| Author(s): | Jeffery, Alison RGN, RM |
|---|---|
| Issue: | Volume 17(32), 23 April 2003, pp 47-55 |
| Publication Type: | [Art&Science: Continuing Professional Development: Endocrine Disorders] |
| Publisher: | © Copyright 2003 RCN Publishing Company Ltd. |
| Institution(s): | Alison Jeffery RGN, RM, is Research Nurse, The EarlyBird Study, Children's Day Beds, Level 12, Derriford Hospital, Plymouth. Email: alison.jeffery@phnt.swest.nhs.uk Date of acceptance: March 17 2003. These key words are based on subject headings from the British Nursing Index. This article has been subject to double-blind review. Online archive: For related articles visit our online archive at: www.nursing-standard.co.uk and search using the key words above. |
Outline
- Summary
- Aim and intended learning outcomes
- Introduction
- Pathology
- Origins of insulin resistance
- Obesity
- Metabolic syndrome
- Prevention of insulin resistance
- Treatment of insulin resistance
- Conclusion
- Acknowledgement
- REFERENCES
- Insulin resistance self-
assessment - Practice profile assessment
- Section Description
Insulin resistance is one of the most important causes of premature death in developed countries (Turtle 2000). In this article, Alison Jeffery examines the basic pathology of insulin resistance and its effect on metabolic health. The role of the nurse is discussed in relation to prevention, health promotion and drug treatments for the management of this condition.
The aim of this article is to provide an overview of insulin resistance and metabolic syndrome. It examines the basic pathology and origins of insulin resistance and its effect on metabolic health. Drug treatments and health promotion advice on the prevention of insulin resistance are discussed. After reading this article you should be able to:
[black small square] List the main features of insulin resistance and metabolic syndrome.
[black small square] Identify individuals at risk of developing insulin resistance.
[black small square] Explain the importance of early recognition of insulin resistance.
[black small square] Identify ways of preventing progression to diabetes and coronary heart disease.
[black small square] Assist patients with lifestyle changes, and help them to understand their importance.
[black small square] Evaluate different methods of treatment of insulin resistance.
Insulin resistance is a disease process whereby an individual becomes resistant to his or her inherent insulin production. This condition exerts a huge toll in terms of illness, quality of life and economic consequences for the individual and society (Narayan et al 2000).
Meigs (2002) suggests a prevalence of 24 per cent in adults in the Unites States. The two major manifestations of insulin resistance are diabetes and cardiovascular disease, both of which have seen a dramatic increase in prevalence in recent years (Meigs 2002). Recent research has indicated that insulin resistance may be responsible for several other diseases (Campbell 2001).
Insulin resistance is a decreased sensitivity of insulin receptors in tissues such as the liver (hepatic insulin resistance), adipose tissue and skeletal muscles (peripheral insulin resistance) (Figure 1). It can be triggered by many conditions, such as pregnancy, ageing or infection, and excess weight plays a major role in its development.
| [Help with image viewing] [Email Jumpstart To Image] | Figure 1. The pathology of insulin resistance |
There is a strong negative correlation between amounts of intra-abdominal fat and insulin sensitivity (Banerji et al 1995). Intra-abdominal fat tissue is thought to provide a signal for a chain of events leading to skeletal muscle insulin resistance. An increased supply of free fatty acids results in their increased uptake in muscle. Increased fat oxidation in the muscle then leads to impaired insulin-stimulated glycogen synthesis. Visceral fat produces a cytokine hormone called tumour necrosis factor (TNF), which desensitises the insulin receptor to insulin (Qi and Pekala 2000). Chronic exposure to free fatty acids impairs insulin secretion by the beta cells (lipotoxicity) in the islets of Langerhans.
