Background: LADA is thought to result from the chronic autoimmune destruction of the insulin-producing pancreatic beta cells. In addition to antidiabetic effects, the newly developed insulin sensitizer-thiazolidinediones have the potential to increase the insulin content of islet cells by downregulating local inflammation and autoimmune response. Therefore, we hypothesized that LADA patients might benefit from thiazolidinediones treatment.

Methods: LADA patients, with a fasting C-peptide (FCP) of 0.3 nmol/L or more, were enrolled and randomly assigned to receive subcutaneous insulin alone (insulin group, n = 12) or rosiglitazone plus insulin (insulin + RSG group, n = 11) to compare the impacts on islet beta cell function. Plasma glucose, HbA 1c, fasting C-peptide (FCP) and C-peptide after 2 h 75-g glucose load (PCP) were determined every 6 months. GAD-Ab and C-peptide were measured with radioimmune assays. Islet beta cell function was evaluated by PCP and DeltaCP(DeltaCP = PCP-FCP).

Results: All of the 23 patients have been followed up for 6 months, 17 cases for 12 months and 14 for 18 months. (1) During 6 months' follow-up, there were no significant changes for DeltaCP and PCP levels in both groups. (2) PCP and DeltaCP levels in insulin + RSG group patients stayed steady during the 12 months' observation (P = 0.161 for both PCP and DeltaCP), while in the insulin alone group, both FCP (P = 0.021) and PCP (P = 0.028) levels decreased significantly. Furthermore, PCP (P = 0.004) and DeltaCP(P = 0.015) differences between 12th month and baseline were higher in insulin + RSG group than those in the insulin group. (3) When observed up to 18 months, PCP and DeltaCP levels in insulin + RSG group patients still stayed steady, while PCP and DeltaCP levels decreased more in the insulin alone group.

Conclusions: This pilot study suggests that rosiglitazone combined with insulin may preserve islet beta cell function in LADA patients.

Download full-text PDF

Source
http://dx.doi.org/10.1002/dmrr.503DOI Listing

Publication Analysis

Top Keywords

islet beta
16
beta cell
16
cell function
16
insulin rsg
16
rsg group
16
pcp deltacp
16
insulin
14
lada patients
12
insulin group
12
deltacp levels
12

Similar Publications

Background: Varicella zoster virus (VZV) reactivation, manifesting as herpes zoster, increases dementia risk. Herein, we review the literature supporting the biological plausibility of VZV contributing to AD pathologies and examine the unique ability of VZV to induce amylin that has been found in blood vessels and parenchyma of AD patients.

Method: We conducted a literature review on VZV and dementia to elucidate a potential model for how VZV reactivation intersects with AD.

View Article and Find Full Text PDF

Developing Topics.

Alzheimers Dement

December 2024

University of Kentucky, Lexington, KY, USA.

Background: Amylin is a systemic hormone that is co-secreted with insulin from pancreatic β-cells. Amylin co-aggregates with brain parenchymal and vascular β-amyloid in persons with Alzheimer's dementia. The present pilot study sought to assess the safety and side effects during and after the treatment period of passive amylin immunotherapy in the APP/PS1 mouse model of Alzheimer's disease.

View Article and Find Full Text PDF

Mechanisms by which Ganglioside GM1, a specific type of glycosphingolipid, ameliorates BMAA-induced neurotoxicity in early-life stage of zebrafish embryos.

Food Res Int

January 2025

State Key Laboratory of Marine Food Processing & Safety Control, College of Food Science and Engineering, Ocean University of China, Qingdao 266404, China; Qingdao Marine Science and Technology Center, Qingdao, Shandong Province 266235, China.

The neurotoxin β-methylamino-L-alanine (BMAA) produced by cyanobacteria is widely present in foods and dietary supplements, posing a significant threat to human health. Ganglioside GM1 (GM1) has demonstrated potential for treating neurodegenerative diseases; however, its ability to prevent BMAA-induced neurotoxicity remains uncertain. In this study, zebrafish embryos were treated with Ganglioside GM1 to investigate its neuroprotective effects against BMAA exposure and the underlying mechanisms.

View Article and Find Full Text PDF

Gestational diabetes mellitus-derived miR-7-19488 targets PIK3R2 mRNA to stimulate the abnormal development and maturation of offspring-islets.

Life Sci

January 2025

Department of Pharmacology, School of Pharmacy, Qingdao University, No. 308 Ningxia Road, Shinan District, Qingdao 266021, China; Key Laboratory of Maternal & Fetal Medicine of National Health Commission of China, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan 250014, China. Electronic address:

Aims: Gestational diabetes mellitus (GDM) provides offspring with a hyper-metabolic intrauterine microenvironment. In this study, we aimed to identify key differential microRNAs in GDM-derived exosomes and explore the potential mechanisms of abnormal embryonic development of islets in offspring.

Main Methods: Exosomes were extracted from umbilical vein blood of GDM and non-GDM (NGDM) parturients for microRNA sequencing.

View Article and Find Full Text PDF

Background: The pancreas exhibits diverse structures and roles across vertebrates. The pancreas has evolved to include both endocrine and exocrine cells, a change that occurred during the transition from fish to amphibian. This event emphasizes the evolutionary significance of amphibians.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!