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Self-directed Learning Assignment Portfolio

Assignment task description: Focus on a single drug or class of drugs, with an emphasis on pharmacology. Depending on your approach, it may also be useful to include the drug’s mechanism of action; a description of the associated disease or condition; relevant and contextual pharmacodynamic and/or pharmacokinetic information; and demonstrate that you have read, understood and analyzed the literature to come up with your own evidence-based conclusions.

  • Read the assignment instructions you were provided carefully - there is plenty of guidance in there to consider. ie examine the evidence published in the last 10 years, use multiple sources, focus on primary research etc.
  • Check your assignment against the assessment criteria form.

View the information and resources within this module to assist you with this self-directed learning assignment. 

  • This assignment is worth 15% of the final PHAR2220 mark
  • To assist with marking, do not change the format or order of sections in this document
  • Student Given Name:
  • Student Surname:
  • Student Number:
  • Drug Name and Class: Metformin (Biguanide class)
  • Word Count: 1506
  • Describe, in the space provided below, how feedback obtained from a previous assignment in PHAR2210 or IMED2002 has assisted with completing this SDL assignment (100 word maximum, 0.1 mark out of 15):
  • Metformin: A Comprehensive Analysis


The oral diabetes drug, metformin, also known chemically as 1,1-dimethylbiguanide is renowned for its exceptional effectiveness in treating type 2 diabetes mellitus. Metformin, a key member of the biguanide medication class is critical in managing and preventing hyperglycemia, constituting a fundamental of diabetic care (LaMoia & Shulman, 2021). Intending to shed light on the many aspects of metformin, this thorough analysis offers evidence-based insights into the drug's clinical efficacy, safety profile, indications, contraindications, absorption kinetics, potential for negative effects, and the wide range of side effects connected with its use. Additionally, this assignment aims to delve deeper into metformin's pharmacology, revealing the complex pathways by, which it exhibits its therapeutic influence. Healthcare professionals and patients can use medications effectively by fully comprehending their pharmacokinetics and the nuances of their mechanisms of action. This will help to control diabetes and its complications effectively leading to better pharmaceutical understanding and enhanced health outcomes.

Pharmacology of Metformin

The pharmacology of metformin supports the drug's efficacy as an antidiabetic. Metformin is effectively absorbed from the gastrointestinal tract when taken orally, often reaching peak plasma concentrations in 2 to 3 hours. Its distinctive quality, nevertheless, is that the body does not metabolise it. Instead, around 90% of the medication is eliminated in the urine, giving it a unique pharmacokinetic profile (Yendapally et al., 2020).

Mechanism of Action

The multifaceted mechanism of action of metformin focuses mainly on peripheral insulin sensitivity and hepatic gluconeogenesis (Rena et al., 2017). Its main mechanisms consist of the following processes-

Suppression of hepatic gluconeogenesis

The liver is essential for synthesizing glucose, especially in those with type 2 diabetes. By preventing mitochondrial glycerophosphate dehydrogenase from functioning, metformin successfully inhibits gluconeogenesis. Due to the reduced rate of lactate and glycerol conversion to glucose, the liver produces less glucose (Rena et al., 2017). Metformin activates AMP-Activated Protein Kinase (AMPK), a cellular energy sensor that controls the metabolism of lipids and glucose. While AMPK activation decreases glucose synthesis in the liver, it increases glucose absorption in peripheral tissues like muscle. The insulin sensitivity is increased due to these actions (Rena et al., 2017).

Enhancement of Insulin Sensitivity

Metformin makes peripheral tissues more sensitive to insulin, which improves their ability to absorb glucose. The enhanced transfer of glucose transporters (GLUT4) to the cell membrane causes this improvement. Reduction in intestinal glucose absorption also occurs in addition to decreasing blood sugar levels. Metformin may also reduce the amount of glucose absorbed from the gastrointestinal tract (Polianskyte-Prause et al., 2019).

Pharmacokinetic Profile

Metformin has a bioavailability of about 50 to 60 per cent, and it absorbs pretty well from the gastrointestinal system. It quickly achieves peak plasma concentrations in 2-3 hours after oral treatment. With respect to dispersion, the plasma is the primary site of metformin's limited dispersion volume. Plasma proteins are not appreciably bound by it (Zake et al., 2021). In addition, one distinctive quality of metformin is that the liver does not metabolise it. Since it is eliminated intact in the urine, renal function is important for its removal. Metformin's pharmacokinetics, particularly its renal excretion, are crucial. Approximately 90% of the dosage that is administered is eliminated in urine unaltered. This characteristic emphasises the need for caution while giving metformin to patients with poor renal function because the medication can build up in the body and possibly cause toxicity (R Betônico et al., 2016).