Type 2 diabetes is characterised by the presence of three major defects (DeFronzo 1988):
Early in the disease process, hypersecretion of insulin compensates for insulin resistance, and glucose levels remain within normal limits. The hypersecretion of insulin places abnormal demands on the beta cells of the pancreas. The first sign of deterioration is an abnormally high rise in blood glucose after meals, which is known as impaired glucose tolerance. As insulin resistance and beta cell failure progress, fasting glucose levels also become elevated. The beta cells become exhausted, insufficient insulin is produced to meet the demands created by insulin resistance and type 2 diabetes develops. Hyperglycaemia can further impair insulin sensitivity and beta cell function. Blood sugar remains high, a situation sometimes called glucose toxicity (Yki-Jarvinen 1990).
Type 2 diabetes mellitus, previously known as non-insulin-dependent diabetes, or maturity-onset diabetes, accounts for 75-90 per cent of cases of diabetes, depending on ethnic background (Campbell 2001). The worldwide incidence has risen exponentially over recent years, and the World Health Organization (WHO) has predicted that the global prevalence will more than double from 135 million in 1995 to 300 million in 2025 (Zimmet 1999). In the UK, type 2 diabetes affects at least 5 per cent of the population, and consumes 9 per cent of the health budget (Currie et al 1997).
The prevalence of insulin resistance is increasing. Write notes on the importance of the following factors in contributing to this trend:
Programming It is suggested that poor nutrition during gestation 'programmes' predisposes a fetus to low birth weight and insulin resistance later in life (Hales and Barker 1992). For a fuller discussion of the programming hypotheses, see Jeffery et al (2002).
Genes The strong association between family history and type 2 diabetes suggests a genetic link (Hattersley and Tooke 1999), but no single gene causing insulin resistance has yet been identified. Some ethnic groups are at much greater risk from insulin resistance than others. Individuals from the Indian subcontinent, Mexican-Americans (in particular the Pima Indians who have diabetes rates of up to 50 per cent), African-Americans and Australian aborigines are particularly at risk (WHO 2001). These differences may result from a genetic susceptibility and lifestyle factors, such as change in diet and physical activity.
Environmental Lucas et al (1999) suggested that the critical period in development of insulin resistance may be the early postnatal period, and rapid weight gain was implicated as a trigger. Cianfarani et al (1999) proposed a 'catch-up weight' hypothesis, whereby those who were born small and whose weight subsequently crossed centiles, were most at risk. The 'accelerator hypothesis' was proposed by Wilkin (2001), who suggested that excess weight gain is the missing link that connects type 1 and type 2 diabetes. Three processes were identified that variably accelerate the loss of beta cells through apoptosis (programmed cell destruction): constitution, insulin resistance and autoimmunity. Body mass is central to the development and rising incidence of all diabetes; the rate of beta cell loss is faster in type 1 than in type 2 diabetes, and is often associated with autoimmunity.
Paradoxically, the insulin resistance that helped primitive man to survive famine throughout evolution may now be catastrophic in our fast food culture. Food is no longer scarce in westernised societies, and what was once a key to survival has become a major cause of obesity, in particular abdominal obesity. Instead of being regarded as an inert store of excess calories, abdominal fat is viewed as being metabolically active and the cause of insulin resistance (Ruderman et al 1998). It is no accident that the rising incidence of abdominal obesity in the western world has been accompanied by a parallel increase in diabetes and metabolic syndrome. According to Meigs (2002), metabolic syndrome is present in nearly one quarter of US adults, who are among the most obese populations in the world. A summary of the risk factors associated with insulin resistance is provided in Box 1.
| [Help with image viewing] [Email Jumpstart To Image] | Box 1. Risk factors for insulin resistance |
Can you identify any diseases associated with insulin resistance that are increasing worldwide?
Over the past 15 years, it has become clear that the action of insulin on glucose is merely one of a number of functions of insulin, and that the development of diabetes is just one manifestation of metabolic syndrome.
