imulate CCK secretion in humans (26–28), and trials have
attempted to establish which hormone is responsible for the
observed effects of MCT on food intake. Barbera et al. (26)
compared effects of MCT and LCT on sensations of satiety,
gastric tone, gastric inhibitory peptide (GIP), pancreatic
polypeptide and CCK. Subjects (n 9) were infused with
saline, LCFA (mainly oleate and linoleate) or MCFA (octanoate
and decanoate) on three separate occasions in random
order. LCFA infusion resulted in a greater rise in satiation
than MCFA, but there was no difference between the two fats
on the perception of fullness and bloating. The rise in gastric
volume was also greater with LCFA infusion than MCFA
infusion. Similarly, LCFA increased baseline levels of plasma
CCK, GIP, neurotensin and pancreatic polypeptide compared
with saline, whereas MCFA infusion did not. The authors thus
concluded that MCFA induce gastric relaxation without increasing
satiation or plasma levels of gut hormones. However,
because Stubbs and Harbron (23) and Van Wymelbeke (24)
have shown lower food intakes with diets rich in MCT, it is
likely that other factors play a role in regulating energy balance
with MCT consumption.