Unravelling the controls that make us over eat

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Unravelling the controls that make us over eat

Once scientists unravell how the brain controls appetite I think we will finally start to see some real controls for over eating.

The offshoot may be a population who are slimmer and therefore healthier, with lower food production required. Guess we all win in that case.

More on the site. ....


However, hopes for easily losing weight by simply taking leptin have not been borne out by human experiments.

The new research helps explain why -- namely, that leptin works in a delicately calibrated system whose workings may be established at least in part even before birth.

The experiments were done in mice that are genetically incapable of making leptin. These so-called ob/ob animals are grossly overweight compared with their brethren.

In both studies, researchers examined cells in an ancient part of the brain called the hypothalamus.

Although it constitutes less than 1 percent of the brain's volume, the hypothalamus contains neural circuits governing numerous vital functions, including body temperature, heart rate, blood pressure, the water content of blood and food intake.

One region contains two cell types with opposite actions on eating. When NPY cells are stimulated, feeding increases and fat accumulates; when POMC cells are stimulated, feeding decreases and, eventually, so does body mass.

Both types are constantly active, and the relative intensity of their action is one of several things that determine how often and how much an animal eats.

Friedman, along with Shirly Pinto of Rockefeller University and Tamas L. Horvath of Yale University, measured both the electrical activity and the number of intracellular connections, called synapses, in both types of cells.

When a mouse is leptin-deficient, the NPY cells that stimulate feeding are more active, and POMC cells are less active, compared with normal animals. In the normal animals' NPY cells, there were more inhibitory than stimulatory connections coming to them from other cells. In the ob/ob mice, that situation was reversed.

The effect of this was to make the leptin-deficient animals eat more and make more fat cells in a futile effort to make leptin.

The researchers then gave the hormone to the deficient animals and watched what happened.

Once exposed to enough leptin, there was a sixfold reduction in the number connections to the NPY cells that stimulate them and promote feeding, and a near doubling of the satiety-inducing connections. Reciprocal changes were seen in the POMC cells. This subtle rewiring occurred within six hours of giving the animals leptin. Two days later, their feeding slowed, and 12 days later their weight began to fall.

While further research must be done to learn what happens in the brain during weight loss, the mouse experiments might determine the "set point" this way:

When a person loses fat, leptin levels in the blood fall. Hypothalamic wiring might then change so that NPY cells get more input that stimulates feeding, and POMC cells get more connections that blunt satiety.

"The net effect is that you would have a stimulus to eat more, eventually deposit more fat and make more leptin -- at which point your wiring diagram normalizes," Friedman said.
By netchicken: posted on 5-4-2004

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