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Regulation of Food Intake

Principle of Nutrition GTN 207

DR. HAMID JAN B. JAN MOHAMED

By the end of this lecture you should be able to:


Define terms related to food intake Explain the main factors determining food intake Explain the role of central nervous system Discuss hunger-satiety signal from the periphery with regard to: Signals from the gastrointestinal tract Aminostatic signals Glucostatic and glycogenostatic signals Lipostatic or adipostat signal
Explain the Integrated models of food intake control

Definitions
Hunger : The internal or physiological drive to find and eat food (energy) Appetite : The external or psychological influences that encourage us to find and eat specific food (pleasure) Palatable : Food that is pleased to the senses. This may include taste, smell and texture Satiety : A physiological state in which there is no longer desire to eat

WHY DO WE EAT?

The main factors determining food intake

Socioeconomic Factors Eg. Income, food price Biological and Physiological factors Cultural and religious factors Eg. Invitation, fasting, halal, belief

Personal and Psychological factors Eg. Emotion food, angry child

Food choice

Educational Factors Eg. Knowledge vs. diet, economy

Extrinstic factors Eg. Media advert., seasons

Food factors, Eg. Senses, taste, appearance

Biological and physiological factors


The discussion will focus on the following areas:
Role of central nervous system Hunger-satiety signal from the periphery
Signals from the gastrointestinal tract Aminostatic signals Glucostatic and glycogenostatic signals Lipostatic or adipostat signals

Integrated models of food intake control

Role of central nervous system


The hypothalamus is the key to control of food intake. Type of studies: Ablation, electrical and chemical stimulation. People with hypothalamus damage (trauma or tumor) often show abnormalities in feeding behaviour. However, many other extra-hypothalamic areas also play a role in the control of food intake

Hypothalamic neurons
Two subpopulations of hypothalamic neurons, whose activations have opposing effects on food intake, has provided some insights into the functions of the hypothalamic centres. Activation of one subpopulation of neurons, which produce the neurotransmitters neuropeptide Y (NPY) and agouti-related peptide (AgRP), induces hunger sensations leading to increased food intake; these neurons are referred to as the orexigenic NPY/AgRP neurons. In contrast, activation of another subpopulation of neurons, which produce propiomelanocortin (POMC), cocaine and amphetamine-related transcript (CART), leads to the formation of -melanocytestimulating hormone (-MSH) which, via melanocortin receptors, induces satiety and reduces food intake; they are referred to as the anorexigenic POMC/CART neurons

Hunger-satiety signal from the periphery


The sensation of hunger and satiety result from the numerous signals originating from variety of peripheral tissues and organs, including the gastrointestinal tract, liver, adipose tissue and skeletal muscle. Hunger-satiety signal from the periphery are as below: Signals from the gastrointestinal tract Aminostatic signals Glucostatic and glycogenostatic signals Lipostatic or adipostat signals

Signals from the gastrointestinal tract


A. Vagal nerve afferent signals. These act on the CNS and are triggered by (1) gastric stretching, (2) the presence of nutrients in the stomach and small intestine and (3) nutrients arriving at the liver via the portal vein. B. Circulating cholecystokinin (CCK). Release of this gut hormone into the circulation stimulates CCK-A receptors in the liver and the central nervous system and inhibits food intake. C. Direct nutrient effects. Circulating glucose and ketones act on responsive neurons in the CNS. D. Ileal hormone release. Release of glucagon-like peptide-1 (GLP1) by L cells in the ileum may act on hepatic sites or inhibit gastric emptying.

Aminostatic signals
Dietary protein induces satiety in the short term, and consumption of low protein diets leads to increased appetite for protein containing foods. Atkins diet? Aminostatic theory: Food intake is determined by the level of plasma amino acids, and that this could be related to the regulation of lean body mass, which is known to be rigorously defended against experimental or dietary manipulation.

Glucostatic and glycogenostatic signals


Glucostatic theory: There are chemoreceptors in the hypothalamic satiety centre which would be sensitive to the arteriovenous difference in glucose or to the availability and utilisation of glucose. Support: the small decrease of blood glucose observed prior to spontaneous meal consumption. The suppression of food intake induced by infusion of glucose the spontaneous decrease in total energy intake when dietary carbohydrate is increased

Lipostatic or adipostat signals


Lipostatic theory: Substances released from the fat stores function as satiety signals. In contra with the discovery of leptin hormone Leptin, released by adipocyte. Inverse correlation with food intake Adiponectin recently discovered.

Ob/Ob mouse and leptin

Integrated model of food intake control

The various signals from the periphery can be integrated in a model in which the control of food intake is considered in three phases, each with a distinct goal:
1. short-term (hour) blood glucose homeostasis by dampening episodes of hypoglycaemia or hyperglycaemia. 2. medium-term (day) maintenance of adequate hepatic stores of glycogen which, consistent with Flatts glycogenostatic theory, would imply corrective responses to offset deviations from carbohydrate balance during the previous day. 3. long-term (> weeks) maintenance of the bodys fat and protein compartments,. Periods of food deprivation that lead to substantial reductions in body weight are normally followed by increased food intake (hyperphagia). Reanalysis of data on food intake and body composition in humans subjected to experimental semistarvation and refeeding in the classic Minnesota Experiment (Keys et al 1950) suggested that the duration and magnitude of such compensatory hyperphagia is determined by (i) the magnitude of fat loss, (ii) the magnitude of fat-free mass loss and (iii) the severity of energy deprivation (Dulloo et al 1998). These findings are consistent with the existence of powerful signals that relate food intake to body composition as well as to psycho-biological reaction to the state of food deprivation. Conversely, in overfeeding trials, subjects often report great difficulty in maintaining high levels of food intake over long periods of time, and they spontaneously lose weight over subsequent weeks and months, apparently by eating less.

Thank you very much