) as compared to control, respectively F4 and G3 diets also increased hepatic glucose production by 16 ± 10% (P < 0.05) and 8 ± 11% (P < 0.05)
Sobrecases et al. (2010)44	30 Healthy men Mean ± SE age: 23.9 ± 0.4 years Mean ± SE BMI: 22.6 ± 0.2 kg/m2	H‐MRS	Isocaloric control (C) diet with 55% carbohydrates (10% simple sugars), 30% fat (10% saturated fat), and 15% protein Followed by one of the following diets: (1) High‐fructose (HFr) diet (3.5 g fructose per kg fat‐free mass per day, +35% energy, n = 12) (2) HF diet (fat: +30% energy, +18% as saturated fat, n = 10) 3) High‐fructose high‐fat (HFrHF) diet (HFr diet combined with HF diet, n = 8)	Control diet: 7 days   HFr diet: 7 days   HF diet: 4 days   HFrHF diet: 4 days	Body weight increased on average by 0.3 ± 0.1 kg and was not different across the three experimental hypercaloric diets Intrahepatocellular lipids increased after each of the experimental hypercaloric diets; HFr diet by 16%, HF diet by 86%, and HFrHF by 133%. The increase after the combined HFrHF diet was significantly higher than with the HFr or HF diets (P < 0.05)
Johnston et al. (2013)45 Randomized parallel arm	32 Healthy but centrally overweight men randomized to one of two groups Fructose group (n = 15) Mean ± SD age: 35 ± 11 years Mean ± SD BMI: 30.0 ± 1.4 kg/m2 Glucose group (n = 17) Mean ± SD age: 33 ± 9 years Mean ± SD BMI: 28.9 ± 1.7 kg/m2	H‐MRS	Pre‐intervention energy balanced (isocaloric) diet, then randomized to HFr, or high glucose (HG) for two separate intervention periods. The first period was an isocaloric diet and the other a hypercaloric diet. For the isocaloric diet, fructose or glucose provided 25% of the predicted total daily energy requirements and were consumed four times a day in divided amounts mixed with 500 mL of water. Remainder of diet provided 75% of energy requirements, and the food was provided to ensure isocaloric status, and overall diet with 55% carbohydrates, 15% protein, and 30% fat. For the hypercaloric diet, ad libitum habitual food consumption plus the same amount of fructose or glucose consumed in isocaloric period. Extra sweetened drinks were forbidden	2 weeks each with a 6‐week washout between diets	Body weight was maintained during isocaloric diets, but significantly increased during the hypercaloric diets by 1.0 ± 1.4 kg in HFr group and 0.6 ± 1.0 kg in HG group with no significant difference between these groups (P = 0.29) Similarly, no change in absolute concentrations of triacylglycerides in liver during isocaloric diets, but significantly increased during the hypercaloric diets by 1.70 ± 2.6% in HFr group and 2.05 ± 2.9% in HG group with no significant difference between these groups (P = 0.73)
Stanhope et al. (2009)46 Double‐blinded parallel arm	32 Healthy men (n = 16) and premenopausal women (n = 16) randomized to one the of two groups. Glucose group (n = 15) Men (n = 7) Mean ± SE age: 54 ± 3 years Mean ± SE BMI 29.3 ± 1.1 kg/m2 Females n = 8 Mean ± SE age: 56 ± 2 years Mean ± SE BMI: 29.4 ± 1.3 kg/m2   Fructose group (n = 17) Men (n = 9) Mean ± SE age: 52 ± 4 years Mean ± SE BMI 28.4 ± 0.7 kg/m2 Females n = 8 Mean ± SE age: 53 ± 2 years Mean ± SE BMI 30.3 ± 1.0 kg/m2	Hepatic fractional DNL via infusion of isotopic acetate	Three phases: (1) Inpatient baseline energy balanced diet with 55% carbohydrates, 15% protein, and 30% fat. Carbohydrate was mostly complex (2) Hypercaloric diet: ad libitum diet plus 25% of daily energy consumed as fructose or glucose (3) Isocaloric diet: inpatient energy balanced diet with 25% of daily energy from fructose or glucose Fructose and glucose were consumed as fructose‐ or glucose‐sweetened beverages with meals	Baseline: 2 weeks   Hypercaloric: 8 weeks   Isocaloric: 2 weeks   Total intervention period: 10 weeks	Both groups significantly gained weight between baseline and 10 weeks. The percentage change at 10 weeks was 1.8 ± 0.5% (P < 0.01) for the glucose group and 1.4 ± 0.3% (P < 0.001) for the fructose group Fractional DNL unchanged during glucose consumption both in fasting (8.8% ± 1.8% vs 9.5% ± 1.8%; P = 0.47) and postprandial 13.4% ± 2.8% vs 14.2% ± 1.7%; P = 0.31) states Fasting DNL was unaffected during fructose consumption but postprandial DNL significantly increased from 11.4 ± 1.3 to 16.9% ± 1.4% (P = 0.02)
