The Timing of Meals.

Strubbe, J.H.; Woods, Stephen C.

doi:10.1037/0033-295x.111.1.128

Cited by 144 publications

(111 citation statements)

References 144 publications

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“…In this light, eliciting a neurally induced slight decrease of glucose can be viewed as an appropriate preparation to circumvent an otherwise excessive increase of glucose. We (Ramsay et al 1996;Strubbe & Woods 2004;Woods 1991;Woods & Ramsay 2000;Woods & Strubbe 1994), as well as other contemporary writers (Dworkin 1993;Schulkin 2003), believe that this better captures the essence of the concept of regulation originally espoused by Bernard.…”

Section: Negative Feedbackmentioning

confidence: 99%

“…In this light, although meals are obviously necessary for the defense of body weight in the long run, it has been argued (e.g., (Bolles 1980)) that feeding per se is not regulated because it is not being driven by deficits. In contrast, body adiposity can be considered to be regulated because perturbations in body fat elicit corrective effector responses to restore adiposity (Ramsay et al 1996;Seeley et al 1997;Strubbe & van Dijk 2002;Strubbe & Woods 2004;Woods et al 1974;Woods & Strubbe 1994). …”

Section: Regulation Vs Control: Body Adiposity Vs Food Intakementioning

confidence: 99%

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Homeostasis: Beyond Curt Richter

Woods

Ramsay

2007

Appetite

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Curt Richter introduced behavioral control into the concept of homeostasis, thereby opening entire fields of research. The prevailing dogma, and the techniques he used, conspired to lead Richter and others to interpret regulation in strict negative feedback terms. Although this point of view continues to be embraced by many contemporary biologists, we believe that prevailing sentiment favors a broader view in which organisms integrate anticipatory pre-emptive control over regulated variables whenever possible.

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Section: Negative Feedbackmentioning

confidence: 99%

Section: Regulation Vs Control: Body Adiposity Vs Food Intakementioning

confidence: 99%

Homeostasis: Beyond Curt Richter

Woods

Ramsay

2007

Appetite

Self Cite

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“…Episodic signals that indicate nutrient availability are derived from the gut, liver and blood. In addition, there are episodic signals that relay information about circadian, seasonal and reproductive rhythms, stress and other factors (Berthoud, 2002;Strubbe & Woods, 2004), which are beyond the scope of the present article.…”

Section: Episodic Homeostatic Regulation Of Feedingmentioning

confidence: 99%

Central regulation of energy balance: inputs, outputs and leptin resistance

Arch

2005

Proc. Nutr. Soc.

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The regulation of energy balance is complex and, in man, imprecise. Nevertheless, in many individuals intake and expenditure are balanced with <1% error with little or no conscious effect. Essential components of such a regulatory system are signals, leptin and insulin, that reflect the size of lipid stores. Leptin receptors signal via phosphatidylinositol 3-kinase (as do insulin receptors) and via the transcription factor signal transducer and activator of transcription-3 to activate various types of neurone. Obese rodents, and possibly man, are resistant to leptin; in some cases because of genetic or perinatal programming (primary resistance), but commonly in response to high leptin levels (secondary resistance). Secondary leptin resistance may be a result of reduced transport of leptin to the brain or down-regulation of leptin signalling. Signals that reflect lipid stores form the tonic homeostatic regulatory system. They interact with episodic homeostatic signals carried by neurones, hormones and metabolites to regulate meal size and frequency. They also interact with signals related to the palatability of food, biorhythms and learning. Many neurotransmitters and hormones mediate responses to more than one input (e.g. gastric and adipocyte leptin), but are nevertheless most involved with particular inputs (e.g. leptin with adipocyte fat stores). Feeding can be divided into appetitive (preparation for feeding) and consummatory phases, which can both be further subdivided. Different sets of neurotransmitters and hormones are involved at each stage. In the long term it may be possible to customise obesity therapies according to those inputs and outputs that are most disturbed and most amenable to intervention in individual subjects.

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“…Th e mechanisms controlling satiation determine the size of the meal. Satiety is a period of time between the meals with no hunger (Strubbe and Woods 2004). Th is time period is variable and its termination coincides with the refeeling of the hunger accompanied by the consumption of the next meal, thus resuming the cycle of the food intake (Hargrave and Kinzig 2012) (Figure 1).…”

Section: Satiety and Adiposity Signalsmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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The Timing of Meals.

Cited by 144 publications

References 144 publications

Homeostasis: Beyond Curt Richter

Homeostasis: Beyond Curt Richter

Central regulation of energy balance: inputs, outputs and leptin resistance

Central and peripheral control of food intake

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