Abstract
The rising incidence of diabetes and its negative impact on quality of life highlights the urgent need to develop biomarkers of early nerve damage. Measurement of total vitamin B12 has some limitations. We want to determine the levels of urinary methylmalonic acid and its relationships with serum vitamin B12 and polyneuropathy. The 176 Chinese patients with Type 2 diabetes mellitus were divided into 3 groups according to the levels of vitamin B12. A gas chromatography mass spectrometric technique was used to determine blood methylmalonic acid and urinary methylmalonic acid. The diagnosis of distal diabetic polyneuropathy was based on the determination of bilateral limb sensory and motor nerve conduction velocity and amplitude with electromyogram. Multiple regression analysis revealed that urinary methylmalonic acid/creatinine, blood methylmalonic acid, and so forth were variables that influenced diabetic polyneuropathy significantly. Nerve sensory conduction velocity and nerve amplitude in the group of urinary methylmalonic acid/creatinine >3.5 mmol/mol decreased significantly. Superficial peroneal nerve sensory and motor conduction velocity and ulnar nerve compound motor active potential amplitude were inversely correlated with urinary methylmalonic acid/creatinine. Urinary methylmalonic acid correlates with serum vitamin B12 levels in person with diabetes and is a sensitive marker of early polyneuropathy.
Highlights
Diabetes mellitus (DM) is caused by genetic and environmental interactions, along with changing lifestyles and an aging population, increasing incidence of diabetes
There was no significant difference in low-density lipoprotein cholesterol (LDL), mean corpuscular volume (MCV), duration, serum creatinine (sCr), TG, BMI, and hemoglobin A1c (HbA1c) among the three groups
Our data showed polyneuropathy was present in 24.7% of our diabetic patients using electromyogram (EMG), which was higher than the previous report [11], maybe because of sample selection or the diagnostic criteria of neuropathy
Summary
Diabetes mellitus (DM) is caused by genetic and environmental interactions, along with changing lifestyles and an aging population, increasing incidence of diabetes. Diabetic neuropathy is one of the major complications of diabetes with both Type 1 and Type 2. Up to 50% of all diabetes have polyneuropathy which is a major cause of morbidity and associated with increased mortality, and up to 26% of diabetics develop painful diabetic neuropathy with debilitating effects on quality of life [1,2,3]. Vitamin B12 (Vit B12) is a cofactor for methylmalonylCoA mutase, which converts methylmalonyl CoA to succinyl CoA. Methylmalonic acid (MMA) may contribute to neuronal injury in many human conditions in which it accumulates, including methylmalonyl-CoA mutase and Vit B12 deficiency [7, 8]. The impaired activity of the enzyme leads to an accumulation of MMA and an elevated
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