GAD Antibody in Multiplex Diabetic Pedigrees of Chinese  

Oleh:

Tao, Chen ; Yan, Ren ; Yang, Long ; and Others

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 30 no. 12 (Dec. 2007), page 3091.
Topik: GADA; GAD antibody • LADA; latent autoimmune diabetes in adults • MODY; maturity-onset diabetes of the young • NGT; normal glucose tolerance

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2007.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

INTRODUCTION Multiplex diabetic families may be caused by mutations in genes of hepatocyte nuclear factors (maturity-onset diabetes of the young [MODY]1, -3, and -5), glucokinase (MODY2), insulin promoter factor-1 (MODY4), NeuroD1 (MODY6), mitochondrion ND1 and tRNALeu(UUR), and some other unknown genetic mutations. Recent studies showed that mutations of MODY are not common causes of diabetes in Chinese diabetic families (1–3), indicating that there may be other causes and mechanisms involved. Latent autoimmune diabetes in adults (LADA) shares some similar clinical phenotypes with MODY and is common in phenotypic type 2 diabetes (10–25%) (4). This study was conducted to investigate the distribution of GAD antibody (GADA) in multiplex diabetic pedigrees from the ChengDu area of China. RESEARCH DESIGN AND METHODS A total of 140 family members of 18 families were recruited. In our previous study, most members had been screened for variants in mitochondrion ND1 and tRNALeu(UUR) and had been proved to be without deficiencies in these genes (5). Among them, 42 subjects in four families had been further screened in the hepatic nuclear factor-1 gene and had been found to have no suspected variant (T.C., Y.R., H.Y., X.Z., H.T., X. Cao, unpublished . . .

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