Continuing Education: Obesity and New-Onset Diabetes Mellitus

By King, Deborah S; Wofford, Marion R | Drug Topics, January 17, 2000 | Go to article overview

Continuing Education: Obesity and New-Onset Diabetes Mellitus

King, Deborah S; Wofford, Marion R, Drug Topics

The incidence of type 2 diabetes mellitus has, like that of obesity, increased significantly in the past decade and is reaching epidemic proportions in the developed world. Approximately 16 million people in the United States have type 2 diabetes, with 800,000 new cases diagnosed each year. This national figure is predicted to increase to 50 million in the next 30 years. Its incidence is steadily rising due to an aging population and to our limited success in controlling risk factors such as obesity and physical inactivity.

Obesity, in addition to being a major risk factor for the development of type 2 diabetes, makes the management of diabetes challenging and complex. Diabetes and obesity are linked to other metabolic aberrations, including hypertension, dyslipidemia, hyperglycemia, and hyperinsulinemia. The coexistence of these metabolic abnormalities is strongly associated with increasing risk of cardiovascular disease. The purpose of this paper is to discuss the management of type 2 diabetes in the obese patient and the role of the pharmacy practitioner in such patients.

What is type 2 diabetes?

This extraordinarily common, complicated, multifactorial disease affects approximately 6% of the United States population. In type 2 diabetes, multiple genes and multiple environmental factors interact, resulting ultimately in development of the diabetic state. Research has demonstrated that type 2 diabetes is strongly genetically determined, but different genetic factors may play a role in different populations or families. Likewise, based on genetics, certain racial and ethnic groups are at very high risk for development of type 2 diabetes-- but only if environmental factors allow or promote its expression. Obesity, physical inactivity, and other lifestyle factors have been identified as important environmental risk factors in genetically susceptible individuals. Figure 1 highlights these complex gene/environment interactions.

Type 2 diabetes is characterized by defects in both insulin secretion and insulin action. A resistance to insulin action in many different tissues in the body, coupled with an inability of the pancreas to deliver insulin in a precisely regulated pattern and quantity to control glucose metabolism, ultimately leads to high blood glucose levels and clinically overt type 2 diabetes.

The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus developed the current guidelines for the diagnosis of type 2 diabetes, as shown in Table 1. There are three ways to diagnose type 2 diabetes, all requiring confirmatory testing on subsequent days: a random plasma glucose of > 200 mg/dl; a fasting plasma glucose (FPG) of > 126 mg/dl; or a 2-hour oral glucose tolerance test with plasma glucose > 200 mg/dl. An FPG < 110 mg/dl is considered normal, while an FPG of > 110 mg/dl and < 126 mg/dl is defined as impaired glucose tolerance or impaired fasting glucose.

Although not the topic of this discussion, Type 1 diabetes results from immune-mediated destruction of the pancreatic beta cells.

What is meant by 'overweight' and 'obese'?

The recently published National Institutes of Health (NIH) Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults defines overweight as a body mass index (BMI) of 25 to 29.9 kg/m^sup 2^. Obesity is defined as an excess of total body fat demonstrated by a BMI of > 30 kg/m^sup 2^.

Several methods have been employed to assess body weight. Waist circumference, waist-to-hip ratio, and measures of skinfold thickness have been used to describe fat distribution. Hydrodensitometry, bioimpedance, computerized tomography, and magnetic resonance imaging have also been used to measure body-fat composition and distribution but are not practical clinically. The BMI is a useful estimate of body fat, regardless of age, race, or gender and correlates well with morbidity and mortality. BMI is recommended as a practical approach for assessment of total body fat for the majority of patients.

BMI is easily calculated: metric formula = weight (kg)/height squared (m)^sup 2^; nonmetric formula = weight(lb)/height(in)^sup 2^ x 703. BMI charts are also available through various sources. For example, a person who is 68 in. tall and weighs 200 lbs. has a BMI of 30 kg/m^sup 2^ and is classified as obese.

