What Does Brown
Adipose Tissue Have to Do with Obesity?
When electron transport generates a proton gradient, some of the
energy produced takes the form of heat. Dissipation of energy as heat is useful
to organisms in two situations: cold-induced nonshivering thermogenesis
(production of heat) and diet-induced thermogenesis. Cold-induced nonshivering
thermogenesis enables animals to survive in the cold once they have become
adapted to such conditions, and diet-induced thermogenesis prevents the
development of obesity in spite of prolonged overeating. (Energy is dissipated
as heat as food molecules are metabolized instead of being stored as fat.)
These two processes may be the same biochemically. It is firmly established
that they occur principally, if not exclusively, in brown adipose tissue (BAT),
which is rich in mitochondria. (Brown fat takes its color from the large number
of mitochondria present in it, unlike the usual white fat cells.) The key to
this “inefficient” use of energy in brown adipose tissue appears to be a
mitochondrial protein called thermogenin, also referred to as the “uncoupling
protein.” When this membrane-bound protein is activated in thermogenesis, it
serves as a proton channel through the inner mitochondrial membrane. Like all
other uncouplers, it “punches a hole” in the mitochondrial membrane and
decreases the effect of the proton gradient. Protons flow back into the matrix
through thermogenin, bypassing the ATP synthase complex.
Very little research on the biochemistry or physiology of brown
adipose tissue has been done in humans. Most of the work on both obesity and
adaptation to cold stress has been done on small mammals, such as rats, mice,
and hamsters. What role, if any, brown fat deposits play in the development or
prevention of obesity in humans is an open question for researchers. Recently,
researchers have devoted much energy toward identifying the gene that encodes
the uncoupling protein involved in obesity. The ultimate goal of this research
is to use the protein or drugs that alter its regulation to combat obesity.
Some researchers have also proposed a link between sudden infant
death syndrome (SIDS), which is also known as crib death, and metabolism in
brown fat tissue. They think that a lack of BAT, or a switch from BAT to normal
adipose tissue too early, could lead to body-temperature cooling in a way that
could affect the central nervous system.
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