This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Kruger, D. F. Search for Related Content PubMed PubMed Citation Articles by Kruger, D. F. Pubmed/NCBI databases Substance via MeSH Medline Plus Health Information Diabetes Social Bookmarking                   What's this?

Exploring the Pharmacotherapeutic Options for Treating Type 2 Diabetes

From the Division of Endocrinology, Diabetes, and Bone Disorders, Henry Ford Medical Center, Detroit, Michigan.

Correspondence to Davida F. Kruger, MSN, APRN-BC, BC-ADM, Certified Nurse Practitioner, Henry Ford Health System, Division of Endocrinology, Diabetes, Bone and Mineral Disorders, 3031 West Grand Blvd., Suite 800, Detroit, MI 48202 (Dkruger1{at}HFHS.org).

There has been a dramatic increase in the prevalence of the most common form of diabetes, with approximately 14.6 million diagnosed and 6.2 million undiagnosed cases of type 2 (non-insulin-dependent) diabetes in the United States since 2005. If diabetes is not diagnosed early and managed properly, patients are at greater risk for microvascular and macrovascular complications, such as nerve damage, heart disease, blindness, and kidney damage. The pathogenesis of type 2 diabetes includes impaired insulin secretion, increased hepatic and muscle/fat insulin resistance, and increased glucagon secretion. Problems commonly associated with type 2 diabetes and consequent hyperglycemia are weight gain, hypertension, and dyslipidemia. The natural progression of type 2 diabetes involves increased insulin deficiency as a result of decreased beta cell function over time, which can raise glycosylated hemoglobin to dangerous levels and consequently increase the risk of death. Lifestyle modifications (eg, diet changes and increased physical activity) remain the cornerstone of early treatment, but glycemic control may worsen despite behavior changes and treatment with oral hypoglycemic agents. Historically, upon failure to maintain glucose levels with exercise and oral medication, insulin was the second-line treatment option. Current treatment algorithms include a new class of agents, incretin mimetics, such as the glucagon-like peptide-1 (GLP-1) receptor agonist exenatide. Exenatide mimics the actions of the hormone GLP-1 that occurs naturally in the gastrointestinal tract and has emerged as an efficacious therapy adjunct to 1 or more oral hypoglycemic agent(s).

The Diabetes Educator, Vol. 34, No. Supplement 3, 60S-65S (2008)
DOI: 10.1177/0145721708319234


CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?