Diabetes risk In the obese individual

It is estimated that more than 80% of the incident cases of type 2 diabetes are associated with obesity. The association between type 2 diabetes and obesity has been demonstrated in many populations and age groups worldwide. In both the Nurse's Health Study and the U.S. Male Health Professionals Study, BMI correlated with the risk of developing type 2 diabetes. Women with a BMI greater than 33 kg/m^sup 2^ had a risk 60 times greater than lean subjects for the development of type 2 diabetes. Men with a BMI greater than 35kg/m^sup 2^ had a risk for developing diabetes more than 40 times greater than lean subjects.

Epidemiologic studies clearly demonstrate that a continuum exists between weight gain in adulthood and the risk for developing type 2 diabetes. The risk for diabetes increases not only with the degree of adiposity but also with the duration and distribution of body fat. Individuals who gain weight as young adults have a greater relative risk of diabetes than middle-aged subjects who gain weight.

Of note, researchers at the American Diabetes Association's 59th Annual Scientific Session, held in June 1999, addressed the disturbing increase in type 2 diabetes among the young. Most of the children identified were obese, many were members of certain ethnic groups, and many had a family history of the disease. Little is known about diagnosis and management of type 2 diabetes in children, and researchers warned that an epidemic could have devastating complications (heart attacks, strokes, blindness) emerging in early adulthood. The rising rates of type 2 diabetes in children are attributed to the increasing prevalence of obesity and inactivity.

Central adiposity, described as the android distribution or visceral adiposity ("apple" shape), poses a greater risk for cardiovascular disease and morbidity than the peripheral fat distribution, or gyenoid ("pear") shape. The reasons for these associations are unclear and the subject of ongoing research.

Does weight reduction decrease diabetes risk?

Weight reduction using lifestyle modification, dietary changes, and pharmacologic treatment for overweight and obesity has been shown to improve control of diabetes. Weight reduction improves insulin sensitivity and carbohydrate metabolism. A decrease in body weight also improves the response to medications such as oral hypoglycemic agents. An ongoing study, the Diabetes Prevention Project, evaluates subjects with impaired glucose tolerance with a primary end point of prevention of type 2 diabetes. One treatment arm will evaluate the benefits of intensive weight loss and increased physical activity on type 2 diabetes prevention.

The insulin resistance syndrome

The coexistence of obesity, hyperinsulinemia/insulin resistance, dyslipidemia, and hypertension has been identified as a powerful predictor of cardiovascular disease. This cluster of metabolic aberrations has been called Syndrome X, the metabolic syndrome or the insulin-resistance syndrome (Table 2).

Insulin resistance is the earliest detectable defect in most individuals with the metabolic syndrome. Insulin resistance is a result of the decrease in action of insulin (both endogenous or exogenous) on peripheral tissues such as liver, muscle, and fat. Insulin resistance often accompanies, and frequently precedes, the development of other metabolic abnormalities, including hypertension, dyslipidemia, and glucose intolerance. Complex relationships link insulin resistance with the development of type 2 diabetes, dyslipidemia, hypertension, and atherosclerosis, and development of one condition often signals the presence of others.

Insulin resistance may occur years before a diagnosis of type 2 diabetes. Insulin resistance leads to elevated blood-glucose concentrations. As glucose concentrations increase, pancreatic beta cells increase the release of insulin in response to impaired glucose utilization, resulting in hyperinsulinemia. Serum glucose levels remain in the range of normal as long as beta cells are able to maintain insulin output. Eventually, beta cells begin to fail, and insulin production declines or ceases completely Hyperglycemia occurs, heralding the onset of type 2 diabetes. Insulin resistance itself may ultimately be the cause of type 2 diabetes and many of the associated cardiovascular complications.

The accumulation of intra-abdominal fat, associated with impaired insulin action and hyperinsulinemia, is closely linked to the development of insulin resistance and type 2 diabetes. First recognized in the 1950s, the adverse effects of central obesity have been associated with an increased risk for diabetes and coronary artery disease in men and women. The use of computerized tomography imaging has provided a method to demonstrate that the preponderance of intra-abdominal fat correlates with subcutaneous fat and total body fat. It is the presence of intra-abdominal fat or central obesity that increases the risk for the metabolic or insulin resistance syndrome.