In 1988, Reaven (1988) described a new syndrome - 'syndrome X' - which has also become known as 'metabolic syndrome' or 'insulin resistance syndrome'. This syndrome comprises a deadly sextet of metabolic disorders, at the centre of which is insulin resistance (Figure 2). These disorders include hyperglycaemia; hyperlipidaemia (raised triglycerides and low density lipoprotein (LDL) cholesterol, reduced high density lipoprotein (HDL) cholesterol); hypertension; hypercoagulability (raised plasminogen activator inhibitor-1, or PAI-1); hyperuricaemia (raised urates, causing gout); and hyperviscosity (raised packed cell volume, or PCV). Since 1988, further components have been added to the insulin resistance syndrome (Box 2).
| [Help with image viewing] [Email Jumpstart To Image] | Figure 2. Insulin resistance as the cause of the metabolic syndrome |
| [Help with image viewing] [Email Jumpstart To Image] | Box 2. Components of the insulin resistance syndrome |
Reflect on any patients you have cared for recently with type 2 diabetes. Make a list of the associated diseases they had in addition to diabetes.
In accordance with the WHO definition, a person has metabolic syndrome if two of the following criteria are fulfilled (Alberti and Zimmet 1998):
[black small square] Type 2 diabetes or impaired glucose tolerance.
[black small square] Hypertension defined as antihypertensive treatment and/or blood pressure >160/90mmHg.
[black small square] Dyslipidaemia defined as elevated plasma triglyceride (1.7mmol/l) and/or HDL cholesterol <1.0mmol/l>
[black small square] Obesity defined as body mass index (BMI) = 30kg/m2 and/or high waist/hip ratio (>0.90 in males, >0.85 in females).
[black small square] Microalbuminuria (albumin excretory rate, or AER >20mcg/min).
It is important to point out that a person with normal glucose tolerance may have metabolic syndrome if he or she fulfils two of the other criteria.
Metabolic syndrome and cardiovascular disease The complications associated with diabetes are both micro- and macrovascular in origin. Microvascular complications, including retinopathy, nephropathy and neuropathy, are caused by hyperglycaemia and generally start with the clinical onset of diabetes (Gerstein 1997). Macrovascular complications, however, are caused by the process of insulin resistance itself, and are often well established by the time diabetes is diagnosed (Groop 2000) (Figure 3). After ten years of overt clinical diabetes, the mortality from cardiovascular disease is 40-50 per cent, about twice that seen in the non-diabetic population (Campbell 2001). A study from Finland showed that a diagnosis of type 2 diabetes, without previous myocardial infarction, carried a similar risk as that in non-diabetic patients who had sustained a previous heart attack (Haffner et al 1998). Smoking has been identified as an independent risk factor for insulin resistance (Bennet et al 2002), and increases morbidity and mortality in coronary heart disease.
| [Help with image viewing] [Email Jumpstart To Image] | Figure 3. Stages in the development of type 2 diabetes with associated levels of insulin sensitivity, insulin secretion and macrovascular disease |
The insulin resistance syndrome presents a complex of risk factors for cardiovascular and cerebrovascular disease. Among the traditional risk factors, dyslipidaemia and coagulation disorders play an important role. The lipid abnormalities of patients with insulin resistance include raised triglycerides, raised LDL, and low HDL cholesterol. This pro-thrombotic risk profile of circulating blood in insulin resistant patients, combined with lipid abnormalities, contributes to an increased risk of vascular events (Betteridge 2001).
From the information given above, compile a list of the factors responsible for increased cardiovascular risk in patients with insulin resistance.
Insulin resistance in children The increasing development of insulin resistance is closely associated with rising obesity rates (Montague and O'Rahilly 2001). Obesity rates in children are increasing alarmingly (Bundred et al 2001), and the Bogalusa heart study found correlations between central fat and raised plasma insulin in school-age children (Freedman et al 1987). Data from the EarlyBird study suggest that current weight, rather than 'catch-up' weight, is more important in determining which children will develop insulin resistance (Wilkin et al 2002). The first British children (aged 9-16 years) with type 2 diabetes, were reported in 2001 (Ehtisham et al 2001), but this is likely to be just the tip of the iceberg. Given the earlier clinical presentation of type 2 diabetes, the likelihood that a young person will go on to develop micro- and macrovascular complications in his or her lifetime is greatly increased.
