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Provedor de dados:  Nature Precedings
País:  United Kingdom
Título:  Low Protein Diet Consumption Antagonize the Age-associated Change in Hypothalamic GABA Receptor activity
Autores:  Bidhan C. Bandyopadhyay
Lina Chakrabarti
Mrinal K. Poddar
Data:  2008-09-10
Ano:  2008
Palavras-chave:  Neuroscience
Pharmacology
Resumo:  Amounts of dietary protein as well as the duration of its supplementation are critical
factors that correlate with the hypothalamic GABAergic activity and immune function
during aging. Here we evaluate the effect of low (5%) and high (40%) protein diet on the
functional state of hypothalamic GABA receptor in the aging brain in albino rats. Longterm
(LT; for 30 consecutive days) supplementation of low protein diet (LDP) retarded
the age-associated (3 to 18 months) (a) loss of both low and high affinity hypothalamic
GABA receptor sensitivity and (b) increase of high affinity GABA receptor density.
Short-term (ST; for 7 consecutive days) consumption of the same protein diet showed
less effect than that observed under LT period. High protein diet (HPD), on the other
hand, under LT period potentiated the age-induced loss of both high and low affinity
hypothalamic GABA receptor sensitivity, without any significant change in age associated
increase in high affinity hypothalamic GABA receptor density. These results thus suggest that the age-induced changes in hypothalamic GABA receptor sensitivity and density may be (i) antagonised by long-term supplementation of LPD by restoring the age-associated loss of sensitivity of both low and high affinity and increase in density of only high affinity hypothalamic GABA receptor and (ii) augmented by long-term intake of HPD by potentiating only the age-associated loss of sensitivity of hypothalamic GABA receptor of both the affinity sites.
Tipo:  Manuscript
Identificador:  http://precedings.nature.com/documents/2284/version/1

oai:nature.com:10101/npre.2008.2284.1

http://hdl.handle.net/10101/npre.2008.2284.1
Fonte:  Nature Precedings
Direitos:  Creative Commons Attribution 3.0 License
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