Published online Apr 30, 2019. doi: 10.13105/wjma.v7.i4.129
Peer-review started: March 19, 2019
First decision: April 13, 2019
Revised: April 20, 2019
Accepted: April 23, 2019
Article in press: April 23, 2019
Published online: April 30, 2019
Processing time: 42 Days and 8.4 Hours
The reciprocal relationship between hyperglycemia and inflammation in the setting of diabetes mellitus has been the subject of extensive research. Insulin resistance, the hallmark of diabetic metabolic dysregulation, has been linked to the inflammatory cascade occurring mainly in adipose tissue. The main pathophysiologic processes facilitating the aforementioned interplay, is a phenotype switch of macrophages to the M1 class following gluco- and lipotoxicity and gut microbial remodeling. Given the correlation between inflammation and metabolic abnormalities, the elucidation of the exact mechanisms linking the two along with exploring the possible role of modulation of one in order to alter the other, could open up the possibility of novel therapeutic approaches for diabetes mellitus and its complications. Therefore, the aim of this review is to summarize the growing body of evidence concerning the molecular basis and results of pro-inflammatory processes in diabetic subjects along with the effect of current antidiabetic treatment options on tissue inflammation.
Core tip: In this review, we aim to create a concise overview of the interplay between hyperglycemia and inflammation, while describing the immunomodulatory potential of each antidiabetic drug and its effects exerted in the inflammatory cascade in subjects with type 2 diabetes.