Functional coupling between transient declines in blood glucose and feeding behavior: Temporal relationships

La, Campfield; Fj, Smith

doi:10.1016/0361-9230(86)90250-9

Cited by 93 publications

(50 citation statements)

References 26 publications

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“…They observed that blood glucose concentration declined 6-8% at 5.0 ± 0.3 min before meal onset in both the dark and light phases of the light-dark cycle. Campfield and Smith 20,21 have confirmed and extended these initial findings. Similar results were obtained in humans who were blinded as to the time of the day.…”

mentioning

confidence: 78%

“…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.…”

mentioning

confidence: 99%

“…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.…”

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confidence: 99%

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

Chaput

Tremblay

2008

Int J Obes

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More than 50 years ago, Jean Mayer proposed that changes in blood glucose concentrations or arteriovenous glucose differences are detected by glucoreceptors that affect energy intake. According to this theory, an increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect. The pioneering work of Mayer has recently received support from our group as low glycemia has been shown to be linked with body weight gain prospectively and has been considered as a strong predictor of the amount of weight regained after weight loss. This state of mild hypoglycemia also predicts the increase in depressive symptoms with weight loss and a greater propensity to glucose intolerance and type 2 diabetes, particularly for individuals having short sleep durations. Furthermore, knowledgebased work has been shown to induce a significant increase in spontaneous energy intake being related to changes in glycemic control. In accordance with the glucostatic theory, this oriented review suggests that factors favoring a trend toward hypoglycemia and/or glucose instability might induce excess energy intake, overweight and impaired glucose tolerance. Data also raise the possibility that fat gain might be protective against mild hypoglycemia by providing compensation to the stimuli promoted by a modern environment. Keywords: body weight; glycemia; glucose homeostasis; glucose intolerance; metabolism; weight gainThe identification of the biochemical basis for hunger and meal initiation, and of the signals controlling these neurobiological processes have been the subject of extensive research and debate for some decades regarding the control of food intake. 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. 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. 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...

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confidence: 78%

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confidence: 99%

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confidence: 99%

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

Chaput

Tremblay

2008

Int J Obes

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“…It has long been known that feeding behavior is stimulated when circulating glucose levels or glucose utilization are reduced (102,123,124), and through studies using pharmacological agents, carbohydrate is now found to be the nutrient of choice under these conditions (125,126). This indicates that alterations in the metabolism or storage of a specific nutrient may be linked to a specific behavioral change designed to rapidly restore this particular nutrient (104,107,115).…”

Section: Nutrient Ingestion and Metabolismmentioning

confidence: 99%

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Tempel

Leibowitz

1994

J Neuroendocrinology

195

127

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The glucocorticoid, corticosterone (CORT), is believed to have an important function in modulating nutrient ingestion and metabolism. Recent evidence described in this review suggests that the effects of this adrenal hormone are mediated through two steroid receptor subtypes, the type I mineralocorticoid receptor and the type II glucocorticoid receptor. These receptors, which have different affinities for CORT, respond to different levels of circulating hormone. They mediate distinct effects of the steroid, which can be distinguished by the specific nutrient ingested and by the particular period of the circadian cycle.Under normal physiological conditions, the type I receptor is tonically activated, either by low basal levels of circulating CORT (0.5-2 pg%) normally available across the circadian cycle or possibly by the mineralocorticoid aldosterone. This type I activation is required for the maintenance of fat ingestion and fat deposition that occurs during most meals of the feeding cycle. In contrast, the type II receptor is phasically activated by moderate levels of CORT (2-1 0 pg%) normally reached during the circadian peak. Activation of this receptor is required for the natural surge in carbohydrate ingestion and metabolism that is essential at the onset of the active feeding cycle when the body's glycogen stores are at their nadir, and gluconeogenesis is needed to maintain blood glucose levels. This receptor is also activated during periods of increased energy requirements, such as, after exercise and food restriction, when CORT levels rise further ( > 10 pg%) and when its catabolic effects on fat and protein stores predominate to provide additional substrates for glucose homeostasis. These functions of CORT on fat and carbohydrate balance are mediated, in part, by type I and type II receptors located within the hypothalamic paraventricular nucleus, which is known to have key functions in controlling nutrient intake and metabolism, as well as circulating CORT levels. Moreover, the type II receptors within this nucleus, in addition to the arcuate nucleus, may interact positively with the peptide, neuropeptide Y, and the catecholamine, norepinephrine, both of which act to enhance natural carbohydrate feeding and CORT release at the onset of the natural feeding cycle.Thus, under normal conditions, endogenous CORT has a primary function in controlling nutrient ingestion and metabolism over the natural circadian cycle, through the coordinated action of the type I and type II steroid receptor systems. Through this action, CORT has impact on total caloric intake and body weight gain over the long term. Moreover, under conditions of obesity, diabetes and food restriction, steroid receptor function is greatly disturbed in association with chronic high circulating levels of CORT and abnormal glucose homeostasis. These disturbances in steroid action, along with dysfunction in brain neurochemical processes, very possibly contribute to the maintenance of hyperphagia and body weight gain in obese and diabetic ...

