Abstract: Feed intake is an important factor affecting the production level of livestock and poultry. Many appetite regulating peptide substances can affect the feed intake of animals. In this paper, the structural functions of neuropeptide Y and leptin and their regulation of animal feeding behavior were reviewed, and the interaction between them was briefly summarized.
Key words: neuropeptide Y; leptin; regulation; feeding intake is an important factor affecting the performance of livestock and poultry production and feed conversion rate. The amount of feed intake directly affects the production level of animals. The regulation of animal feed intake is divided into short-term regulation and long-term regulation: short-term regulation is the regulation within a few hours after the animal feeds, and during the second feeding period; long-term regulation is the regulation of the animal's stable nutritional status. There are many factors involved in feeding regulation, and neural state Y (NPY) and leptin are two of the more important regulatory factors.
1 neuropeptide Y
1.1 Structure and distribution of neuropeptide Y
Since NPY was first isolated from pig brain by Tatermato in 1982, its biological function has been extensively studied. It has been found that NPY promotes animal feeding, affects hormone secretion, regulates body temperature, biological rhythm, sexual behavior and mood. And so on. Franciszek (1999) showed that NPY is an active single-chain polypeptide consisting of 36 amino acids. The peptide chain is folded into a hairpin structure, and Y is a tyrosine residue at both ends of the molecule. Its structure and 36 amino acid pancreatic polypeptide. (Ancreatic polypeptide, pp) and peptide YY (Peptide YY, PYY) are very similar, so it is considered to belong to the same family of pancreatic polypeptides. NPY has two antiparallel helical regions, a proline-rich helix and an alpha helix. Both helix regions have a specific tertiary structure of amphoteric ionization. When a certain factor causes the molecular grade 3 When the structure changes, the biological activity of NPY disappears.
1.2 Regulation of feed intake by neuropeptide Y
1.2.1 Promoting feeding function of neuropeptide Y
NPY is widely distributed in the central nervous system and peripheral tissues, and has a variety of functions, especially the function of promoting food intake has attracted widespread attention. Marsh et al. (1998) showed that NPY regulates animal feeding at the central nervous system level and specifically stimulates animal intake of carbohydrates. In rats, chickens, sheep and pigs, it has been confirmed that the central injection of NPY can increase feed intake, and NPY is injected into the cerebral ventricles and paraventricular nucleus of rats and sheep, and the feed intake and drinking water are greatly improved. The feeding effect of NPY is similar to that of mammals in chickens. After NPY injection into broiler brains, the feed intake of broilers increases and insulin secretion also increases. Injecting NPY into the paraventricular nucleus of the rat hypothalamic found that the increase in animal feed intake was linear with the NPY dose within a certain range, and the effect of promoting feeding was obvious within 4 hours after NPY injection, and then decreased. The results of the study indicate that NPY injection into the ventricles can stimulate animal feeding regardless of whether the animal is full or starved.
Sahu et al. (1992) measured a 3-fold increase in NPY concentration in the hypothalamus during fasting, and the amount of NPY in the paraventricular nucleus increased significantly before feeding and decreased after feeding. The appetite of an animal can be inhibited by antisense nucleotides of NPY or antibodies of NPY. The above test results indicate that NPY is a strong pro-feeding factor.
1.2.2 Pathogenesis of neuropeptide Y promoting feeding
The study found that in the arcuate nucleus (ARC) of the hypothalamus of obese rats, the release of NPY mRNA was more than that of normal mice. The normal animals had larger changes in NPY mRNA in ARC before and after feeding. Thus, it is indicated that most of the NPY associated with feeding regulation is produced in ARC. The feeding-feeding effect of NPY was originally thought to be associated with norepinephrine (NE). Later, a large number of experimental results confirmed that NPY may perform peripheral action by activating parasympathetic nerves and inhibiting sympathetic nerves.
NPY promotes the feeding process: NPY in the paraventricular nucleus binds to the Y1 or Y5 receptor to elicit an efferent signal, inhibits sympathetic nerves, excites parasympathetic nerves, increases appetite and feed intake, promotes digestion, and enhances assimilation. At the molecular level, the level of uncoupling protein in brown fat decreases, and the lipid-producing effect in white adipose tissue is enhanced, increasing body fat content. In this process, NPY also indirectly promotes insulin secretion, thereby increasing the synthesis of hepatic glycogen and triglycerides, and increasing the deposition of glucose and fatty acids in fat. In addition, it is accompanied by symptoms such as decreased body temperature, decreased pulse and blood pressure. The whole process is beneficial to restore the storage of energy in the body, which is of great significance for restoring energy balance and survival.
1.3 The effect of insulin on neuropeptide Y
In general, the average level of insulin in the blood circulation is directly proportional to the body fat content, so insulin has long been considered as a signal for energy storage in the body. There are NPY-positive nerve fiber distribution in endocrine and exocrine tissues of pancreas, and NPY-positive cells and NPY mRNA are also expressed in endocrine cells of islets. This suggests that NPY regulates insulin secretion both through neuroendocrine cells and by paracrine and autocrine. Insulin in the blood acts through sites on the blood-brain barrier that allow macromolecules to pass, such as median bulges and ARC. Studies have shown that neurons in ARC can express high levels of insulin receptors. It is possible that insulin inhibits the excitability of NPY neurons by entering the basal ganglia of the hypothalamus and binding to its receptors, thereby regulating feed intake. Intraventricular perfusion of NPY increases insulin secretion.
