Effect of long-term insulin on body weight and food intake: Intravenous versus intraperitoneal routes

Larue-Achagiotis, Christiane; Magnen, J. Le

doi:10.1016/s0195-6663(85)80001-5

Cited by 17 publications

(1 citation statement)

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“…The role of insulin on appetite in mammals is characterized by a dose-dependent reduction in food intake and body mass when administered directly into the CNS (Woods et al, 2006), although both food intake and body mass were reported to increase after intraperitonal (i.p.) infusion of insulin (Larue-Achagiotis and Le Magnen, 1985). In fish, the effects of insulin treatment on food intake are contradictory.…”

Section: Introductionmentioning

confidence: 99%

In vitro insulin treatment reverses changes elicited by nutrients in cellular metabolic processes that regulate food intake in fish

Blanco

Bertucci

Soengas

et al. 2020

Journal of Experimental Biology

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This research assessed the direct effects of insulin on nutrientsensing mechanisms in the brain of rainbow trout (Oncorhynchus mykiss) using an in vitro approach. Cultured hypothalamus and hindbrain were exposed to 1 µmol l −1 insulin for 3 h, and signals involved in appetite regulation and nutrient-sensing mechanisms were measured. Additionally, the involvement of the phosphatidylinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in the actions of insulin was studied by using the inhibitor wortmannin. Treatment with insulin alone did not elicit many changes in the appetite regulators and nutrient-sensing-related genes and enzymes tested in the hypothalamus and hindbrain. However, we found that, when insulin and nutrients were added together, insulin reversed most of the effects exerted by nutrients alone, suggesting that insulin changes responsiveness to nutrients at the central level. Effects reversed by insulin included expression levels of genes related to the sensing of both glucose (slc2a2, slc5a1, gck, pck1, pklr, g6pcb, gys1, tas1r3 and nr1h3 in the hindbrain, and slc2a2, pklr and pck1 in the hypothalamus) and fatty acid (cd36 in the hindbrain, and cd36 and acly in the hypothalamus). Nutrient-induced changes in the activity of Acly and Cpt-1 in the hindbrain and of Pepck, Acly, Fas and Hoad in the hypothalamus were also reversed by insulin. Most of the insulin effects disappeared in the presence of wortmannin, suggesting the PI3K/Akt pathway is a mediator of the effects of insulin reported here. This study adds new information to our knowledge of the mechanisms regulating nutrient sensing in fish.

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Section: Introductionmentioning

confidence: 99%