Toxicity and Side Effects

Metformin is typically considered a safe and well-tolerated medication when taken as directed. However, it is crucial to consider potential toxicity and side effects. Although uncommon, lactic acidosis is the most severe side effect linked to metformin. Lactic acidosis can be fatal, and people with underlying illnesses, including renal impairment, liver disease, or heart failure, are more likely to experience it. Certain situations may hamper the body's capacity to metabolise lactate. As a result, metformin should only be used with caution in patients with lesser renal impairment and is contraindicated in those with severe renal dysfunction (DeFronzo et al., 2016).

Secondly, gastrointestinal disturbances such as diarrhea, abdominal pain, and nausea are a few of metformin's most frequent gastrointestinal adverse effects (Siavash et al., 2017). When taking metformin with meals, starting at a low dose and gradually increasing it is recommended; these adverse effects frequently go away over time or can be controlled (Corcoran & Jacobs, 2023). Thirdly, metformin use has been linked to vitamin B12 insufficiency over an extended period. This risk can be reduced if required by tracking vitamin B12 levels and supplementation (Kim et al., 2019). Moreover, some people who use metformin may notice changes in their taste buds (Diabetes UK, n.d). Lastly, when taken as monotherapy, metformin rarely results in hypoglycemia. When used with other anti-diabetic medications, particularly insulin or sulfonylureas, the risk of hypoglycemia could rise (J Brouwers et al., 2016).

Indications and Contraindications


Metformin is a first-line treatment for type 2 diabetes mellitus, especially in overweight or obese patients. In the case of prediabetes, metformin may be used as a preventative measure in people at high risk of acquiring type 2 diabetes (Aroda & Ratner, 2018). Metformin is also occasionally used off-label to treat the insulin resistance brought on by polycystic ovary syndrome (PCOS) (Johnson, 2014).


Firstly, metformin is contraindicated in people with a predicted glomerular filtration rate or eGFR less than 30 mL/min/1.73 m due to an elevated risk of lactic acidosis and severe renal impairment. Patients with severe liver illness should use metformin cautiously due to possible changes in medication metabolism (Hur et al., 2020). Secondly, it was considered to increase the risk of lactic acidosis, especially for those with a lower ejection fraction. However, according to more current evidence, this should no longer be the case (Kinsara & Ismail, 2018). Thirdly, while taking metformin, it is essential to ensure that excessive alcohol usage is avoided as it increases the risk of lactic acidosis. Lastly, people who are allergic to metformin and result in hypersensitivity should not take the medication (Corcoran & Jacobs, 2023).

Evidence-Based Conclusions

The effectiveness and safety of metformin in managing type 2 diabetes and related disorders are supported by a considerable body of evidence from clinical trials and studies. Individuals with type 2 diabetes who take metformin have observed significant reductions in blood glucose levels. A fundamental of diabetic care, it has been demonstrated to lower HbA1c, fasting blood glucose, and postprandial glucose levels (Abdalhk et al., 2021). For instance, research by Lv & Guo (2020) reveals that metformin may have advantages for the heart, including fewer heart attacks and better outcomes. Because of this, it is a desirable alternative for people with diabetes with a significant cardiovascular risk.

Metformin is a good alternative for people with diabetes who are overweight or obese because it is thought to have a weight-neutral or weight-loss effect, and it may even help with weight loss (Solymár et al., 2018). Metformin is generally well-tolerated and safe when used correctly and in line with contraindications. When metformin is prescribed to patients with maintained renal function, the risk of lactic acidosis is minimal. Metformin is frequently used over an extended period to manage diabetes, as research has shown that this type of treatment is safe and effective (Corcoran & Jacobs, 2023).

