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300884 Pharmacology

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300884 Pharmacology

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Course Code: 300884
University: Western Sydney University

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Country: Australia


The primary goal of this assignment is to prepare a scientific report based on the above investigation. You need to write your report reflecting a real-life laboratory experiment. You need to recognise that this is a piece of scientific writing, not an opinion piece and therefore you must avoid casual language and colloquialisms and the document must be grammatically correct. The assignment has to be in the form of a scientific report with sections including title, abstract, introduction, methods, results, discussion, references, tables and/or figures. You are advised to familiarise with the detailed marking criteria and standards provided for this assessment task in the Learning Guide. The assignment must include references according to Harvard Referencing Style as shown in below examples:
Nammi S, Sun YT & Chang D. (2014). The effects of ginger on metabolic syndrome: A review of evidence. In D. Ghosh, D. Bagchi& T. Konishi (Eds.), Clinical aspects of functional foods and nutraceuticals (pp. 381-397). Boca Raton: CRC Press.ISBN-10: 1466569107; ISBN-13: 978-1466569102.
Nammi S, Roufogalis BD. Light-to-Moderate Ethanol Feeding Augments AMPK-α Phosphorylation and Attenuates SREBP-1 Expression in the Liver of Rats. Journal of Pharmacy & Pharmaceutical Sciences 2013; 16(2): 342-351.