Insulin resistance in pregnancy The normal physiological response to pregnancy represents a transient metabolic syndrome in which several components are acquired: a relative degree of insulin resistance, hyperlipidaemia and an increase in coagulation factors (Greer 1999). Metabolic changes in pregnancy are likely to result from hormonal changes, either direct or indirect, through regulation of early fat acquisition and the rapid mobilisation of fat in the second half of pregnancy (Sattar et al 1996).
In pregnancy, the temporary state of insulin resistance reveals those individuals with an early beta-cell defect and allows for identification of high-risk individuals at a time when therapeutic interventions could result in primary prevention of disease. Evidence is beginning to demonstrate that pre-eclampsia is at least partly mediated by insulin resistance, and that individuals with pre-eclampsia may have clinically silent but persistent alterations in insulin resistance (Berkowitz 1998, Solomon and Seely 2001).
The gestational environment may have a long-term influence on the metabolic health of both mother and child. Pregnant, overweight, insulin resistant women are relatively hyperglycaemic, causing fetal hyperinsulinaemia, high birth weight and increased long-term risk for developing insulin resistance in the infant (Dabelea et al 2000, Jeffery et al 2003).
Polycystic ovarian syndrome This is characterised by anovulation, menstrual irregularities, hirsutism and infertility, and is associated in the long-term with type 2 diabetes and cardiovascular disease. Recent research suggests that women with recurrent pregnancy loss have an increased incidence of insulin resistance than fertile controls (Craig et al 2002).
The long-term aim for health workers is prevention of insulin resistance. To achieve this, it is essential to identify the high-risk population and to initiate efficient preventive approaches, such as lifestyle changes. The key is to identify and maintain a healthy weight - ideally with a BMI of 20-25kg/m2.
Preventive measures should begin in childhood. Any initiative that reduces obesity - either by increasing physical activity, reducing sedentary behaviour or improving dietary habits - should be given priority in schools and communities. The difficulties in achieving these goals are immense, as demonstrated by several recent intervention trials targeting obesity. A UK study of 634 primary school children evaluated teacher training, modification of school meals and school action plans, focusing on physical education, tuck shops and playground activities (Sahota et al 2001). However, it found no difference in any physical or psychological measures between the intervention and control groups apart from a modest increase in vegetable consumption. A trial of 400 school children in the US achieved dietary improvements and reduced television viewing following intervention (Gortmaker et al 1999), but there is little evidence that short-term interventions have any effect on reducing obesity rates in otherwise healthy children. No intervention studies have so far targeted children in an attempt specifically to reduce insulin resistance.
Trials to prevent or reduce insulin resistance Within the past 20 years, several clinical trials have been initiated involving lifestyle change with and without pharmacological treatment. The majority have been conducted on people with a known high risk of developing of type 2 diabetes, that is, insulin resistance or impaired glucose tolerance.
Weight loss Weight loss through restriction of caloric intake and increased physical activity was shown in one trial to improve insulin resistance and lead to an improvement in glucose control in adults with diabetes (Henry et al 1986).
Finnish Diabetes Prevention Study Group In a randomised trial of 500 middle-aged, overweight people with impaired glucose tolerance, Tuomilehto et al (2001) showed that lifestyle changes can significantly reduce risk of progression to diabetes. Interventions included individualised counselling aimed at reducing weight, reducing intake of total and saturated fat and increasing intake of dietary fibre, and increasing physical activity. Net weight loss at the end of two years was modest: 3.5kg in the intervention group and 0.8kg in the control. However, cumulative incidence of diabetes after four years was 23 per cent in the control and only 11 per cent in the intervention group.
What health promotion advice should you give to a mother with a family history of type 2 diabetes who is worried about the her children developing diabetes?
Diabetes Prevention Programme The Diabetes Prevention Program, based in the US, was a multicentre randomised clinical trial designed to evaluate the safety and efficacy of interventions that may delay or prevent progression to diabetes in those with impaired glucose tolerance. Participants were randomised to one of three groups: intensive lifestyle modification, standard care plus metformin, and standard care plus placebo. The objective of the intensive lifestyle intervention was to attain and maintain a 7 per cent weight loss, and to expend 700Kcal per day through increased physical activity. The metformin group received 850mg twice daily and standard diet and exercise recommendations. After an average follow-up of nearly three years, metformin reduced the incidence of diabetes by 31 per cent, while lifestyle intervention reduced it by 58 per cent, as compared with placebo (Knowler et al 2002).
