Title of article
The Therapeutic Effects of Magnesium in Insulin Secretion and Insulin Resistance
Author/Authors
Hosseini Dastgerdi, Azadehalsadat Department of Physiology - School of Medicine - Isfahan University of Medical Sciences, Isfahan, Iran , Ghanbari Rad, Mahtab Department of Physiology - School of Medicine - Isfahan University of Medical Sciences, Isfahan, Iran , Soltani, Nepton Department of Physiology - School of Medicine - Isfahan University of Medical Sciences, Isfahan, Iran
Pages
11
From page
1
To page
11
Abstract
Insulin resistance (IR) is a chronic pathological condition that is related to reduce the rates of glucose
uptake, especially in the liver, muscle, and adipose tissue as target tissues. Metabolic syndrome and
type 2 diabetes mellitus can occur following progression of the disease. The majority of prior research
has applied that some cations such as magnesium (Mg2+) have important physiological role in insulin
metabolism. Mg2+ is the fourth most abundant mineral in the human body that gets involved as a
cofactor of various enzymes in several metabolic events, such as carbohydrate oxidation, and it has a
fundamental role in glucose transporting mechanism of the cell membrane. This cation has numerous
duties in the human body such as regulation of insulin secretion in pancreatic beta‐cells and
phosphorylation of the insulin receptors in target cells and also gets involved in other downstream
signal kinases as intracellular cation. On this basis, intracellular Mg2+ balancing is vital for adequate
carbohydrate metabolism. This paper summarizes the present knowledge about the therapeutic effects
of Mg2+ in reducing IR in liver, muscle, and pancreases with different mechanisms. For this, the
search was performed in Google Scholar, PubMed, Scopus, and Web of Science by insulin resistance,
skeletal muscle, liver, pancreases, magnesium, Mg2+, and inflammation keywords.
Keywords
Diabetes , glucose , insulin resistance , magnesium
Journal title
Advanced Biomedical Research
Serial Year
2022
Record number
2727803
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