Abstract
Skeletal muscles are important in glucose metabolism and are affected in type 2 diabetes (T2D) and its complications. This study investigated the effect of vanillin on redox imbalance, cholinergic and purinergic dysfunction, and glucose-lipid dysmetabolism in muscles of rats with T2D. Male albino rats (Sprague–Dawley strain) were fed 10% fructose ad libitum for 2 weeks before intraperitoneally injecting them with 40 mg/kg streptozotocin to induce T2D. Low (150 mg/kg bodyweight (BW)) and high (300 mg/kg BW) doses of vanillin were orally administered to diabetic rats. Untreated diabetic rats and normal rats made up the diabetic control (DC) and normal control (NC) groups, respectively. The standard antidiabetic drug was metformin. The rats were humanely put to sleep after 5 weeks of treatment and their psoas muscles were harvested. There was suppression in the levels of glutathione, activities of SOD, catalase, ENTPDase, 5′Nucleotidase and glycogen levels on T2D induction. This was accompanied by concomitantly elevated levels of malondialdehyde, serum creatine kinase-MB, nitric oxide, acetylcholinesterase, ATPase, amylase, lipase, glucose-6-phosphatase (G6Pase), fructose-1,6-biphophastase (FBPase) and glycogen phosphorylase activities. T2D induction further resulted in the inactivation of fatty acid biosynthesis, glycerolipid metabolism, fatty acid elongation in mitochondria and fatty acid metabolism pathways. There were close to normal and significant reversals in these activities and levels, with concomitant reactivation of the deactivated pathways following treatment with vanillin, which compared favorably with the standard drug (metformin). Vanillin also significantly increased muscle glucose uptake ex vivo. The results suggest the therapeutic effect of vanillin against muscle dysmetabolism in T2D as portrayed by its ability to mitigate redox imbalance, inflammation, cholinergic and purinergic dysfunctions, while modulating glucose-lipid metabolic switch and maintaining muscle histology.
Highlights
Skeletal muscles are important in glucose metabolism and are affected in type 2 diabetes (T2D) and its complications
While in the fasting states, skeletal muscle glucose uptake is reduced and the muscle switches to free fatty acids (FFAs) for energy production[4,5]. These normal activities are impaired in T2D owing to diminished pancreatic insulin secretion and/or insulin resistance, culminating in decreased muscle glucose uptake, impaired muscle glucose-lipid metabolic homeostasis, suppressed muscle glycogen levels, perturbed muscle mitochondrial oxidative phosphorylation and muscle cholinergic dysfunction[5,6,7]
Excessive utilization of FFAs and their dysmetabolism over glucose utilization by skeletal muscles in T2D has been involved in the pathogenesis and progression of muscle insulin r esistance[8,9]
Summary
Skeletal muscles are important in glucose metabolism and are affected in type 2 diabetes (T2D) and its complications. Type 2 diabetes (T2D) ranks among the most common types of diabetes as it has been linked to over 90% of mortality and morbidity associated with d iabetes[1] It is typified by poor utilization of insulin secreted by the pancreatic β-cells, causing perturbation in the metabolisms of carbohydrates, proteins, and fatty acids and in turn leads to hyperglycemia[2]. While in the fasting states, skeletal muscle glucose uptake is reduced and the muscle switches to free fatty acids (FFAs) for energy production[4,5] These normal activities are impaired in T2D owing to diminished pancreatic insulin secretion and/or insulin resistance, culminating in decreased muscle glucose uptake, impaired muscle glucose-lipid metabolic homeostasis, suppressed muscle glycogen levels, perturbed muscle mitochondrial oxidative phosphorylation and muscle cholinergic dysfunction[5,6,7]. These factors contribute greatly to skeletal muscle fiber atrophy, sarcopenia and myopathy in the long r un[15,16]
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