A review on the possible molecular mechanism of action of N-acetylcysteine against insulin resistance and type-2 diabetes development.
OBJECTIVE
N-acetylcysteine (NAC), a cysteine pro-drug and glutathione precursor has been used in therapeutic practices for several decades, as a mucolytic agent and for the treatment of numerous disorders including paracetamol intoxication. There is a growing interest concerning the beneficial effects of NAC against the early stages of type-2 diabetes development. Nevertheless, the mechanisms underlying the therapeutic and clinical applications of NAC are not fully understood. In this review we aimed to focus on the protective effects of NAC against insulin resistance.


METHODS
The possible mechanisms of action were reviewed using the major findings of more than 100 papers relating to the antioxidant, anti-inflammatory and anti-apoptotic properties of NAC.


RESULTS
The anti-oxidative activity of NAC has been attributed to its fast reactions with free radicals as well as the restitution of reduced glutathione. Further, NAC has anti-inflammatory and anti-apoptotic properties which can have positive effects during the inflammatory process in insulin resistance. Moreover, NAC can modulate certain signaling pathways in both insulin target cells and β cells.


CONCLUSIONS
The diverse biological effects of NAC may make it a potential adjuvant or therapeutic target in the treatment of type-2 diabetes. So, further studies are required for determining its ability to alleviate insulin resistance and to improve insulin sensitivity.
Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, El Manar University, Tunis, Tunisia. Electronic address: lasram_montassar@yahoo.fr.
Mohamed Montassar
MM
Lasram
Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, El Manar University, Tunis, Tunisia.
Ines Bini
IB
Dhouib
Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, El Manar University, Tunis, Tunisia.
Alya
A
Annabi
Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, El Manar University, Tunis, Tunisia. Electronic address: salouaelfazaa@tunet.tn.
Saloua
S
El Fazaa
Laboratory of Aggression Physiology and Endocrine Metabolic Studies, Department of Biology, Faculty of Sciences, El Manar University, Tunis, Tunisia. Electronic address: najoua.gharbi@planet.tn.
Najoua
N
Gharbi
D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D000111:Acetylcysteine
Anti-apoptotic; Anti-inflammatory; Antioxidant; Insulin resistance; N-acetyl-l-cysteine (NAC) (PubChem CID: 12035); N-acetylcysteine