title: Animal models of catheter-induced intimal hyperplasia in type 1 and type 2 diabetes and the effects of pharmacologic intervention.
abstract: Diabetes is a complex disorder characterized by impaired insulin formation, release or action (insulin resistance), elevated blood glucose, and multiple long-term complications. It is a common endocrine disorder of humans and is associated with abnormalities of carbohydrate and lipid metabolism. There are two forms of diabetes, classified as type 1 and type 2. In type 1 diabetes, hyperglycemia is due to an absolute lack of insulin, whereas in type 2 diabetes, hyperglycemia is due to a relative lack of insulin and insulin resistance. More than 90% of people with diabetes have type 2 with varied degrees of insulin resistance. Insulin resistance is often associated with impaired insulin secretion, and hyperglycemia is a common feature in both types of diabetes, but failure to make a distinction between the types of diabetes in different animal models has led to confusion in the literature. This is particularly true in relation to cardiovascular disease in the presence of diabetes and especially the response to vascular injury, in which there are major differences between the two types of diabetes. Animal models do not completely mimic the clinical disease seen in humans. Animal models are at best analogies of the pathologic process they are designed to represent. The focus of this review is an analysis of intimal hyperplasia following catheter-induced vascular injury, including factors that may complicate comparisons between different animal models or between in vitro and in vivo studies. We examine the variables, pitfalls, and caveats that follow from the manner of induction of the injury and the diabetic state of the animal. The efficacy of selected antidiabetic drugs in inhibiting the development of the hyperplastic response is also discussed.
authors.affiliation: Department of Pharmacology, Tulane University Health Sciences Center, 1430 Tulane Avenue - SL 83, New Orleans, LA 70112, USA. dmcnama@tulane.edu
authors.forename: D B
authors.initials: DB
authors.lastname: McNamara
authors.forename: S N
authors.initials: SN
authors.lastname: Murthy
authors.forename: A N
authors.initials: AN
authors.lastname: Fonseca
authors.forename: C V
authors.initials: CV
authors.lastname: Desouza
authors.forename: P J
authors.initials: PJ
authors.lastname: Kadowitz
authors.forename: V A
authors.initials: VA
authors.lastname: Fonseca
mesh_terms: D000818:Animals; D001645:Biguanides / Q000627:therapeutic use; D002404:Catheterization / Q000009:adverse effects*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000473:pathology*; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000473:pathology*; D004195:Disease Models, Animal; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006965:Hyperplasia; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D009525:Niacin / Q000627:therapeutic use; D009569:Nitric Oxide / Q000502:physiology; D047493:PPAR alpha / Q000819:agonists; D047495:PPAR gamma / Q000819:agonists; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D001645:Biguanides; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007004:Hypoglycemic Agents; D047493:PPAR alpha; D047495:PPAR gamma; D009525:Niacin; D009569:Nitric Oxide