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Pramlintide (Symlin®), a synthetic analog of a neurohormone amylin, was approved by the US Food and Drug Administration for use along with premeal insulin in patients with type 1. In patients with type 2 diabetes, pramlintide is approved for addition to premeal insulin in those patients who are either only on premeal insulin or those receiving the combination of insulin and metformin and/or a sulfonylurea. This article reviews the pharmacology, pharmacokinetics, dosing, clinical trials, safety, contraindications, and drug interactions of pramlintide therapy. A search for published clinical trials and therapeutic reviews in the English language was done in the following databases: Iowa Drug Information Service (1966 to July 2008), MEDLINE (1966 to July 2008), and International Pharmaceutical Abstracts (1970 to July 2008). Pramlintide and amylin were used as keywords and title words. References of key articles were also reviewed to identify additional publications. Amylin is a 37 amino acid peptide neurohormone cosecreted from the beta cells of the pancreas, along with insulin, in response to meals. Amylin lowers serum glucose by decreasing glucagon release, slowing gastric emptying and decreasing food intake. Pramlintide, a synthetic analog of amylin, reduces 2-hour postprandial blood glucose between 3.4 and 5 mmol/L, reduces A1C by 0.2% to 0.7% and has no effect on fasting glucose levels. The use of pramlintide was associated with up to a 1.6 kg weight loss. Nausea was the most commonly reported adverse event. Pramlintide is an amylin analog that was FDA approved for the treatment of type 1 and type 2 diabetes. Its use results in modest reduction of A1C and the most frequent side effects are hypoglycemia and nausea.

RESEARCH DESIGN AND METHODS -Fasting serum lipid profiles of 4,014 AfricanAmericans and 328 Caucasians with type 2 diabetes were retrieved from a computerized re g i s t ry. American Diabetes Association criteria were applied to classify LDL cholesterol, HDL cholestero l , and triglyceride (TG) levels into risk categories. The pro p o rtion of patients who had none, one, two, and three lipoprotein concentrations outside of recommended clinical targets was examined. Multiple logistical re g ression analyses were perf o rmed to determine the influence of sex and race on the probability of having a lipid level outside of the recommended targ e t . R E S U LT S -The percentages of African-Americans with high-, borderline-, and low-risk LDL c h o l e s t e rol concentrations were 58, 26, and 16%, re s p e c t i v e l y, and the percentages for Caucasians w e re 54, 29, and 16%, respectively (P = 0.51). For HDL cholesterol, 41, 33, and 26% of AfricanAmericans were in the high-, borderline-, and low-risk categories, re s p e c t i v e l y, compared with 73, 18, and 9% of Caucasians, respectively (P 0.0001). Nearly 81% of African-Americans had TG concentrations that were in the low-risk category compared with only 50% of Caucasians. M o re women than men had high-risk LDL and HDL cholesterol profiles. The most common patt e rn of dyslipidemia was an LDL cholesterol level above target combined with an HDL cholest e rol level below target, which was detected in nearly 50% of African-Americans and 42% of Caucasians. African-Americans had lower odds of having an HDL cholesterol or TG level outside of target. African-American women, compared to men, had greater probabilities of having a b n o rmal levels of LDL and HDL, but a lower likelihood of having a TG level above goal. C O N C L U S I O N S -In a large sample of urban type 2 diabetic patients receiving care at a diabetes treatment program, race and sex diff e rences in serum lipid profiles were pre s e n t . Because hypertriglyceridemia was rare among African-American subjects, interventions will need to focus primarily on improving their LDL and HDL cholesterol levels. Further studies a re re q u i red re g a rding how to best adapt these observed diff e rences into more effective strategies to optimize lipid levels for this population of diabetic patients and to determine whether similar patterns of dyslipidemia occur in other clinical settings.

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