Background: Emerging evidence suggests the type of dietary fat consumed, irrespective of the amount, may increase intrahepatic triglyceride (IHTG) content, which is a risk factor for cardiometabolic disease (CMD). Previous work demonstrated hypercaloric diets enriched with saturated fat (SFA), compared to unsaturated fat, led to greater IHTG accumulation, despite similar weight gain (1, 2). However, it remains unclear how dietary fat composition influences IHTG accumulation and CMD risk in the absence of weight change.
Aim: To investigate the effects of isocaloric diets enriched with either SFA- or n-6 polyunsaturated fats (PUFA) on IHTG content and CMD risk factors in metabolically healthy men and women.
Methods: 14 adults underwent a baseline MRI scan to measure IHTG content and postprandial metabolic study day, afterwards they were randomly assigned to consume an isocaloric high-fat (HF) diet enriched in either SFA or n-6 PUFA for up to 24 days, before undergoing a post-diet MRI scan and postprandial metabolic study day. Food diaries were collected and analysed using Nutritics software. Fasting and postprandial plasma biochemistry and substrate oxidation rates were measured during metabolic study days.
Results: 6 individuals (2 females, age:48.2±5.5 years, BMI:26.6±2.9 kg/m2; mean ± SD) consumed a high-SFA diet while 8 individuals (3 females, age:50.3±8.6 years, BMI 26.2±3.8 kg/m2) consumed a high-PUFA diet. At baseline, participants randomised to the SFA-enriched HF diet consumed 88±19 g of fat/day, (35.0±2.4% total energy (TE)), of which 33±11 g/day (12.9±2.6%TE) was SFA; during the experimental dietary intervention, lasting 18 (13-24) days (median(range)), participants consumed 135±34 g of fat/day, (47.4±6.2%TE), of which 66±17 g/day (23.3±4.8%TE) was SFA. At baseline, participants randomised to the PUFA-enriched HF diet consumed 95±24 g of fat/day, (38.7±7.8%TE), of which 10±3 g/day (4.1±0.8%TE) was PUFA; during the experimental dietary intervention, lasting 20 (13-23) days, participants consumed 133±54 g of fat/day, (50.9±7.1%TE), of which 27±7 g/day (10.9±3.4%TE) was PUFA. There was no change in body weight from baseline (SFA: 81.2±16.9 kg vs. 81.2±16.6 kg; PUFA: 82.7±16.4 kg vs. 82.9±16.4 kg) with consumption of either isocaloric SFA- or n-6 PUFA-enriched HF diet.
Fasting and postprandial plasma biochemistry were measured before and after consumption of the isocaloric HF diets. Consuming a SFA-enriched HF diet increased fasting total cholesterol (p=0.0046), high-density lipoprotein (HDL) (p=0.013), non-HDL cholesterol (p=0.032), and decreased non-esterified fatty acids (p=0.003) compared to baseline, while consuming a PUFA-enriched HF diet decreased fasting total cholesterol (p=0.026), non-HDL cholesterol (p=0.0096) and plasma triglyceride (TG) (p=0.055) compared to baseline. Neither HF diet significantly altered IHTG, fasting glucose, or insulin, nor changed postprandial TG, NEFA, or very low-density lipoprotein-TG from baseline. There was no change in net fat and carbohydrate oxidation from fasted to fed state, before and after either HF diet, or between experimental groups.
Conclusion: These preliminary results show, despite no change in body weight, dietary fat composition modulates fasting cholesterol, non-HDL cholesterol, and TG, suggesting the type of dietary fat consumed, irrespective of the total amount, may play an important role in influencing well-established CMD risk factors and future CMD risk.