Weight Management Express Report


Medical Management of Obesity and Its Related Metabolic Complications

This report was reviewed for medical and scientific accuracy by Stephen H. Schneider, MD, FACP, Professor of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey


Ken Fujioka, M.D., Director, Nutrition & Metabolic Research Center, Scripps Clinic, San Diego, CA

Obesity is a public health problem that is associated with significant morbidity and mortality due to multiple co-morbid diseases including coronary heart disease (CHD), dyslipidemia, congestive heart failure, Type 2 diabetes mellitus, hypertension, osteoarthritis and certain cancers (e.g., endometrial, breast, prostate, and colon).1 The alarming aspect of obesity is that despite our best efforts, it continues to increase. Over the past 20 years, the percentage of adults with obesity has gone from 15% to 27% and the incidence of children diagnosed as obese has essentially doubled.2,3 Indeed, each year an estimated 300,000 adults die of causes related to obesity.4 Patients with obesity report a significant impairment in quality of life.5,6,7 As expected, there has been a corresponding increase in the incidence of co-morbid diseases such as diabetes.

Treatment options for obesity have been limited by medications that have been associated with drug-induced medical problems. In 1997, two anti-obesity medications [fenfluramine, dexfenfluramine] were voluntarily withdrawn from the market due to a possible association with cardiac valve abnormalities.8 More recently, the Food and Drug Administration (FDA) requested the market withdrawal of phenylpropanolamine due to increased risk of hemorrhagic stroke in certain patients.9 As a result, the clinical development of medications for obesity underwent a fundamental and philosophical change. It had become abundantly clear that if millions of obese individuals were possible candidates for a weight loss medication, safety and efficacy would have to be primary parameters in development and regulatory review.

Treatment of obesity has been characterized with many patients successfully losing weight, only to quickly regain the lost weight. Weight loss agents approved in the current era must not only be safe and effective but also show effective improvement of co-morbid diseases. Currently, clinical research on medications for obesity focuses additional attention on associated co-morbidities: diabetes, hypertension, and dyslipidemias. The direct and indirect costs of healthcare associated with diabetes alone were an estimated $98 billion in 1997.10 By inducing weight loss in a diabetic patient, clinical researchers look to establish a corresponding improvement in significant diabetic parameters such as hemoglobin A1c (HbA1c) and quality of life.

In current medical practice, primary care physicians are treating more and more diabetic patients while facing the complexity of multiple medical problems that accompany diabetes. In the primary care and endocrinologists' offices, the diabetic patient is often the most challenging to medically manage.

The following report examines the weight loss drug sibutramine (Meridia, Abbott Labs), a norepinephrine and serotonin reuptake inhibitor,11,12 particularly its pharmacological effects and therapeutic outcomes in patients with diabetes. It is well known that weight loss is of tremendous clinical benefit to the obese Type 2 diabetic patient. Weight reduction improves insulin sensitivity and carbohydrate metabolism. Therefore, it is critical for the treating physician to understand the clinical consequences and expected metabolic outcomes from prescribing a weight loss medication to the diabetic patient.


Obesity and Type 2 diabetes have well-established associations, so much so that many researchers attribute their relationship to overlapping metabolic defects (e.g., hypertension, dyslipidemia, hyperglycemia, and hyperinsulinemia) and a shared pathophysiology.13 Diabetes is an independent risk factor for CHD, and obesity exacerbates and predisposes to both.14 At the average age of diagnosis, Type 2 diabetes reduces life expectancy by about 35%.15 Lean et al15 have estimated that weight loss could add years to the lives of 3 out of 4 diabetic patients who are overweight with even minor weight loss [each one kilogram weight loss associated with 3-4 months prolonged survival] resulting in rapid metabolic improvement, often approaching normalcy. A 5-10% loss of body weight can substantially improve blood glucose, blood pressure and lipid concentrations.2

Obesity is defined as an excess of total body fat demonstrated by a body mass index (BMI) of > 30 kg/m2 with overweight being 25-29.9 kg/m2.6 BMI is an indicator of relative weight for height and is calculated as weight (in kilograms) divided by height (in meters) squared. The BMI is a convenient and accepted approximation of adiposity and its relation to disease risk. Primary treatment modalities for obesity include dietary therapy, exercise and behavior modification. However, these measures do not always lead to adequate weight loss thereby necessitating concomitant pharmacotherapy.

