Appetite Regulation: From the Gut to the Hypothalamus
Appetite Regulation: From the Gut to the Hypothalamus
Obesity is a serious medical condition whose prevalence is rising. Figures from the Health Survey for England show that, in 1980, 8% of women and 6% of men were classified as obese, as defined by a body mass index (BMI) of greater than 30 kg/m. By 2001, these proportions had increased to 26% and 22%, respectively, with 55% of women and 66% of men being overweight (BMI > 25 kg/m; Health Survey for England, 2001), reflecting a worldwide trend which is most marked in, but not restricted to, the developed world. Most of us in affluent countries live in a privileged land of plenty where high calorie foods are easily available and in which we have a limited need for exercise. The rising prevalence of obesity in children is of particular concern (Chinn & Rona, 2001).
Obesity is associated with significant morbidity and mortality, which can be attributed to increased risk of a number of medical conditions (Kopelman, 2000) including type II diabetes mellitus, hypertension and coronary heart disease, the most common cause of premature mortality in the obese population. Less well known are the associations between obesity and several cancers including breast, endometrial, prostate and bowel cancer (Daling et al., 2001). Obesity predisposes to osteoarthritis particularly in the large weight-bearing joints and to respiratory problems including obstructive sleep apnoea. Thus obesity poses an immense and increasing public health burden.
Despite the increase in population obesity described above, it should not be forgotten, in individual people, energy balance is usually very precise. Daily intake of food is highly variable and correlates poorly with energy expenditure, whereas over longer periods body weight is stable in most adults (Edholm, 1977). In this article, we will explore how appetite and food intake are regulated peripherally by adipose tissue and the gastrointestinal tract, and how these signals are relayed in the hypothalamus (Fig. 1). We will discuss which of these pathways might be pharmacologically manipulated.
Obesity is a serious medical condition whose prevalence is rising. Figures from the Health Survey for England show that, in 1980, 8% of women and 6% of men were classified as obese, as defined by a body mass index (BMI) of greater than 30 kg/m. By 2001, these proportions had increased to 26% and 22%, respectively, with 55% of women and 66% of men being overweight (BMI > 25 kg/m; Health Survey for England, 2001), reflecting a worldwide trend which is most marked in, but not restricted to, the developed world. Most of us in affluent countries live in a privileged land of plenty where high calorie foods are easily available and in which we have a limited need for exercise. The rising prevalence of obesity in children is of particular concern (Chinn & Rona, 2001).
Obesity is associated with significant morbidity and mortality, which can be attributed to increased risk of a number of medical conditions (Kopelman, 2000) including type II diabetes mellitus, hypertension and coronary heart disease, the most common cause of premature mortality in the obese population. Less well known are the associations between obesity and several cancers including breast, endometrial, prostate and bowel cancer (Daling et al., 2001). Obesity predisposes to osteoarthritis particularly in the large weight-bearing joints and to respiratory problems including obstructive sleep apnoea. Thus obesity poses an immense and increasing public health burden.
Despite the increase in population obesity described above, it should not be forgotten, in individual people, energy balance is usually very precise. Daily intake of food is highly variable and correlates poorly with energy expenditure, whereas over longer periods body weight is stable in most adults (Edholm, 1977). In this article, we will explore how appetite and food intake are regulated peripherally by adipose tissue and the gastrointestinal tract, and how these signals are relayed in the hypothalamus (Fig. 1). We will discuss which of these pathways might be pharmacologically manipulated.
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