A variety of dyslipidemias are associated with obesity and diabetes. Obese type 2 diabetics often exhibit increased levels of triglycerides. Hyperinsulinemia encourages the release of free fatty acids from cells throughout the body, leading to multiple alterations in lipid metabolism. The mechanisms in this state are complex and not well understood. Increased levels of triglycerides, lower high-density lipoproteins (HDL), and alterations in low-density lipoprotein (LDL) subtypes correlate with increasing BMI.

Hypertriglyceridemia may result from insulin, causing increased hepatic fatty acid esterification. Alternatively, excess triglycerides related to increasing abdominal fat may be related to alteration of adipose tissue lipoprotein lipase activity.

Low HDL cholesterol may be due to the increased catabolism of HDL, resulting specifically in the decrease in HDL-2. Although the LDL is not usually raised in obesity, the more atherogenic small dense LDL and intermediate LDL may be increased.

There is considerable evidence that insulin resistance and hypertension are linked, although the mechanisms have not been entirely elucidated. Insulin stimulates the sympathetic nervous system, it may impair normal vasodilatation, and it may have direct effects on sodium and water absorption. Elevated insulin concentrations contribute to artery-wall hyperplasia and expanded plasma volume, both of which can lead to hypertension.

Recent evidence also suggests that the metabolic syndrome is associated with impaired fibrinolysis and increased platelet adherence/aggregation. Plasminogen activator inhibitor-1 can also play a role in altering the clotting cascade.

Like diabetes, obesity is the result of a complex interaction between genes and the environment. A variety of endocrine and neural signals that emanate from adipose tissue, various regions of the brain, the endocrine system, and gastrointestinal tract control the delicate coordination of energy intake and expenditure. Fat, no longer regarded as a passive recipient of the overeating process, is known to secrete leptin, an active hormone that may play a major role in appetite regulation, energy storage, and energy expenditure.

Therapeutic strategies for obese type 2 diabetics

Risk-factor reduction through lifestyle modification is crucial to the long-term health of patients with type 2 diabetes. Because type 2 diabetes is associated with multiple comorbid conditions, including a substantially increased risk for cardiovascular disease, reducing risk factors such as obesity and sedentary lifestyle should always be the cornerstone of therapy.

Weight loss and physical activity in diabetes management

Weight loss is recommended for improving glycemic control and other cardiovascular risk factors in overweight and obese persons with type 2 diabetes. Improvements in blood glucose control, as well as a decrease in blood pressure, an increase in insulin sensitivity, and favorable changes in blood lipid profiles, can be realized by addressing the problem of obesity. Often, patients with type 2 diabetes find it more difficult than nondiabetic patients to reduce weight. The combination of increased physical activity and a reduced-calorie diet is recommended, as it produces weight loss, decreases abdominal fat, and increases cardiorespiratory fitness.

Levels of exercise are inversely related to body weight, and longitudinal studies suggest that exercise leads to less weight gained over time. Recently presented research provides evidence that moderateintensity exercise, such as walking, has a protective effect against type 2 diabetes. Appropriate patients should be encouraged to adopt regular activity patterns. Initial exercise goals are for a moderate level of physical activity for 30 to 45 minutes three to five days a weekand long-term, on most (and preferably all) days of the week.

The use of a low-calorie diet for weight loss is appropriate for most overweight or obese type 2 diabetic patients. Dietary fat and carbohydrates should be reduced to create a deficit of 500 to 1000 kcal/day to achieve a weight loss of one to two pounds per week. Even though reductions in dietary fat alone have not been shown to promote weight loss, changes in diet composition have improved the lipid profiles of patients with type 2 diabetes.

Statistically significant benefits have been shown with body weight losses of 5% to 10% (0.6% reduction in HbA^sub 1c^ with 5% loss). Achieving a loss of 5% or greater provides small but significant decreases in HbA^sub 1c^, while decreases of > 10% of body weight can result in clinically meaningful improvements in HbA^sub 1c^. Gastric surgery, though not recommended for the vast majority of patients, has been successful in achieving glycemic control in patients with type 2 diabetes or glucose intolerance.