Pharmacology and Mechanism of Action of Current Obesity Agents

Pharmacotherapeutic options for obesity have decreased over the past several years. Fenfluramine, dexfenfluramine, and phenylpropanolamine have been withdrawn due to severe adverse effects, leaving only sympathomimetics, sibutramine, and orlistat (Xenical, Roche Labs) as FDA-approved weight loss agents.

Sympathomimetics suppress appetite by stimulating the release of norepinephrine and dopamine in nerve terminals in the hypothalamic feeding center. Decreased gastric secretion and increased energy expenditure may also contribute to decreased appetite and weight loss.16 Phentermine (Ionamin, Medeva) is the most prescribed agent in this classification and is indicated for short-term treatment only.17 Because of its pharmacological properties, phentermine must be used cautiously in patients with anxiety disorders, hypertension, and those taking monoamine oxidase (MAO)-inhibitors and tricyclic antidepressants; additional precautions exist.17

Sibutramine inhibits the reuptake of norepinephrine, serotonin, and dopamine in the central nervous system. The increase in norepinephrine and serotonin leads to increased satiety, resulting in decreased caloric intake. The most common adverse effects of sibutramine are headache, dry mouth, constipation and insomnia. Sibutramine is contraindicated in patients receiving MAO inhibitors or centrally acting appetite suppressant drugs and in patients with anorexia nervosa. Regular monitoring of blood pressure is recommended. Concomitant use of sibutramine with other CNS-active drugs, particularly serotonergic drugs (e.g., fluoxetine, paroxetine, sertraline, St. John's wort) has not been systematically evaluated; therefore caution is advised.18

Another strategy in treating obesity is to use digestive inhibitors that interfere with the breakdown, digestion and absorption of dietary fat since a reduction in fat is recommended in most weight loss diets. Orlistat, a gastric and pancreatic lipase inhibitor, prevents the absorption of about 30% of dietary fat.19,20 Because orlistat is not systemically absorbed, fat excretion leads to a number of unpleasant adverse effects21 including abdominal pain, oily spotting, fecal urgency, flatulence with discharge, fecal incontinence. Its use in contraindicated in patients with cholestasis and malabsorption syndrome.22

Clinical Discussion

Fujioka et al23 showed that sibutramine achieved statistically and clinically significant weight loss when combined with recommendations for moderate caloric restriction in obese patients with poorly controlled Type 2 diabetes. The weight loss achieved was associated with improved metabolic control and improved quality of life.

These conclusions were derived from a 24-week, multicenter, placebo-controlled, double blind study involving 175 obese patients (BMI ≥ 27-40 kg/m2) with poorly controlled Type 2 diabetes. At baseline, mean age in the sibutramine group was 53.5 years vs. 55.0 years in the placebo group with mean weight being 99.3 kg vs. 98.2 kg and mean BMI being 34.1 kg/m2 vs. 33.8 kg/m2, respectively. All patients received dietary counseling on an individualized American Diabetes Association nutrition plan24 to achieve moderate calorie restriction (minimum deficit of 250-500 kcal/day). Primary outcome measures included changes in weight, BMI, waist and hip circumference, glycemic control, lipid profile, and quality of life assessments.

At week 24, sibutramine achieved significantly greater absolute (-4.3 kg vs. -0.3 kg, p < 0.001) and percentage (-4.5% vs. -0.5%, p < 0.001) weight loss compared with placebo. Additionally, the mean change from baseline BMI in the sibutramine-treated group was -1.3 kg/m2 compared to -0.2 kg/m2 in the placebo group (p < 0.001).

Waist-hip circumference [marked visceral fat accumulation indicative of higher CHD risk25 as compared to hip/thigh fat] also showed greater improvements in the sibutramine-treated patients. At week 24, the mean change from baseline waist circumference was -3.4 cm in the sibutramine-treated patients and -2.0 cm in the placebo group (p = 0.11). The mean change from baseline hip circumference was -3.0 cm and -0.7 cm, respectively (p = 0.01). Investigators noted that greater weight losses might have been observed had recommendations for caloric restriction been of greater magnitude.

Clinically significant weight loss (≥ 5%) is generally expected to improve glycemic control in obese patients with Type 2 diabetes26,27 as the results of this study corroborated. In sibutramine-treated patients, changes in HbA1c [r = 0.35983, p = 0.001] and fasting plasma glucose (FPG) [r = 0.29890, p = 0.0064] were statistically significantly correlated with percentage change in body weight. For patients losing 5% body weight, the mean change in HbA1c % was -0.28% [mean baseline 8.4%] with the difference in FPG being -9 mg/dL (p ≤ 0.05) [mean baseline 184 mg/dL]. As would be expected, the greatest improvement in HbA1c was found in the patients exhibiting ≥ 10% loss of body weight. Mean HbA1c % differences were -1.40% (p ≤ 0.05) [mean baseline 8.4%] and FPG -52.25 mg/dL (p ≤ 0.05) [mean baseline 184 mg/dL]. Improvements in fasting plasma insulin concentrations were also noted.

