Glucosensing capacity of rainbow trout telencephalon

Abstract

To assess the hypothesis of glucosensing systems present in fish telencephalon, we first demonstrated in rainbow trout by in situ hybridization the presence of glucokinase (GK). Then, we assessed the response of glucosensing markers in rainbow trout telencephalon 6h after ICV treatment with glucose or 2-deoxyglucose (inducing glucoprivation). We evaluated the response of parameters related to the mechanisms dependent on GK, liver X receptor (LXR), mitochondrial activity, sweet taste receptor, and sodium-glucose linked transporter 1 (SGLT-1). We also assessed mRNA abundance of neuropeptides involved in the metabolic control of food intake (NPY, AgRP, POMC, and CART) as well as abundance and phosphorylation status of proteins possibly involved in linking glucosensing with neuropeptide expression such as Akt, AMPK, mTOR, and CREB. The responses obtained support the presence in telencephalon of a glucosensing mechanism based on GK and maybe one based on LXR, but do not support the presence of mechanisms dependent on mitochondrial activity and SGLT-1. The mechanism based on sweet taste receptor responded to glucose, but in a converse way to that characterized previously in hypothalamus. In general, systems responded only to glucose, but not to glucoprivation. Neuropeptides did not respond to glucose or glucoprivation. In contrast, the presence of glucose activates Akt and inhibits AMPK, CREB, and FoxO1. This is the first study in any vertebrate species in which the response to glucose of putative glucosensing mechanisms is demonstrated in telencephalon. Their role might relate to processes other than homeostatic control of food intake such as the hedonic and reward system.

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