Objective: To test the effectiveness at 6 and 12 months' follow-up of group cognitive behavioural therapy (CBT) compared with blood glucose awareness training (BGAT) in poorly controlled Type 1 diabetic patients and to explore the moderating effect of baseline depression.
Research Design And Methods: Adults with Type 1 diabetes (n = 86) with glycated haemoglobin (HbA(1c)) >or= 8% were randomized to CBT or BGAT. Primary outcome was HbA(1c) control. Secondary outcomes were: self-care, diabetes-related distress (Problem Areas in Diabetes scale; PAID), diabetes self-efficacy (Confidence in Diabetes Self-care scale; CIDS) and depressive symptoms (Centre for Epidemiological Studies--Depression scale; CES-D). Measurements were scheduled before CBT and BGAT, and at 3, 6 and 12 months after. Differential effects were analysed for the subgroup of patients reporting low vs. high baseline levels of depression.
Results: Neither CBT nor BGAT had a significant impact on HbA(1c) at 6 and 12 months' follow-up. Both interventions resulted in lower depressive symptoms (CES-D 15.7-13.3, P = 0.01) up to 12 months, but only CBT was effective in lowering HbA(1c) in patients with high baseline depression scores (HbA(1c) 9.5-8.8%) up to 1 year of follow-up (P = 0.03).
Conclusions: Our findings suggest that group CBT can effectively help Type 1 diabetic patients with co-morbid depression achieve and maintain better glycaemic outcomes.
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http://dx.doi.org/10.1111/j.1464-5491.2008.02595.x | DOI Listing |
J Microbiol Immunol Infect
January 2025
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan; Department of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, 70101, Taiwan. Electronic address:
Background: COVID-19 mRNA vaccines have demonstrated 95 % efficacy in the general population. However, their immunogenicity in adolescents with Type 1 Diabetes (T1D), who exhibit weaken immune responses, remains insufficiently explored.
Methods: Longitudinal analysis of innate immune responses following PRR-agonists and BNT162b2 vaccine stimulations, along with S-specific antibody responses, memory T cell recall responses, and RNA-sequencing were assessed in eight T1D adolescents and 16 healthy controls at six different timepoints.
Contemp Clin Trials
January 2025
Kaiser Permanente Washington Health Research Institute, 1730 Minor Ave, Seattle, WA 98101, USA.
Cell Signal
January 2025
Department of Endocrinology, The Third Xiangya Hospital, Central South University, 410007 Changsha, Hunan, China. Electronic address:
Type 1 diabetes (T1D) is an autoimmune disease characterized by hyperglycemia caused by the destruction of insulin-producing β cells. Viral infection is an important environmental factor which is associated with the islet autoimmunity in genetically susceptible individuals. Loss of β-cells and triggering of insulitis following viral infection could result from several non-exclusive mechanisms.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China; Global Health Research Center, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian 116044, China. Electronic address:
Sodium arsenite (NaAsO), the most common form of inorganic arsenic prevalent in the environment, has been closely linked to islet β-cell dysfunction, a critical pathological hallmark of type 2 diabetes (T2D). Even though apoptosis plays a pivotal role in arsenic-induced islet β-cell dysfunction, the explicit underlying mechanisms remain elusive. Here, we have identified that the SET-Rac1 signaling pathway is instrumental in the apoptosis and dysfunction of islet β-cells induced by NaAsO.
View Article and Find Full Text PDFColloids Surf B Biointerfaces
December 2024
Department of Plastic and Cosmetic Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing 400038, China. Electronic address:
The chronic diabetic wounds represented by diabetes foot ulcers (DFUs) are a worldwide challenge. Excessive production of reactive oxygen species (ROS) and persistent inflammation caused by the impaired phenotype switch of macrophages from M1 to M2 during wound healing are the main culprits of non-healing diabetic wounds. Therefore, an injectable DMM/GelMA hydrogel as a promising wound dressing was designed to regulate the mitochondrial metabolism of macrophages via inhibiting succinate dehydrogenase (SDH) activity and to promote macrophage repolarization towards M2 type.
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