Phytosterols protect against diet-induced hypertriglyceridemia in Syrian golden hamsters
1 Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, NY 14214, USA
2 Richardson Centre for Functional Foods and Nutraceuticals, University of Manitoba, Winnipeg, Manitoba R3T 2 N2, Canada
3 Biotechnical and Clinical Laboratory Sciences, University at Buffalo, Buffalo, NY 14214, USA
4 Diabetes and Nutritional Sciences Division, School of Medicine, King’s College London, London SE1 9NH, UK
Lipids in Health and Disease 2014, 13:5 doi:10.1186/1476-511X-13-5Published: 6 January 2014
In addition to lowering LDL-C, emerging data suggests that phytosterols (PS) may reduce blood triglycerides (TG), however, the underlying mechanisms are not known.
We examined the TG-lowering mechanisms of dietary PS in Syrian golden hamsters randomly assigned to a high fat (HF) diet or the HF diet supplemented with PS (2%) for 6 weeks (n = 12/group). An additional subset of animals (n = 12) was provided the HF diet supplemented with ezetimibe (EZ, 0.002%) as a positive control as it is a cholesterol-lowering agent with known TG-lowering properties.
In confirmation of diet formulation and compound delivery, both the PS and EZ treatments lowered (p < 0.05) intestinal cholesterol absorption (24 and 31%, respectively), blood non-HDL cholesterol (61 and 66%, respectively), and hepatic cholesterol (45 and 55%, respectively) compared with the HF-fed animals. Blood TG concentrations were lower (p < 0.05) in the PS (49%) and EZ (68%)-treated animals compared with the HF group. The TG-lowering response in the PS-supplemented group was associated with reduced (p < 0.05) intestinal SREBP1c mRNA (0.45 fold of HF), hepatic PPARα mRNA (0.73 fold of HF), hepatic FAS protein abundance (0.68 fold of HD), and de novo lipogenesis (44%) compared with the HF group. Similarly, lipogenesis was lower in the EZ-treated animals, albeit through a reduction in the hepatic protein abundance of ACC (0.47 fold of HF).
Study results suggest that dietary PS are protective against diet-induced hypertriglyceridemia, likely through multiple mechanisms that involve modulation of intestinal fatty acid metabolism and a reduction in hepatic lipogenesis.