Sipols et al (1992) decreased the level of NPY mRNA, decreased feeding, increased heat production of brown adipose tissue, and decreased body mass after insulin injection in the hypothalamus or third ventricle of rats. This indicates that insulin can inhibit the activity of NPY neurons. Studies have shown that injecting insulin into the second ventricle inhibits the expression of NPY mRNA, thereby inhibiting food intake, stimulating brown fat production and causing weight loss. In addition, Segal et al (1996) showed that insulin has been shown to be one of the important factors in the activation of Leptin gene expression in both human and animal models. Therefore, insulin may inhibit the production of NPY and its effects through its direct and indirect effects.
2 leptin
2.1 Structure and function of leptin
Leptin is an obesity-related gene (ob) encoding a secreted protein consisting of 166 or 167 amino acids with a molecular weight of 14-16 KD. After entering the blood circulation, the N-terminal 21 amino acid signal peptide is removed to form a 146 amino acid mature leptin, which is free in the blood or binds to leptin-binding protein, reaches the central and peripheral regions and binds to various receptors to exert biological effects. Leptin is mainly produced and secreted by white adipose tissue, and brown fat, skeletal muscle, periosteum, placenta, fetal heart, bone, cartilage and other tissues can also be produced. Therefore, in addition to stimulating the feeding behavior and fat metabolism of the hypothalamic satiety center, leptin can also act indirectly or directly on most organs and tissues in the body through the neuro-humidal mechanism. Leptin is a signal of energy metabolism in the body, and its discovery has played an important role in revealing the mechanism of obesity.
2.2 Leptin regulation of feed intake
Leptin has the effects of reducing animal appetite, improving energy metabolism efficiency, increasing energy consumption, reducing fat storage, and reducing body weight. Leptin regulates body fat balance and energy metabolism through binding to its receptor. Leptin binds to the receptor and acts on the hypothalamic satiety center, inhibiting the synthesis of arcuate nucleus neurons and releasing neuropeptides, reducing appetite. Haalas et al. (1995) injected gene recombinant leptin into ob/ob mice with a significant decrease in body weight. Mice were injected intraperitoneally with leptin every day. After 4 days, the feed intake of ob/ob mice was 60% lower than that of the control group, and the body weight decreased by 40% after 4 weeks. At the same time, mice have increased activity, increased metabolism, and decreased plasma insulin and blood glucose levels. Ehrhardt et al. (2000) reported that the concentration of leptin in the serum of Holstein cows has a strong linear relationship with the fat content in the corpus callosum. Leptin can regulate feed intake through the hypothalamus, and can also directly act on adipose tissue to enhance fat metabolism and consume fat. Wang et al. (1999) demonstrated that when the concentration of leptin in the blood is at a normal level, leptin inhibits food intake mainly through the action of the hypothalamus, and has no direct effect on fat metabolism. However, if the concentration of leptin in the blood is higher than the normal level, leptin can directly act on the adipose tissue through the hypothalamus, on the one hand, reducing feed intake, and on the other hand, by increasing fat metabolism to consume body fat. The amount of body fat in humans and rodents under maintenance can be reflected by the amount of leptin expressed and the amount of secretion. When the lean mice were cut off for 12 to 48 hours, the expression of leptin gene was significantly decreased. Kolaczynski et al. (1996) showed that when fat people lose 10% of their body weight, it causes a 53% decrease in serum leptin levels; a 10% weight gain causes a 300% increase in serum leptin levels.
3 Interaction between leptin and neuropeptide Y
Leptin acts on metabolism in vivo through NPY and can antagonize NPY. Studies have shown that the lack of leptin increases the mRNA levels of rats with polyphagia, elevated blood glucose, obesity and arcuate nucleus NPY. Administration of exogenous leptin can make the mRNA expression of NPY in the arcuate nucleus close to normal, and reverse the symptoms of polyphagia, blood sugar and obesity. Peripherally injected leptin can rapidly enter the medial basal part of the hypothalamus and the arcuate nucleus and nearby brain regions after entering the blood circulation, and bind to the leptin receptors at these sites, thereby regulating the expression of NPY mRNA. Baranowska et al (2005) experimental studies have shown that leptin interacts with hypothalamic NPY, and leptin negatively regulates the expression of NPY mRNA. Jang M et al (2000) found that NPY mRNA and NPY levels in specific areas of the hypothalamus were significantly reduced after injection of leptin into mice, accompanied by decreased feeding and weight loss. Leptin may also directly inhibit the activity of NPY neurons by inhibiting cAMP-protein kinase A on NPY neurons to reduce intracellular Ca2+ concentration.
Leptin activates other neuronal activities and produces neurotransmitters that inhibit the action of NPY. If leptin activates melanocyte prohormone (POMC), the α-melanocyte stimulating hormone (α-MSH) produced by POMC can bind to the MCR-4 receptor, thereby blocking the action of NPY. Leptin increases the expression of α-MSH and MCR-4 receptors and increases their inhibition of NPY. These studies indicate that leptin inhibits NPY-induced animal feeding. The NPY gene mutation was caused by ob/ob mice with obesity symptoms, which caused the lack of leptin and NPY. It was found that compared with the original ob/ob mice, the mutated mice had decreased food intake and increased energy consumption, and diabetes occurred. The tendency of growth and growth retardation was significantly reduced, which further confirmed the effect of leptin on metabolism in vivo through NPY. In conclusion, leptin regulates feeding by reducing the synthesis of NPY or by producing neurotransmitters that inhibit NPY.
4 Conclusion
A variety of neurotransmitters and hormones affecting feeding have complex interrelationships in feeding control, and work together to regulate feeding behavior. The mechanism of feeding regulation is a complex physiological and biochemical process, and there are many problems that need further research. Although it is now a research hotspot in animal nutrition by adding some active factors to regulate hormones or related neurotransmitters, it is not a lot of products that can produce significant appetite-promoting effects. Aspect research.
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