Open AccessEffect of Enterostatin on the Feeding Responses to Galanin and NPY
Author(s) -
Lin Ling,
Gehlert Donald R.,
York David A.,
Bray George A.
Publication year - 1993
Publication title -
obesity research
Language(s) - English
Resource type - Journals
eISSN - 1550-8528
pISSN - 1071-7323
DOI - 10.1002/j.1550-8528.1993.tb00610.x
Subject(s) - galanin , medicine , endocrinology , receptor , chemistry , stimulation , neuropeptide y receptor , neuropeptide
We have investigated the possibility that enterostatin may inhibit the intake of dietary fat by inhibiting either galanin or NPY‐induced feeding pathways. Rats, adapted to either high fat (HF) or low fat‐high carbohydrate (HC) diets and fitted with third ventricular cannulas were used to study the effects of intracerebroventricular (icv) enterostatin on icv NPY and galanin induced feeding responses in satiated rats. An equimolar dose of enterostatin (0.1nmoles) inhibited, while a tenfold excess of entersotatin abolished the feeding response to galanin in rats adapted to a HF diet. The galanin stimulation of food intake was reduced in rats adapted to the HC diet and this response was less sensitive to inhibition by enterostatin. Enterostatin had no inhibitory effects on NPY‐induced feeding in rats adapted to the HC diet and only a small inhibitory effect, at tenfold molar excess, in rats adapted to the HF diet. The ability of enterostatin to bind to galanin or NPY Y‐1 receptors was investigated in lig and binding studies. Enterstatin fialed to dispace 125 I‐galanin or 125 I‐PYY from specific binding sites in rat forebrain homogenates or SK‐N‐MC cells respectively. The data provide support for the hypothesis that enterostatin specifically inhibits a galanin‐responsive fat intake system, but indicate that this effect is not modulated by direct interaction with either galanin or NPY‐Y1 receptors.