Study to prevent non-insulin dependent diabetes mellitus The Study to Prevent Non-Insulin Dependent Diabetes Mellitus (STOP-NIDDM) enrolled over 1,400 participants with impaired glucose tolerance who were randomised in a double-blind fashion to receive acarbose or a placebo (Chiasson et al 2002). Forty-two per cent of those receiving placebo, and 32 per cent of those randomised to acarbose, subsequently developed diabetes. The study concluded that acarbose could be used to delay the development of type 2 diabetes, either as an alternative or in addition to lifestyle change in patients with impaired glucose tolerance (Chiasson et al 2002).
Mr Singh's brother has been diagnosed with type 2 diabetes at the age of 25. Mr Singh has a BMI of 29kg/m2, blood pressure of 162/90mmHg, smokes and takes little exercise. He was reassured to find his blood glucose level was only 5.5mmol/l. Do you think Mr Singh has insulin resistance, and what advice would you give him? Compare your advice with the health promotion advice provided in Box 3. Mr Singh displays several risk factors for insulin resistance (Box 1). To confirm or exclude this diagnosis he should have a fasting blood lipid analysis and a glucose tolerance test.
| [Help with image viewing] [Email Jumpstart To Image] | Box 3. Health promotion advice for prevention and treatment of insulin resistance |
Treatment of insulin resistance is by non-pharmacological (lifestyle change) and pharmacological means. Weight loss has been shown to improve insulin resistance (Henry et al 1986, Tuomilehto et al 2001) and may avoid or delay the need for treatment by drugs. Once insulin resistance has been diagnosed, patients should be monitored regularly. Table 1 shows the target levels for glucose, HbA1c, BMI, blood pressure and lipids. Treatment should be initiated once these levels are exceeded. Nonpharmacological treatment is considered in Box 3. Pharmacological treatment is discussed below.
| [Help with image viewing] [Email Jumpstart To Image] | Table 1. Treatment of insulin resistance |
Prevention of cardiovascular disease Multiple factors are associated with the increased risk of cardiovascular disease in insulin resistant patients. Prevention of coronary heart disease should involve a multifactorial approach, including:
Maintaining a HbA1c of less than 7 per cent appears to be crucial in the prevention of cardiovascular disease in diabetes. Patients with diabetes and HbA1c levels higher than 7 per cent had a four-fold risk of death from cardiovascular disease and a two-fold risk of any cardiovascular event compared with those with a lower HbA1c (UKPDS 1998). Tight glycaemic control (mean HbA1c 7.0 per cent compared with 7.9 per cent in the control group) in the United Kingdom Prospective Diabetes Study reduced the risk for myocardial infarction by 16 per cent (UKPDS 1998).
Platelet activation is increased in insulin resistance. Anti-platelet therapy given for one month or more has reduced the incidence of vascular events in randomised trials by 30 per cent in high-risk patients (ATC 1994). The benefit of anti-platelet therapy is similar in patients with and without diabetes. The most widely used anti-platelet therapy is aspirin at a dose of 75-325mg daily, which is recommended for every patient with diabetes who does not have any contraindications (ADA 2000).
Drugs that specifically target insulin resistance Biguanides, for example, metformin, decrease hepatic gluconeogenesis and increase peripheral tissue insulin sensitivity, by improving glucose use in adipose tissue and muscle, thereby reducing peripheral insulin resistance. Metformin is not associated with weight gain or hypoglycaemia and has been shown to reduce insulin resistance in women with polycystic ovarian syndrome (Awartani and Cheung 2002). It may improve menstrual regularity, leading to spontaneous ovulation, and improve ovarian response to conventional ovulation-induction therapies.