Drug discovery and development involves in vitro and in vivo testing. Various models include test tubes, animals, cell cultures, healthy human subjects or even patients. The effects of the drug on the model-based drug metabolism and disposition. The drug absorption, distribution, metabolism, and excretion (DiMasi,2001) assessed. ADME on metabolism parameters such as the amount of insulin, glucose levels, triglycerides, and cholesterol levels can be measured.
Metabolic syndrome is disease related to many conditions. it is known to increase the risk of diabetes, stroke and heart disease. It revolves in situations such as low serum high-density lipoprotein, high blood pressure, elevated serum triglycerides, central obesity, and high blood pressure. It usually arises from insulin resistance that is accompanied by abdominal adipose deposition according to (Alberti, Zimmet and Shaw, 2002). Its clinical manifestations include hypertriglyceridemia, abdominal obesity, hypertension, shortness of breath and hyperglycemia.
According to the American Heart Association (AHA), when a patient at least 3 of these conditions: fasting glucose greater or equal to 100 mg/dl or on hyperglycemia treatment. A blood pressure of above 13/85 mm Hg or on hypertension treatment. Triglycerides more than 150mg/dl or on triglyceridemia drug therapy HDL-C less than 40 mg/dl in men or less than 50mg/dl in women.
Drug X  is a proposed drug to be used in the treatment of metabolic syndrome .theis report will be prepared to prepare clinical trials and report their findings. A conclusion is to be made on the efficacy of the drug.
Three different rats labeled Rat 1, Rat 2 and Rat 3 used. In the beginning of the experiment. Blood samples were taken to measure triglycerides, glucose, total cholesterol, and insulin from the 3 rats before putting them on a high-fat diet. After 10 weeks of high-fat diet, blood samples taken and the drug X  administered. After 4 weeks the blood samples are taken and tested for the respective parameters. The biochemical assay used to check the lipid profile parameters: triglycerides and the cholesterol. Blood glucose levels were measured using a glucometer and testing strips. Drug X was administered after 10-week high-fat diet and is given 4 weeks to work on the system later the blood samples taken for analysis.  
The Sprague- Dawley rats used as the models because of size, its fast production rate, the availability, ease of handling and low cost(Harvey,2008). Best choice because of its calmness hence it is easily handled. It is known to exhibit a notable increase in body weight, triglycerides, basal plasma glucose, total cholesterol, and insulin levels according to (Srinivasan et al.,2005) when given a high-fat diet.
Experimental groups created and the three rats used were assigned to these groups. The normal control group for those whose parameters tested before subjection to the diet. Disease control group for those whose parameters checked after the high fat intake. Drug –X treated group after disease controlled group given the drug X  
The parameters measured were: Insulin levels, Glucose levels obtained by random testing using a glucometer and Serum lipid profile (triglycerides and total cholesterol).
The result obtained is in three tables in figure 1 in the appendixes section
Statistical analysis to be done on the results obtained. The mean and standard estimated mean (SME) done on all the parameters. A comparison is done, and the graphs were plotted to show a clear picture of the changes seen.
The study experiment was done to evaluate the efficacy of ‘Drug X’ in the treatment of a metabolic disorder by measuring its effect on the insulin-glucose and lipid profile levels. The rodent model used was given the drug and assess for 3 weeks. According to the results recorded, the normal values and the values obtained after treatment with’ Drug X’ are almost the same. While those of taken after the 10week treatment with very high-fat diet approximately double the normal values. After 10 weeks the glucose levels increased this is an indication that there was an impact of the high-fat diet on the models. The insulin levels tripled upon the administration of the high-fat diet from the experiment its evident that the insulin abnormalities could have has a significant impact in causing metabolic syndrome. The total cholesterol levels doubled the while triglycerides levels went high almost four times higher than the normal value. Upon treatment with Drug X, the levels reduced to nearly the same levels of the normal. An implication that Drug x was efficient in the treatment of a metabolic disorder.
The insulin levels were elevated upon the high diet uptake because of insulin resistance. This is usually promoted by adipose cell enlargement and the infiltration of macrophages into adipose tissue releasing pro-inflammatory cytokines. It appears to be the primary mediator of the metabolic syndrome as (Grundy, 1999 b) stated. Since insulin is known to promote uptake of glucose in muscle fat and liver cells.it can lead to lipolysis and glucose production by hepatocytes (Albert, Zimmet, Shaw, 2005 a). Obesity increases free fatty acid levels and insulin distribution. leads to impaired glucose disposal, abnormalities in insulin secretion and insulin receptor signaling(Albert, Zimmet, Shaw, 2006 b). This insulin resistance leads to elevated levels of blood glucose levels. Once the body metabolizes carbohydrates food is broken into glucose that is utilized to produce energy (Grundy et, al. 2005). Insulin hormone is made by the pancreas, and it enables sugar to enter the cells. Once there is insulin resistance the cells rarely respond(Grundy,1998 a). Therefore no glucose can enter cells with ease. Increasing glucose levels in the body while insulin is increased to correct glucose levels. the glucose accumulates in the blood
The fat deposited on the body correlates with inflammation this fat is more resistant to insulin hence resulting in higher toxic free fatty acids concentration in circulation. The fat produces harmful levels of cytokines such as plasminogen activator inhibitor, tumor necrosis and adiponectin as illustrated by(Hotamisligil,2006). Initially, there was an imbalance between food intake and energy consumption. This is regulated by the central nervous system by the brain to peripheral nerves as stated by (Hotamisligil,2006). The fat cells enlarge increasing production of inflammatory adipokines and others that promote obesity-induced metabolic disorders. The elevated serum triglycerides associated with insulin resistance. insulin resistance is a clinical marker of metabolic syndrome
According to the graphical representation of the means according to (Bross,1958), there is an indication of the drug x been a very effective metabolic disorder treatment. The drugs used active cleared were almost 100% since the disorder is also due to reduced or no exercise. The cholesterol levels upon drug x treatment the values dropped from 146.6 mg/dl to 76.6mg/dl.  The initial concentration of the control is 67.6 this is an indicator that the drug is very effective .the insulin levels dropped from 16.3 uu/ ml to9.3 uu/ml while the control level was 8.6.this is an indicator that the drug was able to restore insulin resistance to its standard working rates. The glucose levels dropped from 227mg/dl to 125.33mg/dl, which  is not a value away from the normal 125.33mg/.d
The triglyceride levels decreased from 150.3 mg/dl to 45.3mg/dl. The cost is slightly higher but close to the average control value of 37mg/dl.
From this graphical representation and the standard estimation mean obtained.a clear indicator that the drug X was able to act on the mediators that regulate intake of food such as   gut hormones such as ghrelin antagonist, pancreatic hormones such as lipase inhibitors
According to the above report on the use of Drug X in the treatment of metabolic disorder I can conclude that Drug X is an effective treatment therapy for the disease since it can lower all the parameters glucose, triglycerides total cholesterol and insulin to normal. The drug can target the critical factors in the insulin and adipose tissue .the metabolic disorder parameter are high inter grated and their function highly dependent upon each other (Alberti, Zimmet and Shaw, 2002). Drug X is good drug therapy for the treatment of a metabolic syndrome.also lifestyle modification, proper diet, and stress avoided.
Based on the results and discuss the aim of the experiment was successful. Drug x has shown its pharmacotherapy to lower the cholesterol total triglycerides glucose and insulin levels. therefore it’s a right drug in treating the  metabolic syndrome
Alberti, K.G.M., Zimmet, P. and Shaw, J., 2005. The metabolic syndrome-a new worldwide definition. The Lancet, 366(9491), pp.1059-1062 “a.”
Alberti, K.G.M.M., Zimmet, P. and Shaw, J., 2006. Metabolic syndrome—a new world?wide definition. A consensus statement from the international diabetes federation. Diabetic medicine, 23(5), pp.469-480″ b.”
Azizi, F., Salehi, P., Etemadi, A. and Zahedi-Asl, S., 2003. Prevalence of metabolic syndrome in an urban population: Tehran Lipid and Glucose Study. Diabetes research and clinical practice, 61(1), pp.29-37.
Bross, I.D., 1958. How to use credit analysis. Biometrics, pp.18-38.
DiMasi, J.A., 2001. Risks in new drug development: approval success rates for investigational drugs. Clinical Pharmacology & Therapeutics, 69(5), pp.297-307.
Grundy, S.M., 1998. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. The American journal of cardiology, 81(4), pp.18B-25B. “a”
Grundy, S.M., 1999. Hypertriglyceridemia, insulin resistance, and metabolic syndrome. The American journal of cardiology, 83(9), pp.25-29.”b.”
Grundy, S.M., Cleeman, J.I., Daniels, S.R., Donato, K.A., Eckel, R.H., Franklin, B.A., Gordon, D.J., Krauss, R.M., Savage, P.J., Smith Jr, S.C. and Spertus, J.A., 2005. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation, 112(17), pp.2735-2752.
Harvey, A.L., 2008. Natural products in drug discovery. Drug discovery today, 13(19-20), pp.894-901.
Hotamisligil, G.S., 2006. Inflammation and metabolic disorders. Nature, 444(7121), p.860.
Srinivasan, K., Viswanad, B., Asrat, L., Kaul, C.L. and Ramarao, P., 2005. Combination of high-fat diet-fed and low-dose streptozotocin-treated rat: a model for type 2 diabetes and pharmacological screening. Pharmacological research, 52(4), pp.313-320.

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