Regulation of Food Intake
Regulation of Food
Intake
Most animals unconsciously adjust intake of food to balance energy expenditure. If energy expenditure is increased by greater physical activity, more food is consumed. Most vertebrates, from fish to mammals, eat for calories rather than bulk because, if the diet is diluted with fiber, they respond by eating more. Similarly, intake is adjusted downward following a period of several days when caloric intake is too high.
A hunger center located in the hypothalamus of the brain regulates the intake of food. A drop in the blood glucose level stimulates a craving for food. While most animals seem able to stabilize their weight at normal levels with ease, many humans cannot. Obesity is rising throughout the industrial world and is a major health problem in many countries today. According to recent surveys some 60% of the adult population in the United States meets the current definition of clinical obesity. (Assessment of overweight relies on body mass index [weight in kilograms divided by the square of height in meters], waist circumference, and risk factor for diseases associated with obesity.)
It is becoming clear that many obese people do not eat significantly more food than thin people, but rather they have an inherited genetic predisposition to gain weight on a high-fat diet. Many obese people have a reduced capacity to burn excess calories by “nonshivering thermogenesis” . Placental mammals are unique in having a dark adipose tissue called brown fat, specialized for generation of heat. Newborn mammals, including human infants, have much more brown fat than adults. In human infants brown fat is located in the chest, upper back, and near the kidneys. The abundant mitochondria in brown fat contain a membrane protein called thermogenin that acts to uncouple the production of ATP during oxidative phosphorylation. In people of average weight, an increased caloric intake induces brown fat to dissipate excess energy as heat through the uncoupling action of thermogenin. We call this process “dietinduced thermogenesis.” In many people tending toward obesity, this capacity is diminished.
The body of many mammals contains two kinds of adipose tissue that perform completely different functions. White adipose tissue, which comprises the bulk of body fat, is adapted for the storage of fat derived mainly from surplus fats and carbohydrates in the diet. It is distributed throughout the body, particularly in the deep layers of the skin.Brown adipose tissue is highly specialized for mediating nonshivering thermogenesis rather than for the storage of fat. Brown fat, unique to placental mammals, is especially well developed in hibernating species of bats and rodents, but is present also in many nonhibernating species such as rabbits, artiodactyles, carnivores, and primates (including humans). It is brown because it is packed with mitochondria containing large quantities of iron-bearing cytochrome molecules. In ordinary body cells,ATP is generated by the flow of electrons down the respiratory chain . This ATP then powers various cellular processes. In brown fat cells heat is generated instead of ATP. Thermogenesis is activated by the sympathetic nervous system, which responds to signals from the hypothalamus.
There are other reasons for obesity in addition to the fact that many people simply eat too much and get too little exercise. Fat stores are supervised by the hypothalamus, which may be set at a point higher or lower than the norm. A high setting can be lowered somewhat by exercise, but as dieters are painfully aware, the body defends its fat stores with remarkable tenacity. In 1995, a hormone produced by fat cells was discovered that cures obesity in mutant mice lacking the gene that produces the hormone. The hormone, called leptin, appears to operate through a feedback system that tells the hypothalamus how much fat the body carries. If levels are high, release of leptin by fat cells leads to diminished appetite and increased thermogenesis. The discovery of leptin has initiated a flurry of research on obesity and a resurgence of commercial interest in producing a weight-loss drug based on leptin.
Most animals unconsciously adjust intake of food to balance energy expenditure. If energy expenditure is increased by greater physical activity, more food is consumed. Most vertebrates, from fish to mammals, eat for calories rather than bulk because, if the diet is diluted with fiber, they respond by eating more. Similarly, intake is adjusted downward following a period of several days when caloric intake is too high.
A hunger center located in the hypothalamus of the brain regulates the intake of food. A drop in the blood glucose level stimulates a craving for food. While most animals seem able to stabilize their weight at normal levels with ease, many humans cannot. Obesity is rising throughout the industrial world and is a major health problem in many countries today. According to recent surveys some 60% of the adult population in the United States meets the current definition of clinical obesity. (Assessment of overweight relies on body mass index [weight in kilograms divided by the square of height in meters], waist circumference, and risk factor for diseases associated with obesity.)
It is becoming clear that many obese people do not eat significantly more food than thin people, but rather they have an inherited genetic predisposition to gain weight on a high-fat diet. Many obese people have a reduced capacity to burn excess calories by “nonshivering thermogenesis” . Placental mammals are unique in having a dark adipose tissue called brown fat, specialized for generation of heat. Newborn mammals, including human infants, have much more brown fat than adults. In human infants brown fat is located in the chest, upper back, and near the kidneys. The abundant mitochondria in brown fat contain a membrane protein called thermogenin that acts to uncouple the production of ATP during oxidative phosphorylation. In people of average weight, an increased caloric intake induces brown fat to dissipate excess energy as heat through the uncoupling action of thermogenin. We call this process “dietinduced thermogenesis.” In many people tending toward obesity, this capacity is diminished.
The body of many mammals contains two kinds of adipose tissue that perform completely different functions. White adipose tissue, which comprises the bulk of body fat, is adapted for the storage of fat derived mainly from surplus fats and carbohydrates in the diet. It is distributed throughout the body, particularly in the deep layers of the skin.Brown adipose tissue is highly specialized for mediating nonshivering thermogenesis rather than for the storage of fat. Brown fat, unique to placental mammals, is especially well developed in hibernating species of bats and rodents, but is present also in many nonhibernating species such as rabbits, artiodactyles, carnivores, and primates (including humans). It is brown because it is packed with mitochondria containing large quantities of iron-bearing cytochrome molecules. In ordinary body cells,ATP is generated by the flow of electrons down the respiratory chain . This ATP then powers various cellular processes. In brown fat cells heat is generated instead of ATP. Thermogenesis is activated by the sympathetic nervous system, which responds to signals from the hypothalamus.
There are other reasons for obesity in addition to the fact that many people simply eat too much and get too little exercise. Fat stores are supervised by the hypothalamus, which may be set at a point higher or lower than the norm. A high setting can be lowered somewhat by exercise, but as dieters are painfully aware, the body defends its fat stores with remarkable tenacity. In 1995, a hormone produced by fat cells was discovered that cures obesity in mutant mice lacking the gene that produces the hormone. The hormone, called leptin, appears to operate through a feedback system that tells the hypothalamus how much fat the body carries. If levels are high, release of leptin by fat cells leads to diminished appetite and increased thermogenesis. The discovery of leptin has initiated a flurry of research on obesity and a resurgence of commercial interest in producing a weight-loss drug based on leptin.
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