Weight loss is also associated with a decrease in triglycerides, total, and LDL cholesterol. The need for weight loss and for

exercise must be emphasized when diabetes is diagnosed initially and must be reinforced throughout the natural history of the disease. Weight loss and weight maintenance should be facilitated by combined therapy-diet, physical activity, and behavior modification.

Several excellent Internet sites are available as references for both the health-care professional and the patient. The sites listed in Table 3 contain additional information on diabetes and obesity. Diagnostic criteria, BMI charts, sample menus, therapeutic goals, and a wealth of information beyond the scope of this article are available through these organizations.

Pharmacologic options for reducing hyperglycemia

Over the past several decades, substantial progress has been made in the treatment of type 2 diabetes (see Table 4). In most cases, pharmacologic therapy may be initiated with an oral agent. An assessment of the level of glucose lowering is required, and the preferred drugs are those that either improve other risk factors or at least lack negative effects. Most patients eventually will require treatment with insulin, in combination with an oral agent, or alone. Agents that reduce insulin resistance may lead to improvement in coronary risk factors. The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that tight glycemic control decreased the risk of microvascular complications (retinopathy, nephropathy, and neuropathy) in type 2 diabetes.

No consensus exists as to which antidiabetic drug should be first offered to a patient who fails to sufficiently lower blood glucose with diet and weight loss. Older approaches to improving glycemic control, notably insulin or sulfonylureas, often lead to weight gain, which in turn may worsen insulin resistance and other aspects of the metabolic syndrome. As glycemic control steadily declines over time, standard and even intensive treatment regimens for type 2 diabetes gradually lose effectiveness. Treatment of well-established type 2 diabetes often requires multiple therapies, including combinations of drugs designed to increase insulin secretion and improve insulin action. Because obesity may lead to insulin resistance and represents an independent risk factor for coronary artery disease, hypertension, and dyslipidemia, weight gain is an undesirable effect of any therapy.

Six categories of medications are currently available for the management of hyperglycemia: insulins, sulfonylureas, alpha-glucosidase inhibitors, biguanides, meglitinides, and thiazolidinediones. Oral medications either stimulate insulin secretion (sulfonylureas, meglitinides), suppress endogenous glucose production (biguanides, thiazolidinediones), stimulate glucose uptake by peripheral tissues (biguanides, thiazolidinediones,) or interfere with gastrointestinal glucose absorption (alpha-glucosidase inhibitors). Table 5 compares the effects of these different agents. Two antiobesity agents, orlistat and sibutramine, are included; these agents have been shown to have positive effects in the obese diabetic patient.

The UKPDS trial demonstrated that the use of metformin significantly decreased the risk of macrovascular disease (heart attacks, stroke, and peripheral vascular disease) in the obese type 2 diabetic. Compared with insulin or sulfonylurea treatment, metformin therapy decreased the risk for diabetes-related endpoints and resulted in less weight gain and fewer hypoglycemic attacks. Therefore, metformin may be considered appropriate first-line therapy in overweight diabetic patients.

Metformin, a biguanide, enhances the sensitivity of both hepatic and peripheral tissues (primarily muscle) to insulin. It inhibits hepatic gluconeogenesis and may also inhibit hepatic glycogenolysis. Reduction in fasting plasma glucose levels is closely correlated with the decline in basal hepatic glucose production. Muscle insulin sensitivity is enhanced through direct and indirect effects. Metformin has no direct effect on beta-cell function, but fasting and postprandial insulin levels consistently decrease, reflecting the normal compensatory response of the pancreas to enhanced insulin sensitivity.

The thiazolidinediones, such as troglitazone, also enhance insulin sensitivity in both liver and muscle without stimulating insulin release. In individual cases, these may be combined with other antidiabetic agents to provide some synergism. The most important focus of the thiazolidinediones may lie in prevention. Current trials are studying the use of these agents for prevention of type 2 diabetes and its cardiovascular complications. The thiazolidinediones bind to nuclear peroxisome proliferator-activated receptors (PPAR) and to other receptors involved in lipoprotein modulation. PPARs provide a close link between adipocyte metabolism and insulin action. New therapeutic approaches to obesity-associated diabetes and other complications may target cell differentiation through PPARs. As more is learned about treatment and mechanisms, perhaps it may be possible to even forestall and prevent diabetes among those at risk.

