Latent Autoimmune Diabetes in Adults in North Indian Region: Assessment of β-Cell Function, Metabolic and Immunological Features
- 1 December 2017
- journal article
- research article
- Published by Mary Ann Liebert Inc in Metabolic Syndrome and Related Disorders
- Vol. 15 (10), 494-499
- https://doi.org/10.1089/met.2017.0103
Abstract
Background: We undertook a study to assess β-cell function, metabolic and immunological features of patients with latent autoimmune diabetes in adults (LADA) and investigate heterogeneity within LADA based on low and high glutamic acid decarboxylase autoantibodies (GADA) titers. Methods: A total of 139 patients with adult-onset diabetes were examined cross-sectionally in the National capital region of Northern India. Medical history of all subjects was reviewed with the aim of collecting clinical data. Glucose, glycosylated hemoglobin, lipid profile, creatinine, C-peptide, and GADA were measured in 10–12 hrs fasting blood sample. Results: Assessment of metabolic features revealed lower mean systolic blood pressure in subjects with LADA than in those with type 2 diabetes (DM2). Mean triglyceride levels were lower in LADA subjects compared to DM2 subjects. Compared to DM2 subjects, prevalence of metabolic syndrome (MS) was also lower in LADA subjects. Compared to GADA-low, all GADA-high patients were male, had lower waist circumference, fasting C-peptide (FCP), and prevalence of MS. Compared to DM2 patients, GADA-high patients were younger, had lower age at onset, body mass index, waist circumference, systolic blood pressure, triglycerides, FCP, and prevalence of MS. The rate of patients on insulin was higher in GADA-high compared to DM2. There were no significant differences between characteristics of DM2 and GADA-low patients. Conclusions: Our results indicate that LADA patients have distinct metabolic features with lower residual β-cell function than DM2 patients. GADA titer is important parameter in defining the severity of the disease as patients with high GADA titer tend to have significant β-cell impairment.Keywords
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