Clinical applications/ associated diseases

According to several clinical guidelines, including those produced by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), metformin is advised as the first course of treatment for type 2 diabetes. Usually, it is paired with lifestyle changes, including dietary adjustments and exercise (Davies et al., 2022). Secondly, metformin may be used with insulin or other oral antidiabetic medications when metformin alone cannot manage blood sugar levels as part of a combination therapy. This method is frequently modified to meet the unique requirements of every patient (Chaudhary et al., 2017). Thirdly, it may help people at high risk of acquiring type 2 diabetes, such as those with pre-diabetes or a history of gestational diabetes, lower their risk of becoming fully affected by the disease (Madsen et al., 2019). Lastly, the drug is occasionally used off-label to treat PCOS, which affects the ovaries. It can help PCOS sufferers with insulin resistance and menstrual cycle control (Johnson, 2014).


In conclusion, metformin is an effective agent in treating type 2 diabetes and associated diseases. Healthcare professionals and patients can benefit from this medication's distinctive mode of action, clinical uses, pharmacokinetic profile, toxicity, and side effects to maintain optimal blood glucose control. Metformin is a fundamental of diabetic care because evidence-based findings support its efficacy and safety. To provide the best results while minimising potential hazards, its use should be adapted to the needs of each patient, and contraindications must be carefully evaluated. To improve the clinical applications of metformin and maximise its usage in treating diabetes and related disorders, healthcare professionals should continuously monitor and assess new studies on the drug. Millions of people worldwide will benefit from metformin's demonstrated efficacy and safety profile, which make it a crucial part of contemporary diabetes management.


Abdalhk, D., Riddell, M. C., Swayze, S., & Kuk, J. L. (2021). Association between metformin and physical activity with glucose control in adults with type 2 diabetes. Endocrinology, Diabetes & Metabolism (2).

Aroda, V. R., & Ratner, R. E. (2018). Metformin and Type 2 Diabetes Prevention. Diabetes Spectrum : A Publication of the American Diabetes Association 31 (4), 336-342.

Chaudhury, A., Duvoor, C., Reddy Dendi, V. S., Kraleti, S., Chada, A., Ravilla, R., Marco, A., Shekhawat, N. S., Montales, M. T., Kuriakose, K., Sasapu, A., Beebe, A., Patil, N., Musham, C. K., Lohani, G. P., & Mirza, W. (2017). Clinical Review of Antidiabetic Drugs: Implications for Type 2 Diabetes Mellitus Management. Frontiers in Endocrinology , 224539.

Davies, M. J., Aroda, V. R., Collins, B. S., Gabbay, R. A., Green, J., Maruthur, N. M., & Buse, J. B. (2022). Management of hyperglycemia in type 2 diabetes, 2022. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 45 (11), 2753-2786.

DeFronzo, R., Fleming, G. A., Chen, K., & Bicsak, T. A. (2016). Metformin-associated lactic acidosis: Current perspectives on causes and risk. Metabolism 65 (2), 20-29.

Diabetes UK. (n.d). Metformin and diabetes.

Hur, K. Y., Kim, M. K., Ko, S. H., Han, M., Lee, D. W., Kwon, S., & Association, K. D. (2020). Metformin Treatment for Patients with Diabetes and Chronic Kidney Disease: A Korean Diabetes Association and Korean Society of Nephrology Consensus Statement. Diabetes & Metabolism Journal 44 (1), 3-10.

J Brouwers, C. G., A Stehouwer, C. D., Krings, A., M Leufkens, H. G., M Driessen, J. H., & Burden, A. M. (2016). Risk of hypoglycemia in users of sulphonylureas compared with metformin in relation to renal function and sulphonylurea metabolite group: Population-based cohort study. The BMJ 354

Johnson, N. P. (2014). Metformin use in women with polycystic ovary syndrome. Annals of Translational Medicine(6).

Kim, J., Ahn, C. W., Fang, S., Lee, H. S., & Park, J. S. (2019). Association between metformin dose and vitamin B12 deficiency in patients with type 2 diabetes. Medicine98 (46).

Kinsara, A. J., & Ismail, Y. M. (2018). Metformin in heart failure patients. Indian Heart Journal70 (1), 175-176.

LaMoia, T. E., & Shulman, G. I. (2021). Cellular and molecular mechanisms of metformin action. Endocrine Reviews42 (1), 77-96.

Lv, Z., & Guo, Y. (2020). Metformin and Its Benefits for Various Diseases. Frontiers in Endocrinology11

Madsen, K. S., Chi, Y., Metzendorf, I., Richter, B., & Hemmingsen, B. (2019). Metformin for prevention or delay of type 2 diabetes mellitus and its associated complications in persons at increased risk for the development of type 2 diabetes mellitus. The Cochrane Database of Systematic Reviews 2019 (12).