Maersk et al. (2012)47 Randomized parallel arm	47 Healthy men (n = 17) and women (n = 30) allocated to one of the four groups Regular cola (6 men, 4 women) Mean ± SE age: 39 ± 6 years Mean ± SE BMI: 31.3 ± 2.9 kg/m2   Milk (3 men, 9 women) Mean ± SE age: 38 ± 9 years Mean ± SE BMI: 31.9 ± 2.8 kg/m2   Diet cola (3 men, 9 women) Mean ± SE age: 39 ± 8 years Mean ± SE BMI: 32.8 ± 3.8 kg/m2   Water (5 men, 8 women) Mean ± SE age: 39 ± 8 years Mean ± SE BMI: 32.2 ± 4.6 kg/m2	H‐MRS	Participants consumed 1 L per day of one of the four different test drinks: (1) Regular sucrose‐sweetened cola (50% glucose and 50% fructose) (2) Semi‐skim milk, the amount equivalent in energy to the regular cola (3) Aspartame‐sweetened diet cola (4) Still mineral water In addition, they were allowed to drink water, tea, coffee, and usual amount of alcohol	6 months	Body weight increased in a small amount in all groups but difference between groups was not significant (P = 0.8). The percentage increase was 1.28 ± 1.1% in sugar‐sweetened cola group, 1.36 ± 1.1% in milk group, 0.114 ± 1.1% in diet cola group, and 0.576 ± 1.0% in water group Liver fat accumulation was much higher after regular cola (overall P = 0.01) compared with milk (143%; 95% CI: 50, 236; P < 0.05), diet cola (139%; 95% CI: 50, 227; P < 0.05), and water (132%; 95% CI: 43, 222; P < 0.05)
Utzschneider et al. (2013)48 RCT	35 Non‐diabetic men (n = 7) and women (n = 13) from an Alzheimer's disease project randomized to one of the two diets   Low fat/low saturated fat with a low GI (LSAT) diet group (7 men, 13 women) Mean ± SE age: 69.3 ± 1.6 years Mean ± SE BMI: 26.9 ± 0.8 kg/m2   High fat/high saturated fat with a high GI (HSAT) diet group (6 men, 9 women) Mean ± SE age: 68.6 ± 1.8 years Mean ± SE BMI: 28.1 ± 0.9 kg/m2	H‐MRS	Two commercially prepared weight maintenance diets with the following composition (1) LSAT: 23% fat (of which 7% saturated fat), 15–20% protein, 55–60% carbohydrates, and a daily average GI <55 2) HSAT: 45% fat (of which 25% saturated fat), 15–20% protein, 35–40% carbohydrates, and a daily average GI >70	4 weeks	Body weight did not change significantly in either group Liver fat absolute % decreased significantly in the LSAT group compared with baseline from median 2.2 to 1.7% (P = 0.002, unadjusted; P < 0.05 adjusted). Mean ± SE percentage decrease in liver fat was 19.8 ± 6.0% Neither absolute percentage liver fat nor percentage change in liver fat changed significantly on the HSAT diet (median liver fat % 1.2 at baseline and 1.6 at 4 weeks)
Bozzetto et al. (2012)49 Randomized parallel group	45 Men (n = 37) and women (n = 8) with type 2 diabetes with satisfactory glycemic control on diet or diet and metformin assigned to one of the four diets (1) High CHO/fiber Mean ± SE age: 58 ± 5 years Mean ± SE BMI: 30 ± 2 kg/m2 (2) High MUFA Mean ± SE age: 57 ± 8 years Mean ± SE BMI: 28 ± 3 kg/m2 3) High CHO/fiber + physical activity Mean ± SE age: 63 ± 5 years Mean ± SE BMI: 31 ± 3 kg/m2 (4) High MUFA + physical activity Mean ± SE age: 57 ± 9 years Mean ± SE BMI: 30 ± 4 kg/m2	H‐MRS	All diets were isoenergetic in order to keep body weight constant, but differed in macronutrient composition Randomized to either: (1) High carbohydrate high fiber low GI (high CHO/fiber): 52% carbohydrates, 28 g/1000 kcal fiber, GI 60%, 30% fat, and 16% MUFA (2) High monounsaturated