Sulfonylureas and insulin may contribute to weight gain and increase the risk of hypoglycemia. These agents may be necessary for glycemic control, although in the obese patient they may result in adverse effects. The available evidence suggests that a rational combination of antidiabetic agents and nonpharmacologic treatments that produce near-normal glycemia offer the patient the best hope of avoiding the devastating complications of diabetes. The reader may refer to Table 5 for specific metabolic effects of treatment options.

Medications available for weight reduction

The NIH obesity guidelines recommend (after a six month trial of lifestyle modification) that overweight individuals with a BMI > 27 and "concomitant obesity-related risk factors or diseases" or obese persons with a BMI > 30 and no concomitant disease be considered candidates for weight-loss intervention strategies, including pharmacologic treatment. Pharmacologic therapy is recommended for diabetic patients with a BMI > 27 kg/m^sup 2^ who have been unable to lose weight by other means.

Two recently marketed drugs, orlistat and sibutramine, may offer benefits for individual type 2 diabetes in the treatment of obesity. Benefits are primarily through weight loss rather than direct effects of the medications on insulin action, lipid metabolism, or blood pressure. New research into leptin and uncoupling proteins may provide drugs in the future that play an important role in the overall management of obesity. Weight reduction is often difficult to achieve, especially for patients with type 2 diabetes. Agents such as sibutramine and orlistat, used as part of an integrated program, may pose an attractive early option for the management of type 2 diabetes in obese patients.

Orlistat and sibutramine

Introduction of the new antiobesity drugs, sibutramine and orlistat, may allow diabetics to achieve weight loss. Weight loss of at least 10% leads to a reduction in HbAlc of up to 1% and to favorable changes in other aspects of the metabolic syndrome.

Orlistat, a gastrointestinal lipase inhibitor that partially blocks dietary fat absorption, is minimally absorbed from the gastrointestinal tract. It inhibits approximately one-third of dietary fat absorption. In clinical trials among patients with diabetes who were clinically stable on oral hypoglycemic agents, treatment with orlistat for one year exhibited significant beneficial effects on blood lipids and glycemia.

Weight loss in the orlistat group was associated with a 9% reduction in total cholesterol, a 13% reduction in LDL cholesterol, and an 11% decrease in triglycerides. Plasma glucose levels also decreased in the orlistat group, whereas the placebo group showed an increase in glucose levels. Fasting insulin levels declined nearly 5% in the orlistat group, compared with a 4.3% increase in the placebo group.

In clinical trials, orlistat, in combination with a hypocaloric diet, significantly lowered body weight, LDL cholesterol, and HbA^sub 1c^ after one year. Adverse effects of orlistat are primarily gastrointestinal and include rectal incontinence and oily stools. These effects are intensified by the consumption of high-fat foods. The negative reinforcement produced by these adverse effects associated with ingesting excessive fat may reinforce positive dietary behavioral changes.

Sibutramine has been approved for long-term weightloss programs in select patients. Sibutramine inhibits the reuptake of norepinephrine, serotonin, and dopamine. In clinical trials, sibutramine treatment of obese patients with poorly controlled type 2 diabetes was associated with significant improvements in glycemic control, fasting insulin, and serum lipids. These improvements significantly correlated with the amount of weight loss. The sibutramine group experienced a 7.3% average weight loss from baseline, compared with 2.4% with diet and placebo. Reductions in glycemia and fasting glucose correlated with the magnitude of weight loss.

The most common adverse effects associated with sibutramine are dry mouth, anorexia, insomnia, and constipation. The FDA recommends caution in patients with hypertension, and the NIH obesity guidelines provide further, more stringent recommendations that this agent not be used in patients with hypertension.

