Saturday, October 4, 2014

Taste Matters - Bypassing Taste Receptors Boosts Insulin & CCK Satiety Hormone Response to Food - Why Does That Happen & What Are the Implications, If There Are Any?

Infusions of nutrient solutions via a tube is often the last resort for doctors to save anorexic patients' lives - it's yet nothing anyone should do voluntarily for the satiety plus Spetter et al. observed.
As a SuppVersity Reader you are no stranger to "incretin hormones" and their release in response to the interaction of food with the taste receptors that are distributed all over your body. Against that background you will probably not be surprised to hear that Martjee S. Spetter and her colleagues from the University Medical Center Utrecht and the Wageningen University found that bypassing oral the stimulation of oral taste receptors decreases the satiety and alters the appetite hormone response to a given meal.

As the Dutch researchers point out, the interaction between oral and gastric signals is an important part of food intake regulation.
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In that, Spetter et al. are not the first to obversve that bypassing the oral taste receptors may diminish the suppression of hunger and increases gastric emptying rate. The role of appetite hormones, like cholecystokinin-8 and ghrelin, in this process, however, is still unclear.

The objective of Spetter et al.'s latest study was thus to determine the contributions of gastric and oral stimulation to subsequent appetite and hormone responses and their effect on ad libitum intake.
The scientists recruited fourteen healthy male subjects (age 24.6 ± 3.8y, BMI 22.3 ± 1.6 kg/m²) who participated in their randomized, single-blinded, cross-over experiment with 3 treatmentsessions:
  • Stomach distention, only: naso-gastric infusion of 500 mL/0 kJ water, 
  • Stomach distention with caloric content: naso-gastric infusion of 500 mL/1770 kJ chocolate milk, and 
  • Stomach distention with caloric content and oral exposure: oral administration of 500 mL/1770 kJ chocolate milk.
Due to the specific design of the experiment, the distention of the stomach, of which you've learned previously on the SuppVersity that it is a major contributor to the satiety response (see "True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean." | learn more) was fully controlled in the study at hand.
Hunger & desire to eat increase significantly faster after isocaloric liquid vs. solid meals (Tieken. 2007)
No, the study at hand does not imply that you should tube feed yourself: If we take into account that Jones & Mattes observed only recently that the satiety response to liquid meals is generally impaired, even in lean individuals (obese individuals cannot compensate for energy from beverages or solid foods | Jones. 2014), the results may well be different for a solid meal that would be chewed, not just swallowed like the chocolate milk in the study at hand.

Take a look at the data from Tieken et al. (2007) on the left, for example. They found that a liquid meal providing 25% of the daily energy requirement provides a lower and less sustained suppression of hunger and desire to eat than an isocaloric solid meal.
The stomach distention, only, trial can thus serve as a baseline. If we assume that the taste receptors in the mouth were irrelevant and the satiety response would be controlled solely by the amount of type of nutrients that arrive in the stomach, there should be a difference between the control infusion with water and the infusion of chocolate milk, but there should be no difference between the infusion compared to the ingestion of the chocolate milk.
Figure 1: Fullness rating (top) and desire do eat (bottom) in response to infusion (light and dark grey bars) of water and chocolate milk, respectively vs. the ingestion of chocolate milk (dark bars; Spetter. 2014).
As you can see in Figure 1, the latter was not the case. While there were no differences in the fullness ratings (top) and desire to eat (bottom) between chocolate milk and water, when it was infused through the nose, the subjects felt significantly fuller and had a significantly lower desire to eat, when they drank the chocolate milk the way nature intended it.

Things never are as you would expect them to be

Now, everyone would expect that the decrease in desire to eat and the increased fullness in response to the regular (=oral) ingestion of chocolate milk would significantly reduce the energy intake on a subsequent meal, right?
Figure 2: In contrast to what the data in Figure 1 would suggest there was no significant difference between the effects the intra-nasally infused chocolate milk (CM) and the regularly consumed CM had on the ad-lib. intake on a subsequent meal  (Spetter.2014) - How can that be? Maybe the higher satiety hormones in the infusion trial (see Figure 3)
Well, as you can see in Figure 2 this is not the case. There is a reduction in energy intake, but in contrast to the comparison to the water infusion (right), the difference between the oral chocolate milk vs. the intra-nasally infused chocolate milk was not significant.
Figure 3: The increase in the satiety hormones insulin (top) and CCK-8 (bottom) is more pronounced, when the taste receptors in the oral cavity are bypassed (Spetter. 2014)
But why is the intra-nasally administered chocolate milk eventually more "satiating"? Well, if you take a closer look at the previously mentioned CCK-8 and insulin response (see Figure 3), you will see that the increase in these satiety hormones (yes, insulin increases satiety; cf. Anika. 1980; Vanderweele. 1994) is more pronounced, when the taste receptors in the oral cavity are bypassed and the chocolate milk is infused intra-nasally. For the ad-libitum meal that was served 45 minutes later, this increase was more important than the increased feeling of "fullness", let alone the highly subjective desire to eat" (Figure 2).

As Spetter et al. point out, this initially counter-intuitive result provides evidence for the "common but relatively poorly underpinned idea that learned associations between sensory signals and ensuing metabolic consequences serve to adapt hormone responses based on nutrient content" as it was previously observed by Zafra et al. (2006) and Power et al. (2008).

In view of the obesity problem, the results support the idea that a relative lack of oral stimulation, due to e.g. caloric beverage or other fast food consumption can result in overeating by weakening satiety (de Graaf. 2010), an effect of which Jones & Mattes have shown that it is impaired in obese individuals and reduced in lean and obese individuals, when the energy they consume comes from liquid foods, like shakes (Jones. 2014) | Comment on Facebook!
  • Anika, S. M., T. R. Houpt, and K. A. Houpt. "Insulin as a satiety hormone." Physiology & behavior 25.1 (1980): 21-23.
  • de Graaf, Cees, and Frans J. Kok. "Slow food, fast food and the control of food intake." Nature Reviews Endocrinology 6.5 (2010): 290-293.
  • Jones J.B., Mattes R.D. "Effects of learning and food form on energy intake and appetitive responses. Physiol Behav. 21 (2014):1-8.
  • Power, Michael L., and Jay Schulkin. "Anticipatory physiological regulation in feeding biology: cephalic phase responses." Appetite 50.2 (2008): 194-206. 
  • Tieken, S. M., et al. "Effects of solid versus liquid meal-replacement products of similar energy content on hunger, satiety, and appetite-regulating hormones in older adults." Hormone and metabolic research= Hormon-und Stoffwechselforschung= Hormones et metabolisme 39.5 (2007): 389.
  • Vanderweele, Dennis A. "Insulin is a prandial satiety hormone." Physiology & behavior 56.3 (1994): 619-622.
  • Zafra, MarĂ­a A., Filomena Molina, and Amadeo Puerto. "The neural/cephalic phase reflexes in the physiology of nutrition." Neuroscience & Biobehavioral Reviews 30.7 (2006): 1032-1044.