Appetite program in the brain

Is already determined shortly after birth, how much hunger you will develop as an adult?

Two independent groups of scientists introduce surprising new insights over Leptin, that in 1994 discovered proteohormone formed by fatty tie.

The results were able to bring new insights into scientists, as and when Leptin determines his influence on the body weight. Both groups examine laboratory out and discover how leptin influences the nerve tracks in the brain. It is important to the Nucleus Arcuatus of Hypothalamus (ARH), which has numerous receptors for leptin

Sebastian Bouret and colleagues from the Oregon National Primate Research Center report in Science that Leptin unfolds his effect a lot of fruely than previously suspected. Shortly after birth, Leptin provides for the formation of nerve lines in the ARH. These are the same paths that use the hormone later to initiate food intake and energy balance. In other words: Leptin deficiency induces the obesity in childhood – even in the early childhood, the hormone should decide about how much appetite one will have as an adult.

Appetite program in the brain

Leptin demands growth in the Nucleus Arcuatus of Hypothalamus (Arh) (Pictures: Science)

Shirly Pinto and colleagues from the Howard Hughes Medical Institute of Rockefeller University in New York found that fatty-like mausage, which have a leptin deficiency, differ from normal mails based on number and type of connections in the ARH.

The Nucleus Arcuatus of the Hypothalamus (ARH) is considered one of the leading centers for leptin. One group creates the appetite stimulants ("Orexigenic") Neuropeptides, Neuropeptide Y (NPY) and Aguoti Related Protein (AGPR). The second group forms the appetite-underdox neuropeptides, namely POMC (proopio-melanocortin) and Cart (cocaine and ampetamine-regulated peptide). Both nerve cells produce leptin receptors and regulate leptin in a contrastable way.

Appetite program in the brain

The excitatory (red) and inhibitory (blue) influences that act on the NPY and AGPR (yellow) and POMC (GRUN) synapses (normal and fatty mouse)

Thus Leptin activates the POMC / Cart nerves directly, and blocks the activity of the NPY / Agrp nerve cells. NPY / Agrp neurons, in turn, produce the inhibitory neurotransmitter GABA (gammaaminobutary acid), and thus send collateral messengers to the POMC / Cart nerve cells that inhibit these cells. Shirly Pinto and colleagues now report that Leptinarmen Mause the Exititerian Input on the Orexy NPY / Agrp nerve cells exports and at the same time block the anorexy POMC / Cart neurons. Thus, a lack of leptin leads to an increasing activation of the NPY / Agrp neurons and to accept the POMC neurons. Leptin feed reduces this effect in the leptinarms mints both electrophysiologically as well as on the ultrastructural level. These studies suggest that not only the nerve cell activity and the exclusion of neuropeptides is improved, but also the neuronal plasticity in the hyoxhalamic nerve cells, which works the body’s body weight.

Joel Elmquist and Jeffrey Flier from the Harvard Medical School in Boston see in their evaluation a reference to the learning advances in the Hippocampus. They suspect that one "Hypothalamic memorial function" and thus the regulation of the body weight takes place.

Nevertheless, such amptions are still speculation. Thus, the question is unclear how early investigations make the Leptimangel with a stronger influence of the CNS (Ashima, Prabakaran and Flier, Endocrinology 1999), while bouret and colleagues define the influence on a postnatal time window. Also pinto and colleagues stimulate the leptinity of it independently.

The Pinto study also underscores the release of GABA and glutamate, the convenient mediators of the metabolic signal in the brain. Thus, these results could be considered analogously to the stress, since the axis of hypothalamus, zirbeldruse and adrenal bark acts as a long-term effect (Meaney, Annu.Rev.Neurosci. 2001) and thus more meaning preserved than at first glance.

According to the current state of knowledge, Leptin and Ghrelin, a hormone of the pancreatic drum, are the significant circulating peptides that control the food intake. Leptin is present in the high-mabe overweight and should therefore brake food intake, while grelin is clearly suppressed. Accordingly, the overweight beyond a fictitious border had to renew so that they reduce their overweight. This is by no means the case: they survive and accept more important to weight. Therefore, there is a receptor or post receptor defect? The starting point for this could be in the control in the hypothalamus.

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