Sibutramine-treated patients also had improved lipid profiles compared with placebo. Elevated triglycerides and low HDL-cholesterol levels are associated with increased cardiovascular risk in Type 2 diabetes.28 Compared to placebo, the effect of sibutramine on triglycerides was -26.54 mg/dL (p = 0.005) [mean baseline 214 mg/dL] and HDL-C was 5.02 mg/dL (p = 0.083) [mean baseline 42.86 mg/dL]. Similar effects by sibutramine were seen on low-density lipoprotein cholesterol (LDL-C) (2.32 mg/dL, p = 0.340) [mean baseline 128.96 mg/dL] and total cholesterol levels [3.86 mg/dL, p = 0.829) [mean baseline 210 mg/dL].

Sibutramine treatment was generally well tolerated with no differences as compared to placebo. The most commonly reported adverse events (> 10%) [not necessarily drug-related] in either treatment group were: infection (23% vs. 21% in the sibutramine-treated group and the placebo group, respectively); pain (7% vs. 11%); sinusitis (3% vs.10%); back pain (4% vs. 9%) and constipation (9% vs. 5%). Discontinuation rates due to adverse events accounted for 10-12% of patients in each group. This compares favorably to discontinuation rates of 15-46% in non-sibutramine placebo-controlled obesity trials of ≥ 6 months duration.29,30,31

As found in previous studies in patients with uncomplicated obesity,20,32,33 small mean increases in blood pressure (BP) and modest mean increases in pulse rate (PR) were seen with sibutramine. Systolic BP increased a mean of 4.5 mm Hg compared to 2.4 mm Hg with placebo; diastolic BP increased a mean of 2.7 mm Hg compared to 1.4 mm Hg respectively, and PR increased a mean of 6.9 beats/minute (p < 0.001) compared to 0.7 beats/minute, respectively. In general, sibutramine-treated patients who lost weight tended to show smaller increases in BP and PR. Such effects by sibutramine are consistent with the drug's mechanism of action as a norepinephrine and serotonin reuptake inhibitor and are probably mediated through its effect on the sympathetic nervous system.34 Importantly, the number of patients discontinued for hypertension was comparable in the sibutramine-treated group (one) and placebo group (two); no patients were withdrawn for tachycardia.

One limitation to the present study was that patients with a history of marked diabetic complications or a history of significant cardiovascular disease were excluded. Thus, excluding those obese diabetic patients with advanced disease. This exclusion is consistent with sibutramine's prescribing information as it is not recommended for use in patients with serious cardiovascular disease.

Quality of life questionnaires were completed at baseline and weeks 8, 16, and 24. Compared with the placebo group, the sibutramine-treated patients showed significant improvements (p ≤ 0.05) in general health, and social/physical functioning.

Taken together, results of this study suggest that sibutramine is an effective and safe addition to a program that includes caloric restriction for weight reduction, which improves metabolic control and quality of life in obese patients with Type 2 diabetes.

Corroborating conclusions were documented in a randomized, placebo-controlled, double-blind, parallel-group, 12-week study conducted at two hospital-based obesity clinics that found that sibutramine 15 mg once daily when given in combination with a customized, reduced-calorie diet significantly reduced weight in overweight and obese patients (BMI > 26 kg/m2) with Type 2 diabetes.35

The study enrolled 91 patients with treated or untreated Type 2 diabetes having been diagnosed at least 6 months previously. Patients were aged 30 to 65 years, with BMI > 26 kg/m2 and ≤ 35 kg/m2. Fasting blood glucose had to be > 126 mg/dL and < 216 mg/dL on 3 occasions during the month before entry into the study. Concomitant use of appetite suppressants or other weight loss drugs was not allowed. However, patients treated with thyroxine and medications for diabetes (sulfonylureas, metformin, or insulin) were allowed to enroll if the dosage of these drugs was stable over the previous three months. Similarly, hypertensive patients with stabilized blood pressure from antihypertensive pharmacotherapy were allowed to enroll.

