Regulation of Energy Intake and the Body Weight: The Glucostatic Theory and the Lipostatic Hypothesis

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

“…In his 1955 paper, Mayer explicitly argued that the glucostatic theory would account for the short-term control of hunger and food intake, whereas he invoked a lipostatic mechanism to account for the long-term regulation of body weight and energy balance. 9 After the formulation of this hypothesis, there was an increase of research interest in the biological basis of hunger and satiety in both humans and laboratory rats. The initial results of several studies showed that arteriovenous differences in blood glucose concentration were correlated with hunger ratings and food intake under some circumstances.…”

“…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. 8,9 The glucostatic theory of food intake control postulated that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating. Mayer proposed that decreased glucose utilization or 'metabolic hypoglycemia', the point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering 'metabolizing cells', was the signal for meal initiation.…”

“…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.…”

Involvement of neuropeptide Y in glucose sensing in the dorsal hypothalamus of streptozotocin diabetic rats – in vitro and in vivo studies of transmitter release

“…Glucose-sensitive (GS) neurons decrease their firing rate upon increased glucose concentrations, while glucose-responsive (GR) neurons are those that increase their firing in response to increased glucose concentrations. Since the proposal of glucose sensing neurons in the hypothalamus [16], many studies have investigated this question. Effects of systemic glucose on neurons of the lateral hypothalamus (LH), ventromedial nucleus (VMN), paraventricular nucleus (PVN) and arcuate nucleus (ARC) of the hypothalamus, as well as the nucleus tractus solitarius (NTS) of the brainstem have been reported in several mammalian species, including the cat, rat and mouse [17,18,19,20,21].…”