Polianskyte-Prause, Z., Tolvanen, T. A., Lindfors, S., Dumont, V., Van, M., Wang, H., Dash, S. N., Berg, M., Naams, B., Hautala, L. C., Nisen, H., Mirtti, T., Groop, H., Wähälä, K., Tienari, J., & Lehtonen, S. (2019). Metformin increases glucose uptake and acts renoprotectively by reducing SHIP2 activity. The FASEB Journal 33 (2), 2858-2869.

R Betônico, C. C., O Titan, S. M., C Correa-Giannella, M. L., Nery, M., & Queiroz, M. (2015). Management of diabetes mellitus in individuals with chronic kidney disease: Therapeutic perspectives and glycemic control. Clinics 71 (1), 47-53.

Rena, G., Hardie, D. G., & Pearson, E. R. (2017). The mechanisms of action of metformin. Diabetologia 60 (9), 1577-1585.

Siavash, M., Tabbakhian, M., Sabzghabaee, A. M., & Razavi, N. (2017). Severity of Gastrointestinal Side Effects of Metformin Tablet Compared to Metformin Capsule in Type 2 Diabetes Mellitus Patients. Journal of Research in Pharmacy Practice (2), 73-76.
Corcoran, C., & Jacobs, F.T. (2023). Metformin. In Stat Pearls [Internet] . Stat Pearls Publishing.

Solymár, M., Ivic, I., Pótó, L., Hegyi, P., Garami, A., Hartmann, P., Pétervári, E., Czopf, L., Hussain, A., Gyöngyi, Z., Sarlós, P., Simon, M., Mátrai, P., Bérczi, B., & Balaskó, M. (2018). Metformin induces significant reduction of body weight, total cholesterol and LDL levels in the elderly – A meta-analysis. PLOS ONE 13 (11), e0207947.

Yendapally, R., Sikazwe, D., Kim, S. S., Ramsinghani, S., Fraser-Spears, R., Witte, A. P., & La-Viola, B. (2020). A review of phenformin, metformin, and imeglimin. Drug Development Research 81 (4), 390-401.

Zake, D. M., Kurlovics, J., Zaharenko, L., Komasilovs, V., Klovins, J., & Stalidzans, E. (2021). Physiologically based metformin pharmacokinetics model of mice and scale-up to humans for the estimation of concentrations in various tissues. PLoS ONE 16 (4).

PHAR2220 SDL Assignment – University Policies

By submitting this assignment, you acknowledge awareness of the following UWA policies.








Credit has not been awarded since plagiarism was detected. 

See University Policy on:  Academic Conduct




You have lost marks (0.75 marks out of 15 per day) for late submission.  Assessments submitted later than seven days after the deadline receive a mark of zero

See University Policy on:  Assessment




You have lost 1 per cent of the total mark allocated for this assignment applies for each 1 per cent in excess of the 1,500-word limit. 

See University Policy on:  Assessment




“Recycling an item of assessment from one unit and re-submitting it in complete or substantial form for another assessment” is a moderate breach of academic conduct.

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Self-Directed Learning Assignment

Assessment Criteria Form

  • These criteria do not carry equal weight
  • The final mark is not the sum of performance indicated for each criterion
  • Assignments are moderated to ensure consistency
  • A fail mark (< 30%) will be awarded if the topic is not addressed and/or the pharmacology content is unsatisfactory








  1. PHARMACOLOGY content
  • relevance to assigned topic
  • quality, quantity







  1. References
  • use of correct format for in-text citations & reference list (1 mark out of 15)
  • quality and number
  • recent vs outdated







  1. Structure
  • introduction, body, conclusion
  • flow of ideas







  1. Effort
  • evidence of thought and care







  1. Insight
  • evidence that relevant issues have been considered and addressed, evidence-based conclusions







  1. Presentation
  • grammar, spelling, typographical errors
  • readability


  1. Format and submission (0.1 mark out of 15)
  • submission title
  • assignment portfolio used
  • font style, size and spacing


  1. Reflection on how feedback assisted with this assignment

(0.1 mark out of 15)






Related Topic:- Self-directed Learning Assignment Portfolio


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