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Clinical manifestation and islet β-cell function of a subtype of latent autoimmune diabetes in adults (LADA): positive for T cell responses in phenotypic type 2 diabetes.
Acta Diabetol. 2019 Nov; 56(11):1225-1230.AD

Abstract

AIMS

To investigate the possibility of identifying a subtype of latent autoimmune diabetes in adults (LADA), T-LADA (T cell responses-positive and autoantibody-negative) from patients with phenotypic type 2 diabetes (T2D) by enzyme-linked immunospot (ELISPOT).

METHODS

Eighty-two patients with phenotypic T2D were studied. Autoantibodies against glutamic acid decarboxylase (GAD), insulinoma-associated protein-2 and zinc transporter 8 were measured by radioligand assay. Thirty-nine Ab+ and 43 Ab- patients with phenotypic T2D were enrolled for T cell assay of responses to GAD65 and C-peptide antigen by ELISPOT.

RESULTS

(1) Eleven of 43 Ab- participants with phenotypic T2D were demonstrated interferon (IFN)-γ secreting T cells by ELISPOT, while 13 of 39 Ab+ patients with phenotypic T2D were positive for T cells responses to islet antigens. (2) The onset ages of T cell+ people with phenotypic T2D were younger than that of T cell- individuals (42.7 ± 9.3 vs. 48.2 ± 10.2 years, P = 0.025). Moreover, T cell+ patients with T2D displayed a significantly lower fasting C-peptide (FCP) compared with T cell- participants [0.28 (0.02-0.84) vs. 0.42 (0.05-1.26) nmol/L, P = 0.013]. (3) Ab-T+ group had a significantly lower FCP compared with Ab-T- group [0.31 (0.13-0.84) vs. 0.51 (0.07-1.26) nmol/L, P = 0.023].

CONCLUSIONS

By measuring T cell responses to islet antigens in patients with phenotypic T2D, we identified a specific subtype of LADA who may be associated with worse basal β-cell function than classic T2D (Ab-T-).

Authors+Show Affiliations

Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. yanglin_nfm@csu.edu.cn. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China. yanglin_nfm@csu.edu.cn.Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China. zhouzhiguang@csu.edu.cn. Key Laboratory of Diabetes Immunology, Ministry of Education, National Clinical Research Center for Metabolic Diseases, Central South University, Changsha, 410011, Hunan, China. zhouzhiguang@csu.edu.cn.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31367990

Citation

Liang, Huiying, et al. "Clinical Manifestation and Islet Β-cell Function of a Subtype of Latent Autoimmune Diabetes in Adults (LADA): Positive for T Cell Responses in Phenotypic Type 2 Diabetes." Acta Diabetologica, vol. 56, no. 11, 2019, pp. 1225-1230.
Liang H, Cheng Y, Tang W, et al. Clinical manifestation and islet β-cell function of a subtype of latent autoimmune diabetes in adults (LADA): positive for T cell responses in phenotypic type 2 diabetes. Acta Diabetol. 2019;56(11):1225-1230.
Liang, H., Cheng, Y., Tang, W., Cui, Q., Yuan, J., Huang, G., Yang, L., & Zhou, Z. (2019). Clinical manifestation and islet β-cell function of a subtype of latent autoimmune diabetes in adults (LADA): positive for T cell responses in phenotypic type 2 diabetes. Acta Diabetologica, 56(11), 1225-1230. https://doi.org/10.1007/s00592-019-01391-w
Liang H, et al. Clinical Manifestation and Islet Β-cell Function of a Subtype of Latent Autoimmune Diabetes in Adults (LADA): Positive for T Cell Responses in Phenotypic Type 2 Diabetes. Acta Diabetol. 2019;56(11):1225-1230. PubMed PMID: 31367990.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinical manifestation and islet β-cell function of a subtype of latent autoimmune diabetes in adults (LADA): positive for T cell responses in phenotypic type 2 diabetes. AU - Liang,Huiying, AU - Cheng,Ying, AU - Tang,Wei, AU - Cui,Qiuyan, AU - Yuan,Jiao, AU - Huang,Gan, AU - Yang,Lin, AU - Zhou,Zhiguang, Y1 - 2019/07/31/ PY - 2019/05/16/received PY - 2019/07/23/accepted PY - 2019/8/2/pubmed PY - 2019/12/18/medline PY - 2019/8/2/entrez KW - Enzyme-linked immunospot (ELISPOT) KW - Islet β-cell function KW - Latent autoimmune diabetes in adults (LADA) KW - T-LADA KW - Type 2 diabetes SP - 1225 EP - 1230 JF - Acta diabetologica JO - Acta Diabetol VL - 56 IS - 11 N2 - AIMS: To investigate the possibility of identifying a subtype of latent autoimmune diabetes in adults (LADA), T-LADA (T cell responses-positive and autoantibody-negative) from patients with phenotypic type 2 diabetes (T2D) by enzyme-linked immunospot (ELISPOT). METHODS: Eighty-two patients with phenotypic T2D were studied. Autoantibodies against glutamic acid decarboxylase (GAD), insulinoma-associated protein-2 and zinc transporter 8 were measured by radioligand assay. Thirty-nine Ab+ and 43 Ab- patients with phenotypic T2D were enrolled for T cell assay of responses to GAD65 and C-peptide antigen by ELISPOT. RESULTS: (1) Eleven of 43 Ab- participants with phenotypic T2D were demonstrated interferon (IFN)-γ secreting T cells by ELISPOT, while 13 of 39 Ab+ patients with phenotypic T2D were positive for T cells responses to islet antigens. (2) The onset ages of T cell+ people with phenotypic T2D were younger than that of T cell- individuals (42.7 ± 9.3 vs. 48.2 ± 10.2 years, P = 0.025). Moreover, T cell+ patients with T2D displayed a significantly lower fasting C-peptide (FCP) compared with T cell- participants [0.28 (0.02-0.84) vs. 0.42 (0.05-1.26) nmol/L, P = 0.013]. (3) Ab-T+ group had a significantly lower FCP compared with Ab-T- group [0.31 (0.13-0.84) vs. 0.51 (0.07-1.26) nmol/L, P = 0.023]. CONCLUSIONS: By measuring T cell responses to islet antigens in patients with phenotypic T2D, we identified a specific subtype of LADA who may be associated with worse basal β-cell function than classic T2D (Ab-T-). SN - 1432-5233 UR - https://www.unboundmedicine.com/medline/citation/31367990/Clinical_manifestation_and_islet_β_cell_function_of_a_subtype_of_latent_autoimmune_diabetes_in_adults__LADA_:_positive_for_T_cell_responses_in_phenotypic_type_2_diabetes_ L2 - https://dx.doi.org/10.1007/s00592-019-01391-w DB - PRIME DP - Unbound Medicine ER -