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“…An episode of feeding occurs during the rising phase of core temperature, starting some time after its onset and ceasing when it reaches 39.3"C (starting and finishing at lower temperatures during the light phase) (13). A transient dip in blood glucose concentration has been observed prior to the time of meal onset in rats and proposed as part of the initiation signal (8)(9)(10). Attempts to attribute such a dip to pulsatile insulin secretion have not proved entirely successful (47) and its cause has remained obscure.…”

mentioning

confidence: 99%

Does Thermoregulatory Feeding Occur in Newborn Infants? A Novel View of the Role of Brown Adipose Tissue Thermo genesis in Control of Food Intake

Himms‐Hagen

1995

Obesity Research

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HIMMS-HAGEN, JEAN. Does thermoregulatory feeding occur in newborn infants? A novel view of the role of brown adipose tissue thermogenesis in control of food intake. Obes Res. 1995;3:361-369. The physiological significance of the extensive deposits of brown adipose tissue (BAT) in newborn human infants has been the subject of much experimentation and discussion. Because of its large thermogenic capacity, its function has usually been viewed as preparing the infant for producing heat in response to cold exposure at birth. Newborn infants are indeed capable of precise thermoregulation for a limited time over a rather limited range of ambient temperatures, from thermoneutrality (32-34'C) down to common "room" temperatures (24-28'C). During such mild "cold-exposure", in response to a decrease in their skin temperature, their sympathetic nervous system activity increases, and they can more than double their resting metabolic rate, principally by thermogenesis in their BAT. This review puts forward an entirely new role for BAT thermogenesis in the cyclic feeding pattern of newborn infants during their first months of life. BAT thermogenesis is proposed to be an integral element in a physiological thermoregulatory feeding control mechanism in which extended periods of very gradual cooling are interspersed with episodes of increased sympathetic nervous system activity, increased heating via BAT thermogenesis, arousal, and feeding. The cry with which the baby attracts its mother's attention is an integral part of the mechanism, as is the nutritive suckling reflex and the behavior of the mother. Initiation of feeding is attributed to a transient dip in blood glucose concentration that is due to stimulation of glucose utilization in the BAT. Termination of feeding is attributed to the high temperature brought about by the stimulated BAT thermogenesis. The duration of the urge to feed extends from the time of the cry to the time of the peak rise in temperature, when feeding stops. There is no clear circadian rhythm in core temperature in newborn infants, and meals occur at fairly frequent intervals both day and night in infants that are fed on demand. These physiological mechanisms are consistent with the limited information on phenomena attending spontaneous feeding in the newborn human infant and with what is known about the physiological control of feeding in rats. In rats, thermoregulatory feeding is defined as a feeding episode that occurs during a transient but marked increase in sympathetic nervous system activity that has several consequences.It stimulates BAT thermogenesis and increases body temperature. It produces a transient decline in blood glucose concentration secondary to the increased uptake of glucose by the stimulated BAT; this signals the initiation of the feeding episode. Subsequently the high temperature induced by BAT thermogenesis signals termination of the feeding episode. The size of the meal is determined by the balance between the capacity for BAT thermogenesis (heat production) and ambie...

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Functional coupling between transient declines in blood glucose and feeding behavior: Temporal relationships

Cited by 93 publications

References 26 publications

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

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

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Does Thermoregulatory Feeding Occur in Newborn Infants? A Novel View of the Role of Brown Adipose Tissue Thermo genesis in Control of Food Intake

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