Thiazolidinediones, such as pioglitazone and rosiglitazone, have a unique intracellular action that increases peripheral and hepatic insulin sensitivity by inducing insulin receptor activity, which increases insulin receptor numbers and improves hepatic glucose metabolism. The net effects of these actions are reduced hepatic glucose output, increased insulin-dependent glucose disposal and reduced HbA1c levels. Because the normal regulators of glucose metabolism are activated, the thiazolidinediones preserve the normal feedback mechanisms and thus avoid hypoglycaemia (Day 1999).
Thiazolidinediones may alleviate some of the adverse atherosclerotic effects of insulin resistance. They possess anti-inflammatory properties, influence the atherogenic process by affecting endothelial function, monocyte/macrophage function, lipids, smooth muscle cell migration and fibrinolysis (Dandona and Aljada 2002). Pioglitazone has a hypotensive effect and may improve serum lipid profile, reducing free fatty acids and triglycerides, and increasing HDL cholesterol levels, with no changes in total cholesterol and LDL cholesterol (Buchanan et al 1995). Rosiglitazone, however, increases HDL and LDL cholesterol.
Troglitazone, the first thiazolidinedione, was associated with acute liver failure (Gitlin et al 1998, Shibuya et al 1998) and was withdrawn from the market in the UK. Rosiglitazone and pioglitazone do not appear to cause hepatotoxicity (Tolman 2000). Weight gain is a common side effect of all glitazones, but despite this there is an improvement in glycaemic control, with redistribution of visceral fat to the subcutaneous layer (Tan 2000).
Alpha-glucosidase inhibitors, such as acarbose, delay the absorption of glucose from starch and sucrose, thereby reducing post-prandial glucose and insulin elevations. This may reduce the stress on the beta cells and preserve beta cell function. In addition, acarbose has been shown to reduce insulin resistance (Chiasson et al 1996), probably secondary to decreased insulinaemia and glucose toxicity. Acarbose is non-toxic, its main side effect is flatulence related to non-digestion of starch, which tends to decrease over time (Yale 2000).
The compelling evidence that modest lifestyle changes can prevent an epidemic of diseases associated with insulin resistance provides a stimulus for health promotion and preventive medicine. Nevertheless, translating these findings into effective intervention programmes at individual and public health levels is challenging. This challenge is, however, dwarfed by the prospect of treating the consequences of inaction, that is, the lifelong complex and expensive medical and therapeutic regimens used to manage diabetes and its complications. The appeal of lifestyle interventions is that they are inexpensive, have few side effects and can reverse the factors associated with diabetes and cardiovascular disease, for example, obesity, central obesity, physical inactivity, and a high fat and high energy intake.
Many questions remain regarding how to apply these findings in a variety of countries and settings; how to identify and target people who will benefit most from these interventions; and how best to sustain these changes. Lifestyle changes are difficult for individuals to sustain, and there is often insufficient time to promote them in the clinical setting. Ultimately, it is likely that public health measures will be needed to change our increasingly obesogenic environment.
Insulin resistance is responsible for the epidemic of premature cardiovascular deaths, which has gripped industrialised countries for the past 50 years, and now threatens to become a major killer in industrialising countries too. The alarming rise in obesity is paralleled by increasing morbidity and mortality caused by insulin resistance.
The age of onset of insulin resistance is progressively decreasing. Nurses are likely to come across patients with insulin resistance in virtually every area of practice and have a part to play in early identification of high-risk individuals. However, perhaps the most important role for nurses may lie in assisting individuals and/or families to adopt certain lifestyle changes. The greater and longer-lasting the changes, the better the protection afforded against the ravages of diabetes and macrovascular disease. In the process, lifestyle changes promote health, help to make people less reliant on medicine, and improve their quality of life (Tuomilehto et al 2001)
Now that you have completed the article, you might like to write a practice profile. Guidelines to help you are on page 55.
