Insulin resistance syndrome: defective GABA neuromodulation as a possible hereditary pathogenetic factor (the 'GABA hypothesis').
The origin of the insulin resistance syndrome which, mostly through its cardiovascular implications, is characterized by a high incidence of death, is still practically unknown. Energy and glucose homeostasis are under the control of CNS centers and the neurotransmitter GABA modulates the activity of these centers. Alteration of the biochemical structure of GABA receptors is suggested as an interpretation of the origin of the syndrome.
Laboratoires de Recherches Métaboliques, Université de Genéve, Switzerland.
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Blasi
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Jeanrenaud
D000818:Animals; D001921:Brain / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000401:mortality / Q000503:physiopathology*; D030342:Genetic Diseases, Inborn / Q000503:physiopathology*; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology*; D000078790:Insulin Secretion; D008954:Models, Biological; D011963:Receptors, GABA-A / Q000378:metabolism; D013577:Syndrome; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D007328:Insulin; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid