|Title||A feeling of full-filment : Sensory and physiological processes involved in satiation|
|Source||Wageningen University. Promotor(en): K. de Graaf, co-promotor(en): P.A.M. Smeets; M. Mars. - Wageningen : Wageningen University - ISBN 9789463952484 - 251|
Sensory Science and Eating Behaviour
|Publication type||Dissertation, internally prepared|
Satiation is a process that occurs during eating and involves inhibitory signals at a sensory, hormonal, digestive and cognitive level. The taste and texture of food influence this process. Harder foods with an intense taste are more satiating, i.e. we need to eat less of these foods to feel full, compared to softer foods with lower taste intensity. Oro-sensory exposure (OSE), the in-mouth taste perception of food, thus plays an important role in satiation and influences meal size. However, how oro-sensory signals affect satiation is not fully understood. Therefore, the main aim of this thesis was to better understand the role of sensory signals in the physiological processes underlying satiation. To study this we investigated the effect of OSE (duration and intensity) and eating rate on food intake, associated (cephalic) endocrine responses and brain reactivity.
We started by investigating the independent contributions of oral processing duration and taste intensity and their combined effect on satiation (chapter 2). This was done by manipulating texture and sweet taste intensity of model foods (2x2 study design, soft and hard vs. sweet and high sweet). Hard textured model foods decreased food intake through increased OSE duration, whereas sweetness intensity did not affect intake.
To better understand the physiology underlying the effects of oro-sensory exposure on satiation we studied the effect of texture and sweetness intensity on endocrine cephalic phase responses (chapter 3). Cephalic phase responses are neurally mediated anticipatory and conditioned responses to food cues and are considered the first phase of digestion. Insulin, pancreatic polypeptide and ghrelin responses were measured while participants modified sham fed (chew and spit) the same model foods as used in chapter 2. We expected a cephalic peak increase in these hormones 5-15 min after food exposure. However, we did not find a typical cephalic phase peak response for any of the hormones. Insulin levels tended to be higher 5 min after starting to chew but this increase could not be not be attributed to the texture or taste manipulations. In addition, we found that pancreatic polypeptide was more responsive to sweetness. Ghrelin concentrations were higher when chewing the hard texture compared to the soft texture model foods.
Based on the results from chapter 2 and 3 we hypothesized that part of the mechanism behind the oro-sensory exposure duration effect on satiation might be eating rate. When the duration of oro-sensory exposure is increased, eating rate is slowed down. Previous studies have shown that a reduced eating rate also leads to a decrease in food intake. Additionally, we hypothesized that part of the reason why we did not find typical cephalic responses in chapter 2 was because the model foods scored ‘neutral’ on liking, whereas palatability may be important to trigger a cephalic response. We therefore investigated the effect of OSE duration and eating rate on food intake (palatable chocolate custard) and associated endocrine responses (chapter 4). Two studies were set up. In both studies subjects ate until fullness of chocolate custard with and without fudge pieces (low or high oro-sensory exposure) at two different eating rates (slow or fast eating rate). In study 1 participants received a small portion and in study 2 a larger portion. Additionally, blood samples were collected during the meal in study 2. We found that a reduced eating rate (ER) (only in the high oro-sensory exposure condition) (study 1) and increased oro-sensory exposure (study 2) decreased food intake but that this was dependent on the portion size. Eight minutes after starting to eat, insulin concentrations increased for all treatments compared to control. At the end of the meal insulin concentrations were higher in the high OSE, slow ER compared to the low OSE, fast ER condition. Pancreatic polypeptide increased at 5 min after meal onset in the low OSE, fast ER condition. There were no changes in ghrelin concentration. Greater OSE thus increases insulin responsiveness. In contrast, PP responses are stronger when OSE is reduced and ER is fast. Prandial Insulin and PP responses may mediate the independent effects of OSE and ER on food intake.
To determine whether typical cephalic phase responses were specific to certain food cues or sub-populations we quantified outcomes of existing literature on cephalic insulin and pancreatic polypeptide responses in a systematic review (chapter 5). In addition, we aimed to quantify the hypotheses made by previous qualitative cephalic phase reviews that cephalic responses allow for larger meal sizes, induce satiation earlier on in the meal and improve postprandial glucose homeostasis. A cephalic phase insulin and pancreatic polypeptide increase was observed in about half of all included treatments. About one fifth of the treatments induced a significant increase from baseline. The size of the cephalic insulin increase relative to spontaneous fluctuations was small and there was substantial variation in magnitude and onset time of cephalic insulin and pancreatic polypeptide responses between food cues and individuals. Based on this we concluded that cephalic phase insulin responses are small compared to spontaneous fluctuations. Although cephalic pancreatic polypeptide responses are of a larger magnitude, both show substantial variation in magnitude and onset time. Based on the current evidence, we refute the hypotheses that CPRs improve satiation and glucose homeostasis in daily life
Finally, to determine how OSE or taste signals are processed in the brain to affect satiation we performed an fMRI study in which we measured neural reactivity to chocolate milk in the brain(stem) over the course of satiation (chapter 6). Additionally we measured gastric volume such that we could identify regions that respond solely to taste, independent of gastric distention. We found that taste activation in the parabrachial nuclei (PBN) in the brain stem, and bilateral (anterior) insula, amygdala and putamen gradually decreased as satiation increased, in line with the decrease in affective value of the chocolate milk stimuli. When subjects were hungry and completely satiated this effect could completely be explained by gastric filling, whereas this was not the case when subjects felt half full. Responses of these brain regions are thus modulated by gastric volume and sensory satiation seems especially important early in the meal when not completely satiated.
To conclude, we confirmed that increased OSE can decrease food intake. Insulin, PP and ghrelin cephalic phase responses do not mediate the oro-sensory exposure effect on satiation. Instead, we hypothesize that the underlying mechanisms are 1) a direct effect of oro-sensory exposure on satiation through sensory satiation and 2) an indirect effect of increased oro-sensory exposure duration which also slows down ingestion rate. This allows more time for stomach distention signals, hormone secretion, and early uptake of nutrients which are processed by the brain and induce satiation.