Pharmacist management of the obese type 2 diabetic

An integrated multidisciplinary approach to both diabetes and obesity is necessary in order to improve prognosis. As observed by Gerald Bernstein, M.D., past president of ADA, "Certainly by 1999, we have learned that a team approach is the best way to deliver diabetes care. Each health-care professional has a unique contribution to make."

Pharmacists are often the health-care professional most frequently seen by the patient, and opportunities for patient involvement are endless. Being available to communicate with the patient and with the health-care team is the first step to active involvement in patient outcomes.

Pharmacists should be instrumental in choosing appropriate medications, monitoring and adjusting medications, and patient education. Simplifying complicated medication regimens is also an important role of the pharmacist. Patient compliance and adherence are often dictated by the complexity of the regimen, as well as other factors such as cost of therapy and scheduling issues. Patient education in such areas as blood glucose monitoring, medication management, insulin therapy and injection, sick-- day management, and disease symptoms is imperative for improving outcomes.

Pharmacists may be able to forge partnerships with other health-care providers for optimal patient care, education, and referral. Pharmacists can provide patients with the necessary information to help in making informed choices regarding lifestyle modifications and appropriate disease management. A posi five attitude of support and encouragement is crucial to the continuing success of the pharmacist.

References available upon request


An ongoing CE program of

The University of Mississippi School of Pharmacy and DRUG TOPICS


The University of Mississippi School of Pharmacy is approved by the American Council on Pharmaceutical Education as a provider of continuing pharmaceutical education. Accredited in every state requiring CE.


ACPE # 032-999-00-002-H04

This lesson is no longer valid for CE credit after 12/31/02.




This lesson, good for two CE credits, requires a passing grade of 70%.



Upon completion of this article, the pharmacist should be able to:

Review pathophysiologic factors involved with obesity and diabetes

Discuss treatment strategies for obese patients with diabetes

Review the pharmacologic management of diabetes in obese patients

Describe the role of the pharmacist in obesity and diabetes management




To provide a review of the influences of obesity on type 2 diabetes for the pharmacy practitioner


Table 1

Diagnosis of type 2 diabetes mellitus


1. Symptoms of diabetes including polyuria, polydipsia, and unexplained weight loss plus nonfasting plasma glucose of >_ 200 mg/dl



2. FPG >= 126 mg/dl



3. 2-hour postprandial OG1T >= 200 mg/dl


Note: FPG = fasting plasma glucose

OGTT = oral glucose tolerance test


Source: Modified from Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997,;20:1183-1197.


Table 3

Internet sites for patient and provider education

[Sidebar] (American Diabetes Association) (Joslin Diabetes Center)

http://www.niddk.nih.nov (National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases) (National Institutes of Health National Heart, Lung, and Blood Institute)


Table 2

Insulin resistance syndrome (metabolic syndrome)




Type 2 diabetes mellitus



Coronary artery disease


Source: Modified from Conquering Diabetes: A Strategic Plan for the 21st Century. Diabetes Research Working Group, NIH Publication No. 99-4398, 1999.


Table 4

Advances in type 2 diabetes


1923: Insulin becomes available. Diet must be coordinated throughout the day to meet the action of insulin. The recommended diet consists of 70% fat, 20% carbohydrate, and 10% protein.

1924: The liver and its regulation of blood sugar become the focus of investigation.

1925: A Danish physican, Hagedorn, develops delayed-action insulin, "Neutral Protamine Hagedorn," enabling single daily injections in many patients.


1950: Insulin recognized as promoting glucose transport. Diets are still restricted, with fat making up a smaller percentage of total caloric intake (40% fat, 40% carbohydrate, and 20% protein).

1956: Oral hypoglycemics become available for type 2 diabetics.

1957: Immunoassay developed to measure insulin in blood. Researchers show that people with type 1 diabetes produced no insulin, and those with type 2 diabetes have more insulin than normal.

1971: Insulin receptor is identified.

1973-75: Investigators indicate differences in the causes of diabetes. Association of insulin-dependent diabetes with the HLA genes controlling the immune system is described, while no association is found between these genes and non-insulin-dependent diabetes.

