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Review
. 2011 Apr 18;103(1):44-50.
doi: 10.1016/j.physbeh.2011.01.012. Epub 2011 Jan 20.

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

Karen L Teff  1
Affiliations
Review

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

Karen L Teff. Physiol Behav. .

Abstract

Learned anticipatory and compensatory responses allow the animal and human to maintain metabolic homeostasis during periods of nutritional challenges, either acutely within each meal or chronically during periods of overnutrition. This paper discusses the role of neurally-mediated anticipatory responses in humans and their role in glucoregulation, focusing on cephalic phase insulin and pancreatic polypeptide release as well as compensatory insulin release during the etiology of insulin resistance. The necessary stimuli required to elicit CPIR and vagal activation are discussed and the role of CPIR and vagal efferent activation in intra-meal metabolic homeostasis and during chronic nutritional challenges are reviewed.

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Figures

Figure 1
Figure 1
Cephalic phase insulin release (left graph), plasma glucose levels (middle graph) and cephalic phase pancreatic polypeptide release (right graph) during a sham-feed (solid circles) compared to fasting (open squares) in normal weight humans (mean±s.e., n=10)
Figure 2
Figure 2
Differential individual responses to sham-feeding. Upper left graph illustrates a cephalic phase insulin response (CPIR) responder who exhibits a large cephalic phase pancreatic polypeptide response CPPP: upper right graph). Bottom left graph illustrates a CPIR non-responder who exhibits an average CPPP response.
Figure 3
Figure 3
Pancreatic polypeptide (PP) levels prior to (open squares) and following (solid circles) 6 weeks of drinking a flavored polycose solution every other day (left graph, mean±s.e., n=10; treatment effect, P<0.01). Inset: cephalic phase PP in response to the taste of flavored polycose solution prior to ingesting the solution, before and after 6 weeks of exposure. Plasma insulin levels (mean±s.e.) in the same individuals under the same conditions (right graph). Inset: CPIR in response to the taste of flavored polycose prior to ingesting the solution, before and after 6 weeks of exposure. No significant effects of the treatment on cephalic phase or post-prandial insulin were found. (Unpublished data, Teff and Breslin).
Figure 4
Figure 4
Hypothesized effect of a chronic metabolic challenge on vagal efferent activity: During a 48-h glucose infusion in humans, increases in circulating glucose and insulin are recognized by the brain resulting in an induction of vagal efferent activity, thereby contributing to an increase in cephalic phase and compensatory insulin release.
Figure 5
Figure 5
Plasma glucose (left graph) and insulin levels (right graph) (mean±s.e., n=16) following a 48-h saline infusion (dotted line, open squares) or glucose infusion (solid line, solid circles). Post-prandial glucose (P<0.01) and insulin levels (P<0.01) were significantly lower following the glucose solution compared to the saline solution. Inset: cephalic phase insulin release during the saline and glucose infusions. CPIR was significantly greater after the glucose infusion compared to saline control (P<0.05). See (Ref 77).
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