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What primary care clinicians should know about fenofibrate for people with diabetes “In two major randomised placebocontrolled trials, FIELD and ACCORD Lipid, oral fenofibrate has shown multiple protective effects in adults with type 2 diabetes and to be very well tolerated.” retinopathy progression in type 2 diabetes. N Engl J Med 363: 233–44 Ansquer JC, Foucher C, Aubonnet P, Le Malicot K (2009) Fibrates and microvascular complications in diabetes–insight from the FIELD study. Curr Pharm Des 15: 537–52 Australian Medicines Handbook (2015) Australian Medicines Handbook 2015. AMH Pty Ltd, Adelaide, SA. Available at: http://amhonline.amh.net.au/ (accessed 07.10.16) Burgess DC et al (2007) Abstract 3693: Effects of fenofibrate on silent myocardial infarction, hospitalization for acute coronary syndromes and amputation in type 2 diabetes: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Circulation 116(Suppl 16): II_838 Monthly Index of Medical Specialities (2015) Fenofibrates. Haymarket Media Group Ltd, London, UK. Available at: http://www.mims.com.au (accessed 07.10.16) Noonan JE, Jenkins AJ, Ma JX et al (2013) An update on the molecular actions of fenofibrate and its clinical effects on diabetic retinopathy and other microvascular end points in patients with diabetes. Diabetes 62: 3968–75 O’Callaghan CJ, Rong P, Goh MY (2014) National guidelines for the management of absolute cardiovascular disease risk. Med J Aust 200: 454–6 Papademetriou V, Lovato L, Doumas M et al (2015) Chronic kidney disease and intensive glycemic control increase cardiovascular risk in patients with type 2 diabetes. Kidney Int 87: 649–59 Burgess DC, Hunt D, Li L et al (2010) Incidence and predictors of silent myocardial infarction in type 2 diabetes and the effect of fenofibrate: an analysis from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Eur Heart J 31: 92–9 Pedersen O, Gaede P (2003) Intensified multifactorial intervention and cardiovascular outcome in type 2 diabetes: the Steno-2 study. Metabolism 52(8 Suppl 1): 19–23 Chen Y et al (2011) Mechanisms for the therapeutic effect of fenofibrate on diabetic retinopathy in type 1 diabetes models. Presented at: American Diabetes Association 71 st Scientific Sessions. San Diego, Ca, USA, June 24–28 Rajamani K, Colman PG, Li LP et al (2009) Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. Lancet 373: 1780–8 Chen Y, Hu Y, Lin M et al (2013) Therapeutic effects of PPAR-alpha agonists on diabetic retinopathy in type 1 diabetes models. Diabetes 62: 261–72 Rajamani K et al (2015) Abstract 18987: Fenofibrate reduces peripheral neuropathy in type 2 diabetes: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study. Circulation 122(Suppl 21): A18987 Cholesterol Treatment Trialists’ (CTT) Collaborators (2008) Efficacy of cholesterol-lowering therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis. Lancet 371: 117–25 Davis TM, Ting R, Best JD et al (2011) Effects of fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study. Diabetologia 54: 280–90 Riddle MC (2010) Effects of intensive glucose lowering in the management of patients with type 2 diabetes mellitus in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial. Circulation 122: 844–6 Robins SJ, Collins D, Wittes JT et al (2001) Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial. JAMA 285: 1585–91 Authors Professor Alicia Jenkins, Dr Andrzej Januszewski, Dr Emma Scott and Professor Anthony Keech are at the NHMRC Clinical Trials Centre, University of Sydney, Camperdown, NSW. Jenkins AJ, Rowley KG, Lyons TJ et al (2004) Lipoproteins and diabetic microvascular complications. Curr Pharm Des 10: 3395–418 Jones PH, Davidson MH (2005) Reporting rate of rhabdomyolysis with fenofibrate + statin versus gemfibrozil + any statin. Am J Cardiol 95: 120–2 Keech A, Simes RJ, Barter P et al (2005) Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 366: 1849–61 Keech AC, Mitchell P, Summanen PA et al (2007) Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet 370: 1687–97 Manninen V, Tenkanen L, Koskinen P et al (1992) Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation 85: 37–45 Scott R, O’Brien R, Fulcher G et al (2009) Effects of fenofibrate treatment on cardiovascular disease risk in 9,795 individuals with type 2 diabetes and various components of the metabolic syndrome: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study. Diabetes Care 32: 493–8 Tenenbaum A, Motro M, Fisman EZ et al (2005) Bezafibrate for the secondary prevention of myocardial infarction in patients with metabolic syndrome. Arch Intern Med 165: 1154–60 Ting RD, Keech AC, Drury PL et al (2012) Benefits and safety of long-term fenofibrate therapy in people with type 2 diabetes and renal impairment: the FIELD Study. Diabetes Care 35: 218– 25 Tziomalos K, Athyros VG (2006) Fenofibrate: a novel formulation (Triglide) in the treatment of lipid disorders: a review. Int J Nanomedicine 1: 129–47 Vasudevan AR, Jones PH (2006) Effective use of combination lipid therapy. Curr Atheroscler Rep 8: 76–84 34 Diabetes & Primary Care Australia Vol 2 No 1 2017
