Obesity and metabolic disorders are becoming a global health burden, and shifts in dietary compositions and physical activity are believed to be a major contributing factor [1, 2]. Accumulation of liver fat in particular has been considered as a key step in the pathogenesis of diseases such as type-2 diabetes [3, 4] and may lead to steatohepatitis or fibrosis. ¹H MRS provides a powerful, well validated method of measuring fat in vivo which allows non-invasive evaluation of lipids [5] and a robust way of comparing dietary interventions. In previous work a two week hyper energetic diet was shown to increase liver fat regardless of whether excess carbohydrates were fructose or glucose [6]. In the present study this concept was extended to consider the effects of overfeeding carbohydrates vs fat.After obtaining ethical approval, 20 overweight but otherwise healthy males (40.3 ± 2.5 yrs, BMI 31 ± 1.0 kg m-2) were recruited following informed consent. Volunteers visited the test centre on two occasions before and after a dietary intervention. Prior to visit 1 volunteers were given an isocaloric diet for 1 week. Following visit 1 volunteers were randomized into two groups and given a hyper energetic diet (25% excess energy) of either high carbohydrate, HC (65% CHO, 20% fat, 15% protein) or high fat, HF (38% CHO, 47% fat, 15% protein) to be consumed over two weeks before returning for visit 2. During each test day subjects arrived at the test centre following an overnight fast. ¹H MRS was acquired from the liver to determine lipid content, and 2 point mDIXON was acquired from the abdomen to determine subcutaneous and visceral fat. Blood samples were also obtained to measure fasted serum insulin, glucose, triacylglycerol (TAG), free fatty acids (FFAs), Apolipoproteins, total cholesterol and liver function. A 4-point gradient echo sequence was also acquired for comparison with MRS data the results of which are beyond the scope of this abstract.All measurements were performed on a Philips Achieva 3T scanner and ¹H MRS acquired using a Philips XL 32 channel SENSE torso coil. Scout images where obtained and used to position a 20x20x20mm³ voxel for ¹H MRS within the right lobe of the liver avoiding major blood vessels (fig 1). Water suppressed spectra were acquired over four breath holds of varying TE (20ms, 30ms, 40ms, 60ms) using stimulated echo localization (STEAM) with 9 averages at TE = 20ms (fig 2), and 6 averages for the remaining echo times (BW=2Hz, 1024 samples, TR=2046). Water unsuppressed spectra were also acquired during one breath across the same TE range. Spectra were phase corrected and the area of the fat peaks and water peak were quantified using a peak fitting algorithm. Absolute weight fat fractions were calculated using the formula described previously [7] and corrected for T2 relaxation using values derived from spectra at varying echo times for each subjects, with bulk T2 values applied to poorly fitted relaxation curves.Baseline fat fractions were 6.5 ± 2.4% for the HC group and 6.0 ± 1.9% for the HF group. The whole group fat fraction significantly increased from visit 1 to visit 2 (2.6 ± 0.8%, P ≤ 0.005) but there was no significant interaction between group and time (P = 0.3). There was also a significant increase from visit 1 to visit 2 in the HC group (3.5 ± 1.5%, P<0.05) and a smaller non-significant increase in the HF group (1.7 ± 1.1, P=0.3) as shown in figure 3. Fasted serum TAG in the whole group increased (0.33±0.13 mmol/l, P<0.05) and the increase was greater in the HC group (0.45 ± 0.14, P<0.05). Increases in serum Apolipoprotein A and B between visit 1 and visit 2 were greater in the HF group (0.13 ± 0.03 g/dl, P < 0.01 and 0.10 ± 0.03 g/L, P < 0.01 respectively). There were no changes in body mass, visceral fat, IMCL, EMCL, HOMA-IR, fasted insulin, glucose, FFAs, total cholesterol or liver function.Two weeks excess energy consumption increased liver fat fractions, TAG and Apoliprotein A and B. The effects of excess carbohydrate consumption seem to be more pronounced than excess fat consumption. In particular, significant changes in liver fat from visit 1 to visit 2 were only observed in the HC group which suggests that carbohydrate consumptions may play a more deleterious role in on the liver increasing insulin resistance risk.