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Effects of different metabolic states and surgical models

   

Added on  2021-02-20

1 Pages1848 Words72 Views
REFERENCES Celik, A. and et.al., 2016. Effects of different metabolic states and surgical models on glucose metabolism and secretion of ileal L-cell peptides: protocol for across-sectional study.BMJ open,6(3), p.e010245.Gonzalez, R. and Unniappan, S., 2016. Mass spectrometry-assisted confirmation of the inability of dipeptidyl peptidase-4 to cleave goldfish peptide YY (1–36)and the lack of anorexigenic effects of peptide YY (3–36) in goldfish (Carassius auratus).Fish physiology and biochemistry,42(3), pp.831-844.Shi, Y.C., and et.al., 2017. Y5 receptor signalling counteracts the anorectic effects of PYY 336 in dietinduced obese mice.Journal ofneuroendocrinology,29(10), p.e12483.There has been a negative correlation between energy rate of resting state andfasting levels of PYY. The thermic effects of consumed food and postprandialexpenditure of energy is also associated with the PYY circulation level.Hence, for regulation of the body weight PYY not only reduces food intake orthe feeding but it also enhances the energy expenditure.CONCLUSION It can be concluded that PYY3-36 can be used to regulate the energy balanceand feeding mechanisms. However, it is required that its synthesis, actionmechanism and release actions must be elucidated through advanced research.It has been also analysed through drug design that PYY3-36 has potential tomodulate with the hedonic brain circuit and thus can be used to preparetreatment methods of obesity which targets the PYY system. Impact of drug administration on feeding and satiety The Y2 receptors mediate the PYY3-36 effects on feeding by showing highresistance to anorectirc effects. The receptor can lower the adiposity and intakeof the food when it is administered peripherally. The dose dependent action ofPYY3-36 reduces food intake and appetite. Thus, it can be used as potentialtheory of obesity control. The calorie intake in rodents is reduced in normalliving beings. However, the individuals who are deficient of DP-IV agrogateinhibitory feeding effects. This is one of the reason that DP-IV inhibitors arealso used for the type 2 diabetes patients. A PYY3-36 injection into cerebralventricle, hippocampus and paraventricular nucleus stimulates the food intakeand delayed satiety in rodents. The feeding effects generated by PYY depend upon the subtype of Y receptorson which drug is activated. Along with the feeding the central drugadministration of PYY3-36 provides additional advantages of fuel partitioningand energy expenditure. It alters the fat oxidation by encouraging its ratethrough peripheral infusion (Celik and et.al., 2016). Circulation PYY circulation is nutrient dependent and is released from gut. The foodintake can increase its level while the fasting can lower its content. Due to thisreason after few hours of food intake PYY level is maximum. When intakenutireint levels reach L cells, it initiates hormonal or neural actions. Theconsistency of food, caloric load and composition of macronutrients alsoinfluences the peak value of temporal profile of PYY. Site of action The Y2 receptors of PYY are located within vagal afferents, nodose ganglionand throughout the central nervous system. Thus, principal action mechanismis through vagal activation or its combination with the central action. Itenhances the probability of the PYY3-36 to influence the feeding impacts. Thedrug follows hypothalamus path and other non-saturable mechanism. Thedirect injections of PYY3-36 can help in lowering the feeding (Gonzalez andUnniappan, 2016). The intra-arcuate injection of Y2 receptors can also be usedto block the anorectic impacts of peripheral drug administration. The vagasrole in mediating drug efect is controversial but the peripheral PYY3-36enhances the vagal afferent firing. The infusion of PYY3-36 peptide withfunctional MRI gives similar observations as provided by the neuronalactivities within hypothalamus and the mid brain regions. Thus, the drugexerts its acts upon hedonic brain circuit and homeostatic for changing orinfluencing feeding and satiety actions. INTRODUCTIONPeptides are chemical compounds whose functions depend upon shape andsequence of amino acid chain. It also acts as hormone and can be used aspharmacological compound which affects the satiety and feeding operations.The structure based drug design can help to analyse its physiological andpharmacology impact on feeding functionality. Drug descriptionPeptide YY (PYY) is produced postprandially in ileum by endocrine cells inresponse of meal energy. It regulates appetite. The compound can act withneuropeptide and inhibits electrolyte secretions and gastro-intenstinal motility.Thus, it gives indication of satiety by providing feedback signal inhypothalamic circuit pathway. The hormone peptide YY 3-36 plays key role inlowering the feeding and thus can be used for weight management or reduction.It has been analysed that anorectic effect of the drug is caused by the Y2receptors. The individuals with lower level of PYY reduces satiety and thusaffects the obesity development (Shi and et.al., 2017). The PYY is member ofpeptide family and consist of pancreatic polypeptide and neruopeptide. Theyshare tertiary structure in which polyproline and alpha helix are joined by betaturn. PEPTIDE YY 3-36 STRUCTURAL DRUG DESIGN

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