Abstract

BackgroundPhosphatidylethanolamine (PE) is a phospholipid which is biosynthesized into long chain N-acylethanolamines (NAEs) including oleoylethanolamide (OEA), a known inhibitor of food intake. The aim of this study was to investigate whether PE-containing lipids can also inhibit intake. This was a 4 treatment intervention where 18 male participants were given a high-fat test breakfast (2.5MJ, 53 en% fat) containing (i) high-phospholipid, high-PE lipid (ii) high-phospholipid, medium-PE lipid (iii) no-phospholipid, no-PE control lipid or (iv) water control, in a randomised cross-over. Visual analogue scales (VAS) were used to assess post-ingestive hunger and satiety, and energy intake (EI) was measured at an ad libitum lunch meal after 3.5hours.ResultsWhen compared with the water control, the 3 lipid treatments resulted in lower levels of hunger and thoughts of food, greater fullness and satisfaction (all, treatment*time interaction, P<0.001), and a lower EI (P<0.05). However, there was no difference in any of the VAS measures when the 2 PE lipid treatments were compared with no-PE control lipid, nor when medium-PE was compared with high-PE. Unexpectedly participants ate significantly more energy at the lunch meal when the 2 PE lipid treatments (medium-PE:5406 kJ, 334 sem; high-PE:5288 kJ, 244 sem) were compared with the no-PE control lipid (5072 kJ, 262 sem, P<0.05), although there was no dose effect between the medium- and high-PE treatments.ConclusionDespite the close relationship of PE with OEA, there was no evidence from this acute study that dietary phospholipids containing PE can favourably modify eating behaviour.

Highlights

  • The inability to control energy intake (EI), compounded by low levels of physical activity, appears key to the development of obesity

  • OEA is a lipid which has become prominent as an established inhibitor of food intake in animal models and which appears to regulate feeding through activation of the nuclear receptor peroxisome-proliferatoractivated receptor-α (PPAR-α) [15,16]

  • There was no significant difference in body weight at base

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Summary

Introduction

The inability to control energy intake (EI), compounded by low levels of physical activity, appears key to the development of obesity. Regulation of appetite is central to the control of weight gain, and identifying foods which can modulate hunger and satiety and decrease intake is (page number not for citation purposes). Of particular interest in the area of appetite regulation is PE which is known to be metabolized endogenously into a range of ethanolamides of long chain fatty acids, collectively termed the N-acylethanolamines (NAEs), and which include N-arachidonoylethanolamine (anandamide) and its analogue oleoylethanolamide (OEA) [14]. OEA is a lipid which has become prominent as an established inhibitor of food intake in animal models and which appears to regulate feeding through activation of the nuclear receptor peroxisome-proliferatoractivated receptor-α (PPAR-α) [15,16]. Phosphatidylethanolamine (PE) is a phospholipid which is biosynthesized into long chain N-acylethanolamines (NAEs) including oleoylethanolamide (OEA), a known inhibitor of food intake. Visual analogue scales (VAS) were used to assess post-ingestive hunger and satiety, and energy intake (EI) was measured at an ad libitum lunch meal after 3.5hours

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