Food-Related Sensory Stimuli are Able to Promote Pancreatic Polypeptide Elevation Without Evident Cephalic Phase Insulin Secretion in Human Obesity

Abstract

The data concerning the cephalic phase of insulin secretion (CPIS) in human obesity are controversial. We investigated the effect of a variety of sensory challenges on CPIS in 17 non-diabetic obese patients (four males, 13 females, mean age 41.1 years, mean BMI 38.7). Water, saccharin, and lemon juice were used as oral stimuli, and a complete meal was simply presented as visual and olfactory stimulations. Twelve healthy normal-weight subjects (four men, eight women, mean age 39.9, mean BMI 22.5) also underwent oral stimulation as controls, and the patients who underwent the sight and smell stimulations were also tested for pancreatic polypeptide (PP) changes in order to verify the occurrence of truly cephalic reflex during the test. Insulin levels were measured before and after each stimulation (every min for the first 5 min, and then after 10, 20, and 30 min). None of the stimuli (saccharin, lemon juice or water retained in the mouth for 2 min and were then spat out; the combined and separate sight and smell of a meal for 2 min) led to a significant increase in insulin in the obese patients (except in the case of one woman after oral stimulation). The oral stimuli led to a variable CPIS in one female and three male controls. Despite the absence of CPIS, the five obese patients undergoing all three sensory stimulations related to the meal (combined sight and smell, sight alone and smell alone) showed an early and significant increase in plasma PP concentrations within the first 3 min; this was more pronounced after the combined than after the separate exposure. Although only preliminary, these results underline the variability but substantial lack of CPIS in obese patients, thus suggesting that it can be considered a relatively rare and unrelevant event even in the presence of a true brain-mediated reflex revealed by the rapid and consistent increase in PP found in our experiments.

The cephalic phase insulin response to nutritive and low-calorie sweeteners in solid and beverage form

“…Participants also consumed at least 100g of carbohydrate three days prior to testing to standardize carbohydrate metabolism and fasted for 8–10 hours before the visit. Many others have failed to document a response to a variety of sweeteners [16, 19, 23, 66] as well as whole foods [67] or observed it only in subsets of individuals [25, 61, 68, 69] consistent with the present study. However, this variability should not diminish consideration of the likely implications of the CPIR.…”

Exacting Responses: Lack of Endocrine Cephalic Phase Responses Upon Oro-Sensory Exposure

“…However, we also did not find a cephalic PP response. This is not in line with our hypothesis, as several other studies were able to detect a PP response in the absence of a CPIR ( 56 , 57 ).…”

How neural mediation of anticipatory and compensatory insulin release helps us tolerate food

“…While increases in cephalic phase insulin release would be expected to occur coincident with cephalic phase pancreatic polypeptide (CPPP) since both are dependent on vagal activation, we (27) and others (28) have reported increases in CPPP independent of CPIR. This can occur on an individual level as illustrated in Figure 2 where one individual (upper graphs) exhibits robust insulin and PP responses to a sham-feed while the individual in the lower graphs, does not exhibit a CPIR and the PP response is modest.…”