Patients were counseled by a dietitian to follow dietary recommendations36,37 for persons with Type 2 diabetes that included a customized, reduced-calorie diet 500 kcal/day less than the individual's estimated energy needs. Following a test meal, blood samples were obtained for determination of glucose and insulin levels at -5, 0, 30, 60, 120, and 180 minutes.

After a one-week run-in period, patients were randomized to receive sibutramine (47 patients) or matching placebo (44 patients) once a day for 12 weeks in combination with the customized, reduced-calorie diet. Both groups were comparable in terms of age, gender, race, height, weight, BMI, and number taking anti-diabetic drugs. At baseline, mean glycosylated hemoglobin was 9.5% in the sibutramine-treated group and 9.4% in the placebo-treated group.

During the study, no significant differences in dietary intake were found between the two treatment groups for any of the dietary intake variables (calories, protein, fat, and carbohydrate). A progressive, consistent weight reduction was seen in the patients receiving sibutramine 15 mg once daily, whereas weight loss fluctuated and was inconsistent in the placebo group. At the end of the short study, weight loss was significantly greater in those taking sibutramine compared to the placebo (2.4 kg vs. 0.1 kg, respectively, p < 0.001; intent to treat).

Mean reduction in BMI was significantly greater with sibutramine compared to placebo (0.9 kg/m2 vs. 0.1 kg/m2, respectively, p < 0.001). The proportion of patients who lost > 5% of their baseline body weight was significantly greater in the sibutramine-treated group than in the placebo-treated group (19% vs. 0%, respectively, p < 0.001).

A significantly greater loss of body fat was found in those taking sibutramine compared with placebo (1.8 kg vs. 0.2 kg, respectively, p < 0.001). Lean body mass fell in both groups (0.8 kg vs. 0.3 kg, respectively, p > 0.05) as did waist-hip ratios but neither was of statistical difference.

Glycemic Control

Mean peak blood glucose concentration decreased by 19.82 mg/dL in the sibutramine-treated group [baseline to end point] compared to an increase of 9.0 mg/dL in the placebo-treated group (p = 0.04, 95% Confidence Interval (CI), -3.3, -0.1). Mean glycosylated hemoglobin levels decreased by 0.3% units (9.5% to 9.2%) with sibutramine treatment but were unchanged (9.4% to 9.5%) with placebo. More sibutramine-treated patients (30%; 15/45) than placebo-treated patients 5%; 2/41) achieved decreases in glycosylated hemoglobin of 1% unit or more (p < 0.05); this improved diabetic control was associated with a greater reduction in weight. These results corroborate earlier studies38,39 showing that sibutramine produces significant weight loss associated with improved glycemic control in patients with Type 2 diabetes.

Sibutramine was well tolerated during the 12-week trial. The most commonly reported adverse events were headache (14 sibutramine; 19 placebo), constipation (13; 13, respectively), dry mouth (10; 5, respectively), infection (8; 1, respectively), pharyngitis (8; 4, respectively) and dizziness (6; 6, respectively). In almost all cases, patients described adverse events as mild in severity. Five patients were withdrawn from treatment due to adverse events: three in the sibutramine group [insomnia, dizziness and diarrhea] and two in the placebo group [giddiness and vomiting; headache].

No significant differences between groups were recorded for blood pressure, which changed from baseline by -0.2 mm Hg (systolic/diastolic) with sibutramine and by -0.1 mm Hg with placebo. Radial pulse rates increased by 7.5 beats per minute (bpm) with sibutramine treatment and 0.2 bpm with placebo (p = 0.005). ECG heart rate changes were consistent with pulse rate changes. No clinically significant conduction or rhythm abnormalities were seen on ECG. The increase in heart rate associated with the use of sibutramine in this and other studies is an expected consequence of its pharmacologic action as a norepinephrine reuptake inhibitor.


Obesity is now recognized as a chronic disease that requires treatment to reduce obesity-related morbidity and mortality through improvement of cardiovascular and metabolic values. A 5-10% loss of body weight can substantially improve blood glucose, blood pressure and lipid concentrations. Primary treatment modalities include dietary therapy, exercise, and behavior modification. However, these measures do not always lead to adequate weight loss thereby necessitating concomitant pharmacotherapy. In assessing a patient for obesity according to NIH guidelines, BMI, waist circumference and absolute risk status are examined.

Sibutramine is an effective and well-tolerated medication for weight loss management indicated for obese patients with an initial BMI of ≥ 30 kg/m2, or ≥ 27 kg/m2 in the presence of other risk factors (e.g., hypertension, diabetes, dyslipidemia). Improvements in glycemic control make sibutramine well suited for obese, Type 2 diabetic patients fulfilling NIH guideline patient classifications.

