Our previous work has shown that the intake of a high fat high carbohydrate (HFHC) meal results in an increase in endotoxin (LPS) and LPS binding protein (LBP) concentrations concomitant with an increase in the expression of TLR-4, the receptor for LPS, and CD-14, which facilitates the binding of LPS to its receptor. In addition, there is an increase in ROS generation, NFkB binding and the expression of TNF-α and IL-1β. Our work has also demonstrated that an equicaloric meal rich in fiber and fruit (American Heart Association (AHA) recommended meal) does not induce these changes. We hypothesized, therefore, that the addition of fiber to a HFHC meal will prevent the changes induced by HFHC meal. Eight fasting normal subjects (BMI<25 kg/m2) were given 900 Calorie meals of either HFHC or AHA or HFHC with additional fiber (30 g) (Fiber One Original) on three sequential visits one week apart in a randomized crossover design. As expected, the HFHC meal induced an increase in LPS concentrations (by 69±14%) with an increase in ROS generation (by 120±24%) and the expression of TLR-4, CD14 and IL-1β (by 71±14, 86±14 and 127±14%, respectively; P<0.05 for all) in MNC. The AHA meal did not induce any of these changes. The addition of fiber to HFHC meal significantly reduced the increase in LPS concentrations (by 58±10%; P<0.05), ROS generation (by 47±14%; P<0.05) and the expression of TLR-4, CD14 and IL-1β (by 37±11, 46±12 and 52±15%, respectively; P<0.05 for all) observed with the HFHC meal alone. Additionally, the intake of fiber with the HFHC meal reduced postprandial glucose excursion and increased insulin concentrations compared to HFHC meal alone. We conclude that the addition of fiber to a pro-inflammatory HFHC meal has a beneficial anti-inflammatory and metabolic effect. Thus, the fiber content of the AHA meal may account for its non-inflammatory nature. Since ROS, TLR-4 and IL-1 β potentially interfere with insulin signal transduction and are known to be pro-inflammatory in the arterial wall, this action of dietary fiber may contribute to its benefits in the prevention of insulin resistance, type 2 diabetes and atherogenesis.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology