Lab rates were treated with streptozotocin, a naturally occurring chemical that is especially toxic to the insulin producing beta cells of the pancreas in mammals. The chemical induces diabetes.
The study found that B12 supplementation mitigates neuronal morphology and cell death, reduces astrogliosis (the abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system trauma or infection) and improves the neurotrophic support and synaptic density-related proteins.
“Several epidemiological studies showed adults with type 1 diabetes have reduced motor speed, psychomotor activities and reduction in white matter volume or an alteration in white matter microstructure,” wrote researchers from ICMR-National Institute of Nutrition in India. “Additionally, diabetes also reported to induce structural alternations in blood brain barrier, increased blood brain barrier permeability, neuronal cell loss, demyelination, gliosis and degeneration of ganglion cells and nerve fibers in the cerebrum, brain stem and cerebellum.”
Restoring plasticity
Two-month-old Sprague-Dawley rats were randomly assigned into three groups: control, diabetes (induced with streptozotocin), and diabetic rats supplemented with vitamin B12 (50 μg/kg) for four months. At the end of the four months of experimentation, the brains of the rats were dissected to collect the cerebral cortex. The researchers determined whether neuronal apoptosis, or cell death, was determined and found that B12 supplementation ameliorated the diabetes-induced neuronal apoptosis. Further, B12 supplementation restored the markers of neurotrophic support and synaptic plasticity in diabetic rats. Interestingly, B12 supplementation also attenuated astrogliosis, endoplasmic reticulum stress and ameliorated autophagy-related proteins in diabetic rats.
“Overall, these findings suggest that B12 acts as a neuroprotective agent by inhibiting the neuropathological changes in streptozotocin-induced type 1 diabetes,” the researchers wrote. “Thus, B12 supplementation could produce beneficial outcomes including neuroprotective effects in diabetic patients.”
Vitamin B12 deficiency
Diabetes mellitus is a metabolic disease characterized by elevated glucose levels or hyperglycemia stemming from the body's inability to produce insulin and/or use insulin, the researchers described.
“Diabetes and its complications are increasing at an alarming rate and that is the growing concern for morbidity and mortality in diabetic patients,” they added.
About 537 million people worldwide were diabetic in 2021 and expected to reach 783 million in 2045 according to the International Diabetes Federation. Several neurological complications are associated with diabetes including retinopathy, peripheral neuropathy, brain atrophy, neuropathic pain and cognitive deficit.
Additionally, many studies established that diabetes can lead to alterations in brain morphology and functions.
“Several epidemiological studies showed adults with type 1 diabetes have reduced motor speed, psychomotor activities, reduction in white matter volume or an alteration in white matter microstructure,” the scientists noted.
Vitamin B12 is a water-soluble vitamin important for red blood cell formation and maintenance of neuronal and cognitive health. Moreover, B12 is also necessary for proper brain development and functioning, suggesting that it has neurotrophic effects.
“Experimental diabetes causes a depression of several water-soluble vitamins including B12 in various tissues of rats. Besides, several studies proposed that metformin therapy in diabetic patients is associated with a higher prevalence of B12 deficiency,” the researchers stated.
Even short-term metformin therapy reduced the serum B12 and folate levels while increasing the homocysteine. Metformin-induced vitamin B12 deficiency is associated with hematological and neurological side effects.
Source: Chemico-Biological Interactions
Volume 387, 110823, doi: doi.org/10.1016/j.cbi.2023.110823
“Neuroprotective role of vitamin B12 in streptozotocin-induced type 1 diabetic rats”
Authors: Udaykanth Suryavanshi et al.