Impairment of the serotonergic control of feeding in adult female rats exposed to intra-uterine malnutrition.

We have previously shown that adult female rats exposed to intra-uterine malnutrition were normophagic, although obese and resistant to insulin-induced hypophagia. The present study aimed at examining aspects of another important catabolic component of energy homeostasis control, the hypothalamic serotonergic function, which inhibits feeding and stimulates energy expenditure. Pregnant dams were fed ad libitum or were restricted to 50 % of ad libitum intake during the first 2 weeks of pregnancy.

Feeding induced by increasing doses of neuropeptide Y: dual effect on hypothalamic serotonin release in normal rats.

Endogenous neuropeptide Y (NPY) levels increase during fasting and before dark onset in rats. The feeding that follows these states elicits the release of serotonin in the lateral hypothalamus (LH), as part of the physiological mechanisms controlling satiety. With the hypothesis that exogenous NPY-induced feeding should also stimulate serotonin, we measured its release in the LH of non-fasted rats, which received a single intracerebroventricular injection of either 1.

The cross-talk between angiotensin and insulin differentially affects phosphatidylinositol 3-kinase- and mitogen-activated protein kinase-mediated signaling in rat heart: implications for insulin resistance.

Insulin and angiotensin II (AngII) may act through overlapping intracellular pathways to promote cardiac myocyte growth. In this report insulin and AngII signaling, through the phosphatidylinositol 3-kinase (PI 3-kinase) and MAPK pathways, were compared in cardiac tissues of control and obese Zucker rats. AngII induced Janus kinase 2 tyrosine phosphorylation and coimmunoprecipitation with insulin receptor substrate 1 (IRS-1) and IRS-2 as well as an increase in tyrosine phosphorylation of IRS and its association with growth factor receptor-binding protein 2.

Effect of leptin on the acute feeding-induced hypothalamic serotonergic stimulation in normal rats.

Both hypothalamic serotonin and leptin reduce energy intake and stimulate expenditure. There are evidence that increased serotonin metabolism may be involved in leptin actions. Using microdialysis, we directly assessed the effect of an intracerebroventricular leptin injection on 5-HT release in the lateral hypothalamus of normal rats.

Adrenalectomy abolishes the food-induced hypothalamic serotonin release in both normal and monosodium glutamate-obese rats.

Corticosteroids influence energy homeostasis through centrally-mediated stimulation of energy intake and inhibition of expenditure, while central serotonin (5-HT) has opposite effects. Both serotonergic dysfunction and high glucocorticoid levels may be relevant in obesity. The neurotoxin monosodium glutamate (MSG) induces a non-hyperphagic and hypometabolic obesity with hypercorticosteronemia.