1. Potential Effect of Cinnamaldehyde on Insulin Resistance Is Mediated by Glucose and Lipid Homeostasis.
- Author
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Frederico MJS, Sulis PM, Pereira LL, Rey D, Aragón M, and Silva FRMB
- Subjects
- Animals, Male, Rats, Calcium metabolism, Signal Transduction drug effects, Rats, Wistar, Lipids blood, Liver metabolism, Liver drug effects, Insulin Resistance, Acrolein analogs & derivatives, Acrolein pharmacology, Homeostasis drug effects, Muscle, Skeletal metabolism, Muscle, Skeletal drug effects, Glucose metabolism, Lipid Metabolism drug effects, TRPA1 Cation Channel metabolism
- Abstract
Diabetes mellitus is a metabolic syndrome that has grown globally to become a significant public health challenge. Hypothesizing that the plasma membrane protein, transient receptor potential ankyrin-1, is a pivotal target in insulin resistance, we investigated the mechanism of action of cinnamaldehyde (CIN), an electrophilic TRPA1 agonist, in skeletal muscle, a primary insulin target. Specifically, we evaluated the effect of CIN on insulin resistance, hepatic glycogen accumulation and muscle and adipose tissue glucose uptake. Furthermore, the in vitro role of CIN in glucose uptake and intracellular signaling was determined in insulin-resistant rats whose calcium influx was analyzed. Moreover, the serum lipid profile was assessed following short-term CIN treatment in rats, and lipid tolerance was analyzed. The effects of CIN on insulin resistance were mediated by TRPA1, with downstream signaling involving the activation of PI3-K, MAPK, PKC, as well as extracellular calcium and calcium release from intracellular stores. Additionally, cytoskeleton integrity was required for the complete action of CIN on glucose uptake in muscle. CIN also ameliorated the serum lipid profile and improved triglyceride tolerance following acute vivo exposure.
- Published
- 2025
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