Equivalent insulin resistance in latent autoimmune diabetes in adults (LADA) and type 2 diabetic patients

• Published in: Diabetes research and clinical practice Vol. 77; no. 2; pp. 237 - 244
• Main Authors: Chiu, Harvey K, Tsai, Elaine C, Juneja, Rattan, Stoever, James, Brooks-Worrell, Barbara, Goel, Amit, Palmer, Jerry P
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 01.08.2007
• Subjects: Adult; Age of Onset; Autoantibodies - blood; Blood Glucose - analysis; Body Mass Index; Body mass index (BMI); Diabetes Mellitus, Type 1 - immunology; Diabetes Mellitus, Type 1 - physiopathology; Diabetes Mellitus, Type 2 - immunology; Diabetes Mellitus, Type 2 - physiopathology; Endocrinology & Metabolism; Female; Glutamate Decarboxylase - immunology; Homeostasis model assessment (HOMA); Humans; Insulin - blood; Insulin Resistance; Insulinoma - immunology; Islets of Langerhans - immunology; Isoenzymes - immunology; Latent autoimmune diabetes in adults (LADA); Male; Middle Aged; Pancreas - immunology; Pancreatic autoantibody; Pancreatic Neoplasms - immunology; Insulin resistance; Homeostasis model assessment (HOMA); Body mass index (BMI); Latent autoimmune diabetes in adults (LADA); Pancreatic autoantibody
• ISSN: 0168-8227; 1872-8227
• DOI: 10.1016/j.diabres.2006.12.013

Abstract Insulin resistance is a primary component in the pathophysiology of type 2 diabetes. In latent autoimmune diabetes in adults (LADA), insulin resistance has been reported to be significantly lower than in autoantibody-negative type 2 diabetes (T2DM), but whether this might be related to differences in body mass index (BMI) has not been excluded. Furthermore, previous studies have used limiting inclusive criteria for LADA, requiring only the presence of GADA or IA-2A. To apply more inclusive criteria for LADA, consistent with recent recommendations, we defined LADA by clinical manifestations characteristic of T2DM, but with the presence of any combination of GADA, IA-2A, ICA, or IAA. We recruited 43 LADA patients, 70 T2DM patients, and 150 non-diabetic controls. Insulin resistance was assessed by both the homeostasis model assessment and the quantitative insulin sensitivity check index, and BMI was calculated. We found that insulin resistance in LADA is equivalent to that of T2DM. When insulin resistance is assessed as a function of BMI, both diabetic populations demonstrated an insulin resistance equally greater than normal controls. The interaction between insulin resistance and BMI in the two diabetic groups was significantly different from that demonstrated in non-diabetic controls. In summary, LADA demonstrates insulin resistance of similar magnitude to T2DM, but with the concurrent component of an immune attack against the pancreatic beta-cells. LADA patients may be at significant risk for metabolic consequences of insulin resistance other than glucose metabolism, such as those described in the metabolic syndrome. As complications and treatment regimens specific to LADA are realized, improved means of identification of LADA will become increasingly important.