Article Glucagon-like peptide-1 analogues – a practical guide to initiation Ralph Audehm and Laura Dean Glucagon-like peptide-1 (GLP-1) analogues are one of the more recent additions to the type 2 diabetes armamentarium and work by mimicking the incretin system to lower glucose and increase insulin. The drug class also exerts associated non-glycaemic advantages, such as weight loss. The first GLP-1 analogue was approved for use in Australia in 2007 and has been subsidised by the Pharmaceutical Benefits Scheme since 2008, yet its use remains relatively low. This article discusses the mode of action of GLP-1 analogues, their use in Australia and how to use and initiate GLP-1 analogues in people with type 2 diabetes, using case studies. Glucagon-like peptide-1 (GLP-1) is a hormone released by the gut when sensory receptors in the small intestine detect dietary glucose and other nutrients. GLP-1 forms part of the “incretin effect” – the increased secretion of insulin when the same amount of glucose is ingested orally compared to when it is administered intravenously (Willard and Sloop, 2012). The incretin system potentiates glucose-induced insulin secretion and may be responsible for up to 70% of postprandial insulin secretion (Holst et al, 2009). GLP-1 is also known to be involved in the inhibition of glucagon release (thus decreasing hepatic production of glucose and fasting blood glucose levels), delayed gastric emptying (thus decreasing post-prandial blood glucose levels) and the suppression of appetite, which, in theory, leads to decreased calorie intake (Gupta, 2013). The roles of GLP-1 make it an attractive target for drug development, especially for the management of type 2 diabetes where the incretin effect is severely reduced or absent in patients (Holst et al, 2009). In addition, the half-life of endogenous GLP-1 is less than 2 minutes, so creating GLP-1 analogues that can be active for longer is of great benefit. Dipeptidyl peptidase-4 (DPP-4), an endogenous enzyme also involved in the incretin system, rapidly inactivates GLP- 1, leading to its short half-life (Willard and Sloop, 2012). It is now possible to artificially prolong the half-life of GLP-1 and its effect by using DPP-4 inhibitors, or “gliptins”. The first DPP-4 inhibitor to be approved by the US Food and Drug Administration was saxagliptin in 2006. The drug class is well tolerated by users, is weight neutral and has a low risk of hypoglycaemia unless used in combination with medications with a risk of hypoglycaemia, such as sulfonylureas (Prasad-Reddy and Isaacs, 2015). They are administered in tablet form and are available in a combined tablet with metformin. Studies have shown they can reduce HbA 1c by 4.4–7.7 mmol/mol (0.4–0.7%; Brunton, 2014). Around the same time, GLP-1 analogues were developed to be more resistant to the actions of DPP-4 inhibitors and with a longer halflife than endogenous GLP-1. The advantages and disadvantages of using GLP-1 analogues are presented in Table 1. GLP-1 analogues have been shown to reduce HbA 1c by around 10.9 mmol/mol (1%; Kenkre et al, 2013) and they can be combined with insulin as GLP-1 analogues are weight negative and insulin is weight positive (Cohen et al, 2013). Devices that contain both basal insulin and a GLP-1 analogue in a single injection have been Citation: Audehm R, Dean L (2017) Glucagon-like peptide-1 analogues – a practical guide to initiation. Diabetes & Primary Care Australia 2: 35–9 Article points 1. The incretin system is used to develop pharmacological therapies for type 2 diabetes. 2. The incretin mimetics, glucagon-like peptide-1 (GLP-1) analogues, represent a useful and effective tool in the management of type 2 diabetes 3. GLP-1 analogues are an under utilised resource in the type 2 diabetes armamentarium. Key words – Administration – Glucagon-like peptide-1 analogues – Glucose-lowering medication – Incretin system Authors Ralph Audehm, Associate Professor, Department of General Practice, University of Melbourne, Vic, and Director, Primary Care Diabetes Society of Australia; Laura Dean, Course Director, Graduate Certificate in Pharmacy Practice, Faculty of Pharmacy and Pharmaceutical Sciences, Monash University, Vic. Diabetes & Primary Care Australia Vol 2 No 1 2017 35
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Page 3 and 4: Contents Diabetes & Primary Care Au
Page 5 and 6: Editorial Diabetes education We are
Page 7 and 8: From the desktop From the desktop P
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