Neurotensin is a 13 amino acid neuropeptide found both in the central nervous system, where it is secreted by neurotensin neurons, and in epithelial cells of the gastrointestinal tract. Its presence was first discovered in the bovine hypothalamus by Leeman and Carraway3, in 1973. Several studies have investigated the functions of neurotensin and it has been shown that its effects are different depending on whether it is secreted centrally. or device. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Neurotensin is involved in temperature regulation, pituitary hormone secretion1, blood pressure regulation, and vascular permeability2. Three different neurotensin receptors (NTRs) have been discovered: NTR1, NTR2 and NTR3; these receptors recognize the C-terminal 8-13 fragment of the neuropeptide and mediate the actions of neurotensin3. The term appetite is generally used to characterize the desire for food. Eating behavior represents a major survival response, and it has been shown that it is mainly regulated at the level of the central nervous system2: several types of hormones are secreted and can induce either an appetite stimulation response (orexigenic hormones ), or an appetite reduction response (anorexigenic hormones). Alongside this survival response, it is important to regulate energy homeostasis, to control body weight. We will therefore address the physiological role of Neurotensin in the regulation of appetite and fat metabolism. To do this, we will first present the role of neurotensin in appetite. We will successively address its actions on fat metabolism. Neurotensin plays a role in regulating appetite. Indeed, since its discovery, several studies have been carried out, and the anorexigenic role of neurotensin has been highlighted2. Many studies have investigated the pharmacological effects of neurotensin and administration of exogenous neurotensin has been shown to reduce food intake. This important pharmacological role could reflect a physiological function of neurotensin. Exogenous administration of neurotensin causes an increase in normal neurotensin levels in the body. Therefore, a higher amount of this neuropeptide could enhance its physiological roles. However, the amount of Neurotensin injected into the test subjects must be controlled, to ensure that too high a quantity is not injected which could, potentially, disrupt the physiological roles of Neurotensin. Research by Remaury A. et al4 (5) focused on the inactivation of Neurotensin. Receptor 1 (NTR1) to identify the role of the neuropeptide in regulating appetite. The study was carried out on mice expressing NTR1 (NTR1+/+ mice) and NTR1 knockout mice (NTR1-/- mice). It was observed that NTR1-/- mice spontaneously consumed a greater amount of food than NTR1+/+ mice (10% increase in food consumption), which resulted in a significant increase in body weight. This therefore indicates that the absence of NTR induces an increase in food consumption. Furthermore, following administration of 10 ng of Neurotensin (into the right intracerebral lateral ventricle), a significant decrease in food consumption was observed in NTR1+/+ mice, and no change was observed in mice NTR1-/-: Neurotensin, binding to NTR, decreased food consumption. The combination of these two observations demonstrates theanorexigenic role of Neurotensin, mediated by NTR1: food consumption increases in mice lacking NTR1; when exogenous neurotensin is injected, food consumption increases in mice expressing NTR1 (the neurotensin therefore binds to the receptor) and remains unchanged in mice lacking NTR1. The role of neurotensin in the regulation of appetite is also elucidated by its importance in the action of leptin: this was studied by a study carried out by Sahu A. et al5. (6). Leptin, an anorexigenic hormone, is secreted by adipose cells, and regulates the body's fat mass: the more fat there is present, the more leptin is secreted and the more the appetite is reduced. Food-deprived rats were first injected with either a control rabbit serum or a neurotensin antiserum (NT-AS). They were then administered 4 µg of leptin and food consumption was measured. A significant increase in food consumption was observed in rats administered leptin and NT-AS compared to the control. Therefore, NT-AS reversed the anorexigenic action of leptin: this suggests that neurotensin may be involved in the appetite regulatory functions of leptin. To explore this observation further, a second experiment was carried out. Rats received leptin plus 40 µg/kg of the neurotensin receptor (NTR) antagonist SR48692 or vehicle control. An increase in food consumption was observed in rats given the NTR antagonist compared to rats given vehicle. Additionally, rats receiving only SR48692 (without leptin) showed no change in food intake compared to vehicle, showing that the NTR antagonist alone had no influence on food intake. The NTR antagonist therefore reversed the action of leptin on