content and food intake settle at levels at
which the positive and negative effects on
feeding are in balance.
Kennedy’s ‘lipostatic’ theory of intake
control envisaged the monitoring of the
state of the adipose stores by the brain so
that an excess of fat could be countered by
a reduction in food intake, and depletion of
body energy reserves could be compen-
sated by an increase in intake. The
existence of a humoral factor was shown
by joining pairs of rats in parabiotic union
and destroying the ventromedial hypo-
thalamus of one by electrolytic lesions. The
lesioned rat overate and became obese,
while the unlesioned partner lost weight,
presumably due to a reduction in its food
intake (Hervey, 1959). The parabiotic union
provides a slow exchange of blood between
the partners, presumably allowing suffi-
cient of the ‘feedback from fat factor’ to
reach the unlesioned animal from the
obese one but insufficient to allow enough
of the excess nutrients being taken in by
the latter to provide sufficient nutrition to
maintain the former. The nature of the
humoral factor was unknown but it was
speculated that it might be a steroid
hormone. However, more recent evidence
has implicated insulin, and it now seems
clear that the most important feedback
signal from adipose tissue to the CNS is
leptin.
Insulin
In the 1970s, it was shown that insulin
infused at a low rate into the ventricular
cavities of the brain, from which it can
quickly reach the hypothalamus, caused
reduced food intake in monkeys. Plasma
insulin levels rise as an animal gets fatter
(Vandeermeerschen-Doize et al., 1983), due
to progressive insulin resistance, providing
a link between body fatness and intake
control. However, treatment of animals
with exogenous insulin has often been
observed to cause an increase in intake,
probably in response to the increase in rate
of fat deposition and growth, suggesting
that an insulin-mediated control of intake
by fatness is not a primary means of
control of intake.
In the short term, it has been suggested
that the rise in insulin secretion during
spontaneous meals is responsible for their
termination.Leptin
In 1994, the nature of the deficit of one of
the genetically obese strains of mice was
elucidated with the discovery of ob-protein
(leptin). Recent evidence shows that there
is a similar hormone in sheep (Dyer et al.,
1997), pigs (Barb et al., 1998) and chickens
(Taouis et al., 1998).
Leptin is a hormone, secreted by
adipose cells in proportion to their size,
which circulates in the bloodstream and
influences receptors in the brain. It appears
to interact with the insulin and NPY
systems and thus to be part of an important
control system for food intake in relation to
fatness and metabolism. At the time of
writing, there has been little published on
this subject concerning farm animals, but its
discovery seems likely to prove very impor-
tant in view of the reduced food intake in fat
animals. However, it is not easy to see how
knowledge of the leptin system could be
made use of commercially in farm animals:
if intake is being limited by this feedback
signal from excessive adipose stores, then
neutralizing leptin (e.g. with specific anti-
bodies) would allow food intake to increase
but the extra nutrients would be used for fat
synthesis which is not usually required. If,
on the other hand, the animal is eating
insufficient to support its metabolic needs,
then adipose tissue will have been depleted
and its production of leptin will be very
low, rendering neutralization ineffective.
If it is required to reduce voluntary
intake as, for example, in pregnant sows and
broiler breeder stock, then treatment with
leptin (or an analogue or secretagogue)
would limit intake but likely effects on
reproduction would have to be contended
with (Houseknecht et al., 1998).Integration of factorsAlthough it has sometimes been stated that
only one factor controls intake in any givenPhysiological and Metabolic Aspects 327