fat (high MUFA): 40% carbohydrates, 10 g/1000 kcal fiber, GI 95%, 42% fat, 28% MUFA, 18% protein, 7% saturated fat, and 4% polyunsaturated fat (3) High CHO/fiber+Ex: high CHO/fiber diet plus physical activity program (4) High MUFA + Ex: high MUFA diet plus physical activity program Other dietary components were similar in the two diets including saturated fat (7%), protein (18%), and PUFA (4%)	8 weeks	Body weight did not change significantly in any group Liver fat content significantly decreased in MUFA group from 7.4 ± 2.8 to 5.2 ± 2.7% (P = 0.01) and MUFA + Ex group from 11.6 ± 8.0 to 9.1 ± 7.4% (P = 0.02) Liver fat content did not change in the CHO/fiber group (17.7 ± 9.7% vs 16 ± 6.8%; P = 0.295) or CHO/fiber + Ex group (8.8 ± 4.9% vs 8.9 ± 5.7%; P = 0.794) There was a significant effect on liver fat content for diet (P = 0.006), with no effects for exercise training (P = 0.789)
Faeh et al. (2005)50 Randomized crossover	7 Healthy males Age range: 22–31 years BMI range: 20.2–25.4 kg/m2	Hepatic fractional DNL via infusion of isotopic acetate. Fractional DNL calculated by isotopomer distribution analysis technique.	Preceding each experimental diet, each subject consumed a provided control diet: isoenergetic with 15% protein, 35% fat, and 50% carbohydrates (40% starch and 10% from monosaccharide and disaccharide) Experimental diets: (1) Fish oil supplementation: control diet plus 7.2 g of fish oil (1.2 g eicosapentaenoic acid and 0.8 g docasahexaenoic acid) per day (2) Hyperenergetic high fructose (HHFr): control diet plus 3 g of fructose per kg body weight per day (additional 800–1000 kcal/day) taken with three main meals. Overall 11% protein, 26% fat, and 63% carbohydrates (30% starch and 8% from monosaccharide and disaccharide, and 25% fructose) (3) Combination: control diet plus fish oil supplementation and HHFr	Control only diet: 3 days   Fish oil: 28 days   HHFr: 6 days   Washout of 12 weeks following each of fish oil supplement diets	Body weight was stable in all groups DNL was very low among fish oil only group and control group (1.9 ± 0.44 and 1.6 ± 0.34%, respectively). DNL significantly increased after both high‐fructose diets but was higher after HHFr diet (9.4 ± 2.8%, P < 0.05) compared with combination diet (7.5 ± 1.8%, P < 0.05). The difference between these two high‐fructose diets was not significant
Theytaz et al. (2012)51 Randomized crossover	9 Healthy, but sedentary men Mean ± SE age: 23.3 ± 0.9 years Mean ± SE BMI: 22.6 ± 0.5 kg/m2	H‐MRS	Three dietary interventions: (1) Control diet: weight maintenance diet with 55% carbohydrates, 30% fat, and 15% protein. (2) Hypercaloric high‐fructose + essential amino acid diet (HFrAA): control diet plus 3 g fructose per kg per day and 6.77 g of five essential amino acids three times per day (3) Hypercaloric high‐fructose + placebo (HFr): control diet plus 3 g fructose per kg per day and a placebo three times per day	6 days with 4–10 weeks washout period between each diet	Both HFr and HFrAA diets increased IHCL content compared with the control diet (P < 0.05) but the increase was 16.1% lower with HFrAA than with HFr (P < 0.05) IHCL (vol %) was 1.27 ± 0.31% with the control diet, 2.74 ± 0.55% with the HFrAA diet, and 2.30 ± 0.43% with the HFr diet No difference in body weight between the three diets

ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; CT, computed tomography; DNL, de novo lipogenesis; FA, fatty acid; GI, glycemic index; H‐MRS, 1H‐magnetic resonance spectroscopy; HOMA‐IR, homeostatic model assessment of insulin resistance; IHCL, intrahepatocellular lipid concentration; IHTG, intrahepatic triglyceride; IQR, interquartile range; MRI, magnetic resonance imaging; MUFA, monounsaturated FA; PUFA, polyunsaturated FA; RCT, randomised controlled trial; SFA, saturated FA; TE, total energy.