source: Lehninger Principles of Biochemistry (5th Ed, 2008), Chapter 23.4, pg 930-932
I've recently bought the latest edition of Lehninger Principles of Biochemistry ( 5th Edition, 2008). Chapter 23.4 & 23.5 summarises Obesity & the Regulation of Body Mass. Also see my summary of September 2007 Scientific American article.
To a first approximation, obesity is the result of taking in more calories in the diet than are expended by the body's energy consuming activities. The body can deal with an excess of calories in 3 ways:
- convert excess fuel to fat and store it in adipose tissue.
- burn excess fuel by extra exercise.
- "waste" fuel by diverting it to heat production (thermogenesis) by uncoupled mitochondria.
Adipose tissue has important endocrine functions
FIGURE 23-33 Set-point model for maintaining constant mass. When the mass of adipose tissue increases (dashed outline), released leptin inhibits feeding and fat synthesis and stimulates oxidation of fatty acids. When the mass of adipose tissue decreases (solid outline), a lowered leptin production favors a greater food intake and less fatty acid oxidation.
FIGURE 23-34 Obesity caused by defective leptin production. Both of these mice, which are the same age, have defects in the OB gene. The mouse on the right was injected daily with purified leptin and weighs 35 g. The mouse on the left got no leptin, and consequently ate more food and was less active; it weighs 67 g.
FIGURE 23-35 Hypothalamic regulation of food intake and energy expenditure. (a) Anatomy of the hypothalamus and its interaction with adipose tissue. (b) Details of the interaction between the hypothalamus and an adipocyte, described later in the text.
FIGURE 23-36 Hormones that control eating. In the arcuate nucleus, two sets of neurosecretory cells receive hormonal input and relay neuronal signals to the cells of muscle, adipose tissue, and liver. Leptin and insulin are released from adipose tissue and pancreas, respectively, in proportion to the mass of body fat. The two hormones act on anorexigenic neurosecretory cells to trigger release of α-MSH (melanocortin); this produces neuronal signals to eat less and metabolize more fuel. Leptin and insulin also act on orexigenic neurosecretory cells to inhibit the release of NPY, reducing the "eat" signal sent to the tissues. As described later in the text, the gastric hormone ghrelin stimulates appetite by activating the NPY-expressing cells; PYY3-36, released from the colon, inhibits these neurons and thereby decreases appetite. Each of the two types of neurosecretory cells inhibits hormone production by the other, so any stimulus that activates orexigenic cells inactivates anorexigenic cells, and vice versa. This strengthens the effect of stimulatory inputs.