1974: Added evidence that type 1 diabetes is an autoimmune disease comes from reports of antibodies to insulin-producing cells in newly diagnosed patients with insulin-dependent diabetes.

1976: Evidence for altered insulin receptor function in obesity and diabetes is reported. Assessment of blood sugar control in the preceding two to three months becomes available with the discovery that hemoglobin becomes easily glycosylated (attached to glucose molecules).

1979: The cDNA for human insulin is cloned. The National Diabetes Data Group publishes new classification criteria for diabetes, distinguishing insulin-dependent from non-insulin-dependent.

1980s: Diets become much lower in fat (30% of total calories) to help prevent heart disease. Human insulin is available.

1993: The Diabetes Control & Complication Trial (DCCT) proves conclusively that tight diabetes control reduces or delays the risk of diabetic eye disease, kidney disease, and nerve damage in type 1 diabetes.

1997: Several new drugs with different methods of therapeutic action become available to treat type 2 diabetes.


Source: Modified from Conquering Diabetes: A Strategic Plan for the 2ist Century. Diabetes Research Working Group, NIH Publication No. 99-4398,1999.




A 52-year-old woman with obesity presents with complaints of fatigue and inability to lose weight. She notes a decreased energy level, particularly in the afternoons. She is tearful at times and has had difficulty concentrating on clerical work. She denies constipation or cold intolerance but describes polyuria and polydipsia.

She has no prior medical problems. She had a total hysterectomy at the age of 45. She has one older sister with diabetes, and her father died of heart disease at the age of 62.

She has been employed as an office clerk for 10 years. She usually eats out for lunch and often "picks up a sandwich" for dinner. Her hobbies include reading and watching old movies. She played high school basketball but since then has made no time for exercise.

On review of systems, she reports palpitations in the chest but no chest pain. She avoids walking upstairs, as she gets short of breath. At night she notices a burning sensation on the feet. She also mentions a recent vaginal yeast infection.

Her physical exam is remarkable for a blood pressure of 154/94, pulse of 84. She is 64 in. tall and weighs 175 lbs. Her BMI is 30 kg/mZ. The mucus membranes are moist, and there is no palpable thyroid nodule. The cardiovascular exam is normal, and the lungs are bilaterally clear. The extremities appear normal except for trace edema in the ankles.

Fasting laboratory values are as follows: CBC normal; serum glucose 255 mg/dl; BUN 10 mmol/L; TSH normal; creatinine 0.8mg/dl; urinalysis normal; total cholesterol 194 mg/dl, HDL 35 mg/dl, triglycerides 712 mg/dl.


Management of the multiple metabolic abnormalities seen in the patient presents complex decisions. Most likely her presenting complaints of fatigue and inability to lose weight are related to the sedentary lifestyle and poor dietary habits developed since early adulthood. Patient education in behavioral modification, nutrition, and exercise will provide a foundation for improvement in her quality of life, sense of well-being, and complexity of the medical regimen required to improve all aspects of the metabolic syndrome. Fundamental to the management of diabetes, dyslipidemia, and hypertension will be the patient's adherence to recommendations for lifestyle modification. Providing the necessary education and guidance for this patient may require a team of health-care providers prepared for the challenge of treating patients with the metabolic syndrome.

The health-care provider must decide which chronic illness to address first, along with the appropriate choices. Thought must be given to strategies that are effective yet do not have adverse metabolic effects. If the focus is on achieving glycemic control with oral sulfonylureas, for example, there may be an associated weight gain resulting in hypertension and increased insulin resistance. On the other hand, if diuretics and beta-blockers are used for the treatment of hypertension, there may be even higher triglyceride levels as a result of either agent.

Addressing the problem of obesity and sedentary lifestyle initially in this patient may lead to improvement in blood glucose control, blood pressure control, and aberrations of the lipid profile.

[Author Affiliation]

By Deborah S. King Pharm.D.

Assistant Professor of Clinical Pharmacy Practice, University of Mississippi Medical Center, Division of Hypertension


Marion R. Wofford, M.D., M.P.H.

Assistant Professor of Medicine, University of Mississippi Medical Center, Division of Hypertension

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