Protective effects of 1-alpha-hydroxyvitamin D3 on residual beta-cell function in patients with adult-onset latent autoimmune diabetes (LADA).
BACKGROUND
Previous in vitro and in vivo studies have demonstrated that vitamin D could prevent pancreatic beta-cell destruction and reduce the incidence of autoimmune diabetes. In children with type 1 diabetes, vitamin D treatment produces moderate protective effects on residual beta-cell function and has proven to be safe. Therefore, we hypothesized that vitamin D might have protective effects on beta-cell function in patients with latent autoimmune diabetes in adults (LADA), a form of slowly progressive autoimmune type 1 diabetes.


METHODS
Thirty-five patients with LADA were randomly assigned to receive subcutaneous insulin alone (n = 18) or insulin plus 1-alpha-hydroxyvitamin D3 (1-alpha(OH)D3; 0.5 microg per day) (n = 17) for 1 year. Plasma C-peptide levels in fasting state (FCP) and 2 h after 75-g glucose load (PCP) were measured every 6 months with radioimmunoassay.


RESULTS
Both FCP and PCP levels stayed steady in the insulin plus 1-alpha(OH)D3 group, while FCP decreased in insulin-alone group (P = 0.006) during the 12-month intervention. Seventy percent of patients treated with 1-alpha(OH)D3 maintained or increased their FCP concentrations after 1 year of treatment, while only 22% of patients treated with insulin alone maintained stable FCP levels (P < 0.01). Further analysis on LADA subgroups with different durations of diabetes demonstrated that islet beta-cell function was better preserved (as reflected by significantly higher FCP and PCP levels) in the 1-alpha(OH)D3 plus insulin group only in patients with diabetes duration no longer than 1 year. No severe side effects were observed in any group.


CONCLUSIONS
Our data suggest that 1-alpha(OH)D3 plus insulin therapy can preserve pancreatic beta-cell function in patients with LADA.
Li
Xia
X
Diabetes Center, Institute of Metabolism and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, China.
Liao
Lan
L
Yan
Xiang
X
Huang
Gan
G
Lin
Jian
J
Lei
Minxiang
M
Wang
Xiangbing
X
Zhou
Zhiguang
Z
D000328:Adult; D001327:Autoimmune Diseases / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D002096:C-Peptide / Q000097:blood / Q000187:drug effects; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D004338:Drug Combinations; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000008:administration & dosage* / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000008:administration & dosage*; D007328:Insulin / Q000008:administration & dosage*; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000276:immunology; D007515:Islets of Langerhans / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D016896:Treatment Outcome
D002096:C-Peptide; D004338:Drug Combinations; D006887:Hydroxycholecalciferols; D007004:Hypoglycemic Agents; D007328:Insulin; C008088:alfacalcidol