ABSTRACT
AIM: The present study was undertaken to investigate mechanisms of peripheral nerve dysfunction in latent autoimmune diabetes in adults (LADA). MATERIALS AND METHODS: Participants with LADA (n = 15) underwent median nerve ultrasonography and nerve excitability to examine axonal structure and function, in comparison to cohorts of type 1 diabetes (n = 15), type 2 diabetes (n = 23) and healthy controls (n = 26). The LADA group was matched for diabetes duration, glycaemic control, and neuropathy severity with the type 1 and type 2 diabetes groups. A validated mathematical model of the human axon was utilized to investigate the pathophysiological basis of nerve dysfunction. RESULTS: The most severe changes in nerve structure and function were noted in the LADA group. The LADA cohort demonstrated a significant increase in nerve cross-sectional area compared to type 1 participants and controls. Compared to type 1 and 2 diabetes, measures of threshold electrotonus, which assesses nodal and internodal conductances, were significantly worse in LADA in response to both depolarising currents and hyperpolarising currents. In the recovery cycle, participants with LADA had a significant increase in the relative refractory period. Mathematical modelling of excitability recordings indicated the basis of nerve dysfunction in LADA was different to type 1 and 2 diabetes. CONCLUSIONS: Participants with LADA exhibited more severe changes in nerve function and different underlying pathophysiological mechanisms compared to participants with type 1 or 2 diabetes. Intensive management of risk factors to delay the progression of neuropathy in LADA may be required.
Subject(s)
Diabetic Neuropathies/physiopathology , Latent Autoimmune Diabetes in Adults/physiopathology , Median Nerve/physiopathology , Neural Conduction/physiology , Adult , Aged , Case-Control Studies , Diabetes Mellitus, Type 1/diagnostic imaging , Diabetes Mellitus, Type 1/physiopathology , Diabetic Neuropathies/diagnostic imaging , Disease Progression , Female , Humans , Latent Autoimmune Diabetes in Adults/diagnostic imaging , Male , Median Nerve/diagnostic imaging , Middle Aged , Risk Factors , UltrasonographyABSTRACT
In this paper, we will describe a novel lable-free electrochemiluminescent (ECL) immunosensor for the detection of glutamate decarboxylase antibody (GADA) in which Au nanoparticles (AuNPs) had pre-functionalized the indium tin oxide (ITO) glass to support the sensing interface. The preparation of the basal electrode only need a simple two-step drop coating, a thin polymer of hydrolyzed 3-aminopropyl trimethoxysilane, and the AuNPs gel on the ITO substrate. The AuNPs not only enhanced the ECL signal of luminol, but also acted to immobilize the glutamate decarboxylase (GAD) to build the sensing host. This immunosensor exhibits excellent specificity, reproducibility and stability. On resultant sensor, after the direct immunoreaction, the decreased ECL intensity has a good linear regression toward the logarithm of GADA concentration in the range of 0.30â¯ngâ¯mL-1 to 50â¯ngâ¯mL-1 with a detection limit of 0.10â¯ngâ¯mL-1. The proposed senor has prospective capability for the clinical detection of GADA in human serums, which had important value for diagnosis and precaution of type-1 diabetes or latent autoimmune diabetes in adult (LADA).
