Blood Glucose Dynamics and Control of Meal Initiation: A Pattern Detection and Recognition Theory

Abstract

A new framework for understanding the control of feeding behavior, with special emphasis on the evolution of hunger, the initiation of feeding, and its dependence on patterns of blood glucose, is the subject of this review. A perspective on the current status and future directions of this search for a more complete understanding of the regulation of feeding behavior in laboratory rats and humans is presented including theoretical and experimental components. First, a historical perspective on the role of blood glucose in the control of feeding is presented. Next, the theoretical approaches that have been applied to the control of feeding and had a strong influence on experimental feeding research are summarized. This is followed by a statement and overview of a current theory that has emerged from studies of the role of transient declines in blood glucose in the control of meal initiation. The current working hypothesis that transient declines in blood glucose are endogenous metabolic patterns that are detected and recognized by the central nervous system and are mapped into meal initiation in rats and are correlated with meal requests in humans are then presented. Then, the experimental studies on meal initiation and its dependence on patterns of blood glucose, first in rats and then in humans, are reviewed in detail. Finally, the future directions of the work, limitations, and the implications for the understanding of the control of feeding behavior and the regulation of energy balance are discussed.

Effect of the glycemic index of carbohydrates on day-long (10 h) profiles of plasma glucose, insulin, cholecystokinin and ghrelin

“…The concentration of the 'hunger' hormone, GHR, also rose and fell in a predictable meal-related pattern, but there was no detectable difference between the high and low GI diets. 'Dynamic' falls in blood glucose, however, have been associated with meal initiation in animal and human studies (Campfield and Smith, 2003) and a rise in counterregulatory hormones and food energy intake in obese adolescents (Ludwig et al, 1999). The findings therefore provide a mechanism to explain higher satiety and greater falls in body fat on low GI diets in some settings.…”

“…Mayer's glucostatic theory of food intake regulation postulates transient declines in blood glucose are the most important determinant of feeding drive (Mayer, 1953). There is substantial evidence supporting the detection of low blood glucose by the central nervous system as a signal for meal initiation and/or hunger in both rats and humans (Campfield and Smith, 2003). Insulin itself may also influence acute satiety (Holt et al, 1992) and act as a long-term adiposity signal (Woods et al, 2006).…”

The glucostatic theory of appetite control and the risk of obesity and diabetes

“…These studies led to the classical lipostatic, 1 aminostatic, 2 and thermostatic 3 theories of food intake control as well as more recent hypotheses. [4][5][6] However, all of these theoretical ideas were preceded by the notion that glucose uptake and utilization played a central and metabolically privileged role in the control of hunger, satiety and the regulation of body energy balance. Although these notions were first discussed and suggested by Carlson in a classic text published in 1916, 7 they were formalized by Jean Mayer into the classical glucostatic theory in the mid 1950s.…”

“…The accentuation of the glucose area below fasting levels observed at plateau is a matter of preoccupation if one refers to the glucostatic theory of appetite control and subsequent studies. [6][7][8][9][19][20][21][22][23][24][25] Taken together, these findings suggest that blood glucose fluctuations may have biopsychological consequences and may be perceived as a source of signaling favoring weight regain.…”

“…Indeed, at the 180th minute of this test, the glycemia was significantly lower than that before treatment. Even though these values do not necessarily represent clinical hypoglycemia, they might carry some importance as a fall in blood glucose may trigger episodes of feeding [6][7][8][9][19][20][21][22][23][24][25] and some metabolic counterregulation such as hyperglucagonemia 33 as discussed above. Interestingly, the span between the maximal and minimal glucose concentrations was the same before and after weight loss, suggesting that a shift toward hypoglycemia has occurred over the course of the programme.…”