Additional Reading Materials

Effects of Sibutramine in Obese Female Subjects with Type 2 Diabetes and Poor Blood Glucose Control. Gokcel et al. Diabetes Care 2001;24:1957-1960.

Dickerson L, Carek P. Drug Therapy for Obesity. Am Fam Physician 2000;61:2131-8, 2143.

ASHP Therapeutic Position Statement on the Safe Use of Pharmacotherapy for Obesity Management in Adults. Am J Health-Syst Pharm 2001;58(17):1645-1655.


1. Pi-Sunyer FX. Medical Hazards of Obesity. Ann Intern Med 1993;119 (7, pt. 2):655-660.

2. National Heart Lung and Blood Institute. Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults-The Evidence Report. Obes Res 1998;6(Suppl 2):S51-S290.

3. Troiano et al. Overweight Prevalence and Trends for Children and Adolescents. The National Health and Nutrition Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc Med 1995;149:1085-1091.

4. Allison et al. Annual Deaths Attributable to Obesity in the United States. JAMA 1999;282:1530-1538.

5. Must et al. The Disease Burden Associated with Overweight and Obesity. JAMA 1999;282:1523-1529.

6. Fontaine K, Bartlett S. Estimating Health-Related Quality of Life in Obese Individuals. Dis Manage Health Outcomes 1998;3:61-70.

7. Ford et al. Self-Reported Body Mass Index and Health-Related Quality of Life: Findings From the Behavioral Risk Factor Surveillance System. Obes Res 2001;9:21-31.

8. Cardiac Valvulopathy Associated With Exposure to Fenfluramine or Dexfenfluramine: U.S. Department of Health and Human Services Interim Public Health Recommendations, November 1997. MMWR Morb Mortal Wkly Rep 1997;46:1061-1066.

9. Food and Drug Administration. Washington, DC: U.S. Department of Health and Human Services 2000 Nov. 6. (Talk Paper T00-58.)

10. American Diabetes Association. Economic Consequences of Diabetes Mellitus in the U.S. in 1997. Diabetes Care 1998;21:296-309.

11. Luscombe et al. The Contribution of Metabolites to the Rapid and Potent Down-Regulation of Rat Cortical Beta-Adrenoceptors by the Putative Antidepressant Sibutramine Hydrochloride. Neuropharmacology 1989;28:129-134.

12. Luscombe et al. Effect on Radiolabelled-Monoamine Uptake in vitro of Plasma Taken From the Healthy Volunteers Administered the Antidepressant Sibutramine HCL. Psychopharmacology (Berlin) 1990;100:345-349.

13. Porte et al. Obesity, Diabetes and the Central Nervous System. Diabetologia 1998;41:863-881.

14. Grundy et al. Diabetes and Cardiovascular Disease: A Statement for Healthcare Professionals From the American Heart Association. Circulation 1999;100:1134-1146.

15. Lean et al. Obesity, Weight Loss and Prognosis in Type 2 Diabetes. Diabetic Med 1990;7:228-233.

16. USP DI - Volume I: Drug Information for the Health Care Professional. 21st ed. Englewood, CO: Micromedex; 2001.

17. Ionamin Prescribing Information. Physician's Desk Reference 2001. Medical Economics Company, Montvale, NJ.

18. Meridia Prescribing Information, Abbott Labs. Available at http://www.4meridia.com. Accessed December 7, 2001.

19. Drent et al. Lipase Inhibition: A Novel Concept in the Treatment of Obesity. Int J Obes Relat Metab Disord 1993;17:241-244.

20. Orlistat for Obesity. Med Lett Drugs Ther 1999;41(1055):55-56.

21. Schrefer J, ed. Mosby GenRx: A Comprehensive Reference for Generic and Brand Prescription Drugs. 11th ed. St. Louis: Mosby; 2001.

22. Xenical Prescribing Information, Roche Labs. Available at http://www.rocheusa.com/products/xenical/pi.html. Accessed December 7, 2001.

23. Fujioka et al. Weight Loss With Sibutramine Improves Glycaemic Control and Other Metabolic Parameters in Obese Patients With Type 2 Diabetes Mellitus. Diab Obes Metab 2000;2:175-187.

24. American Diabetes Association. Nutrition Recommendations and Principles for People With Diabetes Mellitus. Position Statement. Clinical Practice Recommendations 2001. Diabetes Care Vol.24; Suppl 1.

