Tine Maria Hansen1, Birgitte Brock2, Anne Juhl3, Asbjørn Mohr Drewes4, Henrik Vorum5, Carl Uggerhøj Andersen5, Poul Erik Jakobsen6, Jesper Karmisholt7, Jens Brøndum Frøkjær8, Christina Brock9. 1. Mech-Sense, Department of Radiology, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark. 2. Clinical Biochemistry, Aarhus University Hospital and Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 82, 8200 Aarhus, Denmark; Steno Diabetes Center Copenhagen, Niels Steensens Vej 6, 2820 Gentofte, Denmark. 3. Department of Clinical Neurophysiology, Aalborg University Hospital, Ladegårdsgade 5, 9000 Aalborg, Denmark. 4. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark; Mech-Sense, Department of Gastroenterology & Hepatology, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark; Steno Diabetes Center North Jutland, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark. 5. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark; Department of Ophthalmology, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark. 6. Steno Diabetes Center North Jutland, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark; Department of Endocrinology, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark. 7. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark; Department of Endocrinology, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark. 8. Mech-Sense, Department of Radiology, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark. Electronic address: jebf@rn.dk. 9. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 11, 9000 Aalborg, Denmark; Mech-Sense, Department of Gastroenterology & Hepatology, Aalborg University Hospital, Mølleparkvej 4, 9000 Aalborg, Denmark; Department of Drug Design and Pharmacology, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark.
Abstract
AIMS: Emerging evidence shows, that distal symmetric peripheral neuropathy (DSPN) also involves alterations in the central nervous system. Hence, the aims were to investigate brain metabolites in white matter of adults with diabetes and DSPN, and to compare any cerebral disparities with peripheral nerve characteristics. METHODS: In type 1 diabetes, brain metabolites of 47 adults with confirmed DSPN were compared with 28 matched healthy controls using proton magnetic resonance spectroscopy (H-MRS) in the parietal region including the sensorimotor fiber tracts. RESULTS: Adults with diabetes had 9.3% lower ratio of N-acetylaspartate/creatine (NAA/cre) in comparison to healthy (p < 0.001). Lower NAA/cre was associated with lower sural (p = 0.01) and tibial (p = 0.04) nerve amplitudes, longer diabetes duration (p = 0.03) and higher age (p = 0.03). In addition, NAA/cre was significantly lower in the subgroup with proliferative retinopathy as compared to the subgroup with non-proliferative retinopathy (p = 0.02). CONCLUSIONS: The association to peripheral nerve dysfunction, indicates concomitant presence of DSPN and central neuropathies, supporting the increasing recognition of diabetic neuropathy being, at least partly, a disease leading to polyneuropathy. Decreased NAA, is a potential promising biomarker of central neuronal dysfunction or loss, and thus may be useful to measure progression of neuropathy in diabetes or other neurodegenerative diseases.
AIMS: Emerging evidence shows, that distal symmetric peripheral neuropathy (DSPN) also involves alterations in the central nervous system. Hence, the aims were to investigate brain metabolites in white matter of adults with diabetes and DSPN, and to compare any cerebral disparities with peripheral nerve characteristics. METHODS: In type 1 diabetes, brain metabolites of 47 adults with confirmed DSPN were compared with 28 matched healthy controls using proton magnetic resonance spectroscopy (H-MRS) in the parietal region including the sensorimotor fiber tracts. RESULTS: Adults with diabetes had 9.3% lower ratio of N-acetylaspartate/creatine (NAA/cre) in comparison to healthy (p < 0.001). Lower NAA/cre was associated with lower sural (p = 0.01) and tibial (p = 0.04) nerve amplitudes, longer diabetes duration (p = 0.03) and higher age (p = 0.03). In addition, NAA/cre was significantly lower in the subgroup with proliferative retinopathy as compared to the subgroup with non-proliferative retinopathy (p = 0.02). CONCLUSIONS: The association to peripheral nerve dysfunction, indicates concomitant presence of DSPN and central neuropathies, supporting the increasing recognition of diabetic neuropathy being, at least partly, a disease leading to polyneuropathy. Decreased NAA, is a potential promising biomarker of central neuronal dysfunction or loss, and thus may be useful to measure progression of neuropathy in diabetes or other neurodegenerative diseases.
Authors: Allison L O'Kell; Clive Wasserfall; Joy Guingab-Cagmat; Bobbie-Jo M Webb-Roberston; Mark A Atkinson; Timothy J Garrett Journal: Metabolomics Date: 2021-11-14 Impact factor: 4.290