Wow - mixing blood/vascular systems causes weight loss in mice...

[Guest guest]

This is a very odd little piece of research with some awfully

interesting aspects, if you ask me... not that it's too practical.

(Find a skinny person and glom onto them?)

--

From:

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/pregastric/f

atgenes.html

....To understand the physiology behind the " obesity genes " currently

under investigation, it is valuable to first look back at some

experiments conducted in the 1960's using parabiotic mice. The

technique of parabiosis, which is rarely used today, involves making

an incision along the lateral aspect of two animals, then suturing

them together to form a parabiotic pair. The key utility of this

technique is that it unites the vascular systems of the two animals,

allowing exchange of blood-borne molecules.

Many years ago, geneticists identified in mice two recessive

mutations which, if homozygous, led the mice to become grossly obese.

The two genes were termed ob and db. Parabiotic pairs constructed

between ob/ob, db/db and normal mice led to the following

observations:

Pairing an obese ob/ob mouse with a normal mouse: the ob/ob mouse

lost weight

Pairing an obese db/db mouse with a normal mouse: the normal mouse

stopped eating and lost weight

Pairing an obese ob/ob mouse with an obese db/db mouse: the ob/ob

mouse stopped eating and lost weight, whereas the db/db mouse was

unaffected.

An additional experiment showed that when one of a pair of normal

parabiotic mice was overfed, its " twin " lost weight.

These observations were consistent with the idea that a satiety

hormone, presumably the ob gene product, is produced which binds to

receptors, presumably the db gene product, in the hypothalamus and

suppresses hunger.

Considerable support was recently obtained for this model by the

cloning of the ob and db genes from several species. The ob gene

encodes the hormone leptin and the db gene the leptin receptor.

Leptin is secreted by fat cells and has dual activity of decreasing

food intake and increasing metabolic rate, which makes the

old " lipostatic theory " for control of food intake very appealing...

[Guest guest]

LOL. I think the idea is to use the genetic products, not put two humans

together. However, I don't know if they have been able to use this in

practicum.

cinnamonbelle <cinnamonbelle@...> wrote:

This is a very odd little piece of research with some awfully

interesting aspects, if you ask me... not that it's too practical.

(Find a skinny person and glom onto them?)

--

From:

http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/pregastric/f

atgenes.html

....To understand the physiology behind the " obesity genes " currently

under investigation, it is valuable to first look back at some

experiments conducted in the 1960's using parabiotic mice. The

technique of parabiosis, which is rarely used today, involves making

an incision along the lateral aspect of two animals, then suturing

them together to form a parabiotic pair. The key utility of this

technique is that it unites the vascular systems of the two animals,

allowing exchange of blood-borne molecules.

Many years ago, geneticists identified in mice two recessive

mutations which, if homozygous, led the mice to become grossly obese.

The two genes were termed ob and db. Parabiotic pairs constructed

between ob/ob, db/db and normal mice led to the following

observations:

Pairing an obese ob/ob mouse with a normal mouse: the ob/ob mouse

lost weight

Pairing an obese db/db mouse with a normal mouse: the normal mouse

stopped eating and lost weight

Pairing an obese ob/ob mouse with an obese db/db mouse: the ob/ob

mouse stopped eating and lost weight, whereas the db/db mouse was

unaffected.

An additional experiment showed that when one of a pair of normal

parabiotic mice was overfed, its " twin " lost weight.

These observations were consistent with the idea that a satiety

hormone, presumably the ob gene product, is produced which binds to

receptors, presumably the db gene product, in the hypothalamus and

suppresses hunger.

Considerable support was recently obtained for this model by the

cloning of the ob and db genes from several species. The ob gene

encodes the hormone leptin and the db gene the leptin receptor.

Leptin is secreted by fat cells and has dual activity of decreasing

food intake and increasing metabolic rate, which makes the

old " lipostatic theory " for control of food intake very appealing...