Neuropathic phenotypes of type 1 diabetes are related to different signatures of magnetic resonance spectroscopy-assessed brain metabolites

• Published in: Clinical neurophysiology Vol. 166; pp. 11 - 19
• Main Authors: Hansen, Tine M., Croosu, Suganthiya S., Røikjer, Johan, Mørch, Carsten D., Ejskjaer, Niels, Frøkjær, Jens B.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.10.2024
• Subjects: Adult; Aspartic Acid - analogs & derivatives; Brain - diagnostic imaging; Brain - metabolism; Brain metabolites; Central nervous system; Diabetes Mellitus, Type 1 - metabolism; Diabetic Neuropathies - diagnostic imaging; Diabetic Neuropathies - metabolism; Diabetic neuropathy; Female; Humans; Magnetic resonance spectroscopy; Magnetic Resonance Spectroscopy - methods; Male; Middle Aged; Peripheral nervous system; Phenotype; Peripheral nervous system; T1DM; ACC; DPN; MRI; Central nervous system; Diabetic neuropathy; MRS; NAA; Magnetic resonance spectroscopy; Glu; TE; Brain metabolites; MEDON; SNR; Cre; FWHM; FLAIR; GPC; mI; HbA1c; TR
• ISSN: 1388-2457; 1872-8952; 1872-8952
• DOI: 10.1016/j.clinph.2024.06.017

•Brain alterations have been described in type 1 diabetes and diabetic neuropathy.•Metabolic profiles of neuropathic phenotypes using relevant brain regions were explored.•Specific metabolic brain profiles were linked to phenotypes of diabetes, neuropathy, and neuropathic pain.•Metabolic brain profiles could be relevant for detailed understanding of central neuropathy. The study aimed to investigate brain metabolites in type 1 diabetes and the associations with disease characteristics. We explored the metabolic profiles predicting different neuropathic phenotypes using multiple linear regression analyses. We compared brain metabolites in 55 adults with type 1 diabetes (including painful diabetic peripheral neuropathy (DPN), painless DPN, without DPN) with 20 healthy controls. Proton magnetic resonance spectroscopy measurements (N-acetylaspartate (NAA), glutamate (glu), myo-inositol (mI), and glycerophosphocholine (GPC) were obtained in ratios to creatine (cre)) from the parietal region, anterior cingulate cortex and thalamus. The overall diabetes group revealed decreased parietal NAA/cre compared to healthy controls (1.41 ± 0.12 vs. 1.55 ± 0.13,p < 0.001) and increased mI/cre (parietal: 0.62 ± 0.08 vs. 0.57 ± 0.07,p = 0.025, cingulate: 0.65 ± 0.08 vs. 0.60 ± 0.08,p = 0.033). Reduced NAA/cre was associated with more severe DPN (all p ≤ 0.04) whereas increased mI/cre was associated with higher hemoglobin A1c (HbA1c) (p = 0.02). Diabetes was predicted from decreased parietal NAA/cre, increased parietal ml/cre, and decreased thalamic glu/cre. DPN was predicted from decreased parietal NAA/cre and increased GPC/cre. Painful DPN was predicted from increased parietal GPC/cre and thalamic glu/cre. Specific metabolic brain profiles were linked to the different phenotypes of diabetes, DPN and painful DPN. Assessment of metabolic profiles could be relevant for detailed understanding of central neuropathy in diabetes.