The author would like to thank Dr Linda Voss, Professor Terry Wilkin and the EarlyBird team at Peninsula Medical School, Plymouth, for their help in preparing this article
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Yale J (2000) Prevention of type 2 diabetes. International Journal of Clinical Practice. Suppl 113, 35-39. [Context Link]
Yki-Jarvinen H (1990) Acute and chronic effects of hyperglycaemia on glucose metabolism. Diabetologia. 33, 10, 579-585. [Context Link]
Zimmet P (1999) Diabetes epidemiology as a tool to trigger diabetes research and care. Diabetologia. 42, 5, 499-518. Bibliographic Links [Context Link]
This self-assessment questionnaire (SAQ) will help you to test your knowledge. Each week you will find ten multiple-choice questions broadly linked to the continuing professional development (CPD) article. The answers might not be found in the article itself and you may wish to use reference books to assist you.
Note: There is only one correct answer for each question.
There are several ways that you can make use of this assessment.
[black small square] You could test your subject knowledge by attempting the questions before reading the article, and then go back over them to see if you would answer differently.
[black small square] Alternatively, you might like to read the article to update yourself before attempting the questions.
[black small square] The answers will be published in Nursing Standard in two weeks' time.
Each week there is a draw for correct entries. If you wish to enter, send your answers on a postcard to: Nursing Standard, Nursing Standard House. 17-19 Peterborough Road, Harrow, Middlesex HA1 2AX, or via email to: zena.latcham@rcnpublishing.co.uk
Ensure you include your name and address and the SAQ number. This is SAQ No 188. Entries must be received by 10am on Tuesday May 6. This week's successful entrant will receive £50 in book tokens.
[black small square] When you have completed your self-assessment, cut out this page and add it to your professional portfolio. You can record the amount of time it has taken you, and don't forget to include any time spent consulting other sources to find answers. Space has also been provided for you to add any comments and additional reading you might have undertaken.
[black small square] If you wish to further your professional development, you might consider writing a practice profile, see page 26.
| [Help with image viewing] [Email Jumpstart To Image] | Figure 1. No caption available. |
[black small square] Using the information in Box 1 to guide you, write a practice profile of between 750 and 1,000 words - ensuring you have related it to the article you have studied. See the practice profile on page 26 and the examples in Box 2.
| [Help with image viewing] [Email Jumpstart To Image] | Box 1. Framework for reflection |
| [Help with image viewing] [Email Jumpstart To Image] | Box 2. Examples of possible practice profile entries |
[black small square] Write practice profile at the top of your entry, followed by your name, the title of the article, which is Insulin resistance, and the article number, which is NS188.
[black small square] Complete all the requirements of the cut-out form provided and attach it securely to your practice profile. Failure to do so will mean your practice profile cannot be considered for accreditation.
[black small square] RCN members are entitled to unlimited free entries. Using an A4 envelope, send for your free RCN assessment or enclose the fee (£15 for non-RCN members) to: RCN CPD articles, Royal College of Nursing, Freepost CF 3790, Cardiff CF23 8ZY by April 23 2004 (cheques payable to RCN). Please do not staple cheques or vouchers to your practice profile and cut-out slip - paper-clips are recommended. You can also email practice profiles to RCNDCPD/Events@rcn.org.uk. You must also provide the same information that is requested on the cut-out form. Type 'Practice Profile' in the email subject field to ensure you are sent a response confirming receipt of your profile.
[black small square] You will be informed in writing of your result. Ten continuing education points are awarded for successful completion of this CPD article. You are entitled to one retake if you are unsuccessful.
[black small square] Feedback is not provided: notification of accreditation indicates that you have been successful. If you wish your practice profile to be considered for publication in Nursing Standard (page 26), indicate this in the place provided on the cut-out form.
[black small square] Keep a copy of your practice profile and add this to your professional profile-copies are not returned to you.
[black small square] Study the checklist (Box 3).
| [Help with image viewing] [Email Jumpstart To Image] | Box 3. Portfolio submission |
| [Help with image viewing] [Email Jumpstart To Image] | Figure 2. Continuing professional development |
Key words: Diabetes: health promotion; Endocrine system and disorders; Metabolic disorders
By reading this article and writing a practice profile, you can gain ten continuing education points (CEPs). You have up to a year to send in your practice profile. Guidelines on how to write and submit a profile are featured at the end of this article.
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