food consumption. This study highlights that leptin and neurotensin work together to reduce appetite. Neurotensin appears to be necessary for leptin to induce its anorexigenic effect. Finally, the physiological role of neurotensin in appetite was also studied in a research paper led by Ratner. C et al1 (2). This study particularly focuses on the function of neurotensin in Roux-en-Y gastric bypass (RYGB) surgery. Gastric bypass surgery is a surgical operation, performed mainly in obese people, which consists of reducing the volume of the stomach and is characterized in particular by a reduction in appetite. Relative neurotensin expression was measured in the gastrointestinal tract (by qPCR) in rats that underwent RYGB (RYGB rats) and in sham-operated rats (sham rats) (rats received approximately 15 g of food per day). RYBG rats weighed less than sham rats, and neurotensin gene expression was significantly higher in RYGB rats. Additionally, both cohorts of rats received the neurotensin antagonist SR142848A: increased food consumption and body weight were observed in RYBG rats compared to sham rats. These observations therefore support the role of neurotensin as an appetite-regulating neuropeptide in gastric bypass surgery. Although several studies confirm the general anorexigenic effect of neurotensin, it is important to consider neurotensin secretion. Neurotensin is produced by several neurotensin neurons, located in the central nervous system. Neurotensin secreted in the Accumbens nucleus does not appear to affect appetite and eating behavior, unlike neurotensin secreted by neurons located in the ventral tegmental area or hypothalamic arealateral6. Therefore, the role of neurotensin as an appetite-reducing neuropeptide appears to depend on the site of secretion: further research is needed to more precisely identify neurotensin neurons that play a role in appetite. It is crucial to take into account the condition in which famine occurs. The anorexigenic role of neurotensin has been shown to be particularly effective in fasting-induced feeding, but less evident in homeostatic feeding (food intake to regulate energy)2. Along with its role in appetite, the physiological function of neurotensin in fat metabolism has been studied. Neurotensin has been shown to be involved in lipid absorption in the gastrointestinal tract. After exposure to a diet containing a significant amount of fat, lipid absorption was significantly lower in the absence of neurotensin. A study by Li J. et al 7 examined the function of neurotensin in lipid absorption in mice exposed to high-fat diets (60% of kcal from fat). Two cohorts of mice were studied: wild-type mice (expressing Neurotensin (NT), called NT+/+ mice) and NT-deficient mice (NT-/- mice). When exposed to a high-fat diet, NT-/- mice's epididymal, retroperitoneal, and pericardial fat pads were smaller than those of NT+/+ mice: this resulted in lower body weight for NT-/- mice . NT deficiency appears to decrease the amount of fat in the body. Subsequently, the action of neurotensin on intestinal lipid absorption was studied. The fecal triglyceride content of NT-/- mice was 25% higher than that of wild-type mice, indicating decreased lipid absorption. To confirm this observation, the mice were given SR48692, a neurotensin receptor 1 (NTR1) antagonist, and olive oil, rich in fatty acids. Decreased fatty acid absorption was observed in NT+/+ mice. When NTR1 is blocked (by the antagonist), neurotensin is no longer able to carry out its function: lipids are less absorbed, highlighting the role of neurotensin in fat absorption. Insulin represents another major regulator of lipid metabolism. Among other functions, it exerts different roles in the synthesis of fatty acids and the degradation of lipids. Béraud-Dufour s. et al 8 aimed to analyze the pharmacological effect of neurotensin on insulin secretion. Isolated rat pancreatic islets and insulin-secreting beta cells were first exposed to 0.1 µM neurotensin and glucose, at two different concentrations (2 mM and 20 mM). A similar trend was observed after 45 minutes incubation in both populations. While neurotensin increases insulin secretion in cells exposed to 2 mM glucose, it significantly decreases insulin secretion in cells exposed to 20 µM glucose. Therefore, because neurotensin appears to regulate insulin secretion, it is involved, albeit indirectly, in lipid metabolism (through the effects of insulin). This observation, however, suggests that the action of neurotensin on insulin is not fully understood. If glucose is administered in low doses, neurotensin increases insulin secretion, which therefore promotes the synthesis of fatty acids and stimulates the accumulation of fat in adipose tissues. On the other hand, if glucose is administered in higher doses, Neurotensin has the opposite effect: it decreases insulin secretion, which results in a reduction in the production of fatty acids and an., 23(1), 41-47.