Ultrastructural aspects of cranial and peripheric nerves of cronically diabetic and malnourished rats: a short biochemical panorama

Abstract

Diabetes Mellitus is one of the most common causes of neuropathies, which can be caused by molecular imbalances that impair metabolic pathways. Studies in rats showed the importance of sirtuins (SIRT), deacetylases that use NAD + as a cofactor, which have a widespread function in metabolism, and their relation when food deprived or calorie restricted. Additionally, diabetic neuropathy presents different structural biomarkers that cause morphological alterations in fibers that can be partially treated. SIRT1 is the principal sirtuin, which acts on hypothalamus, liver, kidney, among other organs, up regulating or down regulating the expression of some genes or enzymes crucial in the process of glucose absorption.

SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis

“…In mammals, SIRT1, SIRT6 and SIRT7 are located in the nucleus, SIRT3, SIRT4 and SIRT5 are located in the mitochondria and SIRT2 is located in the cytoplasm (13). SIRT1 has been shown to be associated with the regulation of apoptosis, inflammation, metabolism and mitochondrial biogenesis, and play a pivotal role in neural development and age-related diseases, including type 2 diabetes (14). SIRT3 enhances lipid catabolism, regulates the tricarboxylic acid cycle and reduces the levels of ROS (15).…”