25. Pouliot et al. Waist Circumference and Abdominal Sagittal Diameter: Best Simple Anthropometric Indexes of Abdominal Visceral Adipose Tissue Accumulation and Related Cardiovascular Risk in Men and Women. Am J Cardiol 1994;73:460-468.

26. Wing et al. Long-Term Effects of Modest Weight Loss in Type II Diabetic Patients. Arch Intern Med 1987;147:1749-1753.

27. Goldstein et al. Test of Glycemia in Diabetes. Diabetes Care 1995;18:896-909.

28. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). [No authors listed]. JAMA May 16, 2001;285(19):2486-2497.

29. Hollander et al. Role of Orlistat in the Treatment of Obese Patients With Type 2 Diabetes: A 1-Year Randomized Double Blind Study. Diabetes Care 1998;21:1288-1294.

30. Davidson et al. Weight Control and Risk Factor Reduction in Obese Subjects Treated for 2 Years With Orlistat. A Randomized Controlled Trial. JAMA 1999;281:235-242.

31. Sjostrom et al. Randomized Placebo-Controlled Trial of Orlistat for Weight Loss and Prevention of Weight Regain in Obese Patients: European Multicentre Orlistat Study Group. Lancet 1998;352:167-172.

32. Hanotin et al. Efficacy and Tolerability of Sibutramine in Obese Patients: A Dose-Ranging Study. Int J Obes Relat Metab Disord 1998;22:32-38.

33. Bray et al. Sibutramine Produces Dose-Related Weight Loss. Obes Res 1999;7:189-198.

34. Wynne et al. A Single-Dose, Placebo-Controlled, Comparative Evaluation of the Cardiovascular Effects of Sibutramine and Amitriptyline in Normal Volunteers.Int J Pharmaceut Med 1997;11:65-70.

35. Finer et al. Sibutramine is Effective for Weight Loss and Diabetic Control in Obesity With Type 2 Diabetes: A Randomized, Double Blind, Placebo-Controlled Study. Diab Obes & Metab April 2000;2:105-112.

36. Lean MEJ, James WPT. Prescription of Diabetic Diets in the 1980s. Lancet 1986;1(8483):723-725.

37. Nutrition Subcommittee of the British Diabetic Association's Professional Advisory Committee. Dietary Recommendations for People With Diabetes: An Update for the 1990s. Diabet Med 1992;9:189-202.

38. Rissanan A. Sibutramine in the Treatment of Obese Type II Diabetics. Int J Obes Relat Metab Disord 1999;23 (Suppl): S63.

39. Fujioka et al. Sibutramine Induces Weight Loss and Improves Glycemic Control in Obese Patients With Type 2 Diabetes Mellitus. Diabetologia 1998;41 (Suppl): A215.

Jointly sponsored by:

UMDNJ - Center for Continuing and Outreach Education
P.O. Box 573 . Newark . NJ . 07101-0573
973.972.4267 or 1.800.227.4852 . Fax 973.972.7128

6 Merrill Drive . Hampton . NH . 03842 . USA
603.929.5078 . Fax 603.926.3942

Stephen H. Schneider, MD
Research Grants-Aventis, Bristol Myers Squibb, Eli Lilly, Merck

Ken Fujioka, MD
Consultant, Research Grants, Speaker's Bureau-Abbott, Amgen, Roche; Research Grants, Speaker's Bureau-Bayer, Wyeth; Speaker's Bureau-GlaxoSmithKline, Johnson & Johnson, Regeneron, Sanofi, Schering

David C. Howard
Has no significant relationships to disclose.

This report contains no information on commercial products that are unlabeled for use or investigational uses of products not yet approved.

This report is supported by an educational grant from Abbott Laboratories.

Medical Writer
David C. Howard, BS Pharmacy, Director of Research, Millennium Medical Communications, Inc., Hampton, NH

The opinions expressed in this publication are those of the participating faculty and do not necessarily reflect the opinions or the recommendations of their affiliated institutions: University of Medicine & Dentistry of New Jersey; MMC, Inc.; or any other persons. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this publication should not be used by clinicians without evaluation of their patients№ conditions, assessment of possible contraindications or dangers in use, review of any applicable manufacturer№s product information, and comparison with the recommendation of other authorities. This Weight Management Express Report was made possible through an unrestricted educational grant from Abbott Laboratories.

© 2001 Millennium Medical Communications, Inc. and UMDNJ - Center for Continuing and Outreach Education