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Autonomic diabetic neuropathy (ADN) is a complication of diabetes mellitus (DM), to which there is no specific treatment. In this study, the efficacy of the essential oil of Croton zehntneri (EOCz) in preventing ADN was evaluated in the rat vagus nerve. For the two fastest conducting myelinated types of axons of the vagus nerve, the conduction velocities and rheobase decreased, whilst the duration of the components of the compound action potential of these fibers increased. EOCz completely prevented these DM-induced alterations of the vagus nerve. Unmyelinated fibers were not affected. In conclusion, this investigation demonstrated that EOCz is a potential therapeutic agent for the treatment of ADN.

This article summarizes the latest epidemiology of diabetic autonomic neuropathy (DAN), and provides a brief overview on epidemiology, current outcomes measures for screening and diagnosis in research and clinical settings, the latest evidence on effective management, and novel perspectives on the impacts of social determinants of health in development and management of DAN. Among the various forms of diabetic neuropathy, distal symmetric polyneuropathy and diabetic autonomic neuropathies, particularly cardiovascular autonomic neuropathy, are by far the most studied. However, emerging data highlight the impact of other forms of autonomic neuropathies such as gastrointestinal and urogenital autonomic neuropathies, on healthcare and patients' reported outcomes [1]. [ABSTRACT FROM AUTHOR]

Objective: The established marker for tubular damage, urinary n-acetyl-beta-d-glucosaminidase is significantly increased in type 1 and 2 diabetes patients and is related to albuminuria and other diabetic complications. In this cross sectional study of type 2 diabetes patients with a history of albuminuria, we studied the relationship between excretion of n-acetyl-beta-d-glucosaminidase in urine and diabetic neuropathy. Methods: 160 type 2 diabetes patients were screened for diabetic peripheral neuropathy and cardiovascular autonomic neuropathy. N-acetylbeta- d-glucosaminidase excretion was detected in 24 h urine samples. Results: Urinary excretion of n-acetyl-beta-dglucosaminidase correlated significantly with glucose control (fasting glucose r = 0.18; p = 0.04; HbA1c r = 0.20; p = 0.02) and urine albumin excretion (r = 0.22; p = 0.01). Binary regression analyses showed that increased urinary n-acetyl-betad- glucosaminidase concentration is an independent predictor for presence of clinical symptoms of peripheral neuropathy (OR 1.8 [95 %CI 1.2-2.74] and vibration deficiency [OR 1.7; 95 % CI 1.2-2.66]. There was also a significant negative association between urinary n-acetyl-beta-d-glucosaminidase and E/I-Ratio (r = - 0.21, p < 0.02) as well as the 30:15-Ratio (r = - 0.24; p < 0.01) of heart rate variability. Furthermore, increased n-acetyl-beta-d-glucosaminidase excretion independently predicted cardiovascular autonomic diabetic neuropathy with an OR for decreased E/I-Ratio of 1.7 [95 %CI 1.1-2.75]; (p < 0.02) and 30:15-Ratio:OR 2.4 [95 % CI 1.26-4.45]; (p < 0.01). Conclusion: Urinary n-acetyl-beta-d-glucosaminidase excretion is an independent marker for diabetic peripheral and cardiovascular autonomic neuropathy in type 2 diabetic patients [ABSTRACT FROM AUTHOR]

Autonomic diabetic neuropathy (ADN) is a complication of diabetes mellitus (DM), to which there is no specific treatment. In this study, the efficacy of the essential oil of Croton zehntneri (EOCz) in preventing ADN was evaluated in the rat vagus nerve. For the two fastest conducting myelinated types of axons of the vagus nerve, the conduction velocities and rheobase decreased, whilst the duration of the components of the compound action potential of these fibers increased. EOCz completely prevented these DM-induced alterations of the vagus nerve. Unmyelinated fibers were not affected. In conclusion, this investigation demonstrated that EOCz is a potential therapeutic agent for the treatment of ADN. [ABSTRACT FROM AUTHOR]

Two diabetic women (case 1, 75 years old; case 2, 49 years old) being treated with glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1 RAs) showed no suppression of cortisol secretion on a dexamethasone suppression test (DST). However, its secretion was suppressed after switching from GLP-1 RAs to insulin. We also checked the cortisol secretion by a DST in five consecutive inpatients (case 3-7) being treated with GLP-1 RAs. The coefficients of R-R interval variation at rest and during deep breathing were lower in the two false-positive cases (case 1 and 2) than in the five true-negative cases (case 3-6). GLP-1 RAs can be switched to insulin in order to eliminate the slow absorption effect of dexamethasone by GLP-1 RAs if a DST is planned in diabetic patients receiving GLP-1 RAs.