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In the past 20 years of groundbreaking diabetes research, Anath Shalev, MD, demonstrated that the TXNIP protein regulates the survival and function of β cells, β cells are pancreatic cells that produce insulin to lower glucose levels
in the blood.
β cells play a key role
in the pathogenesis of both type 1 and type 2 diabetes.
To further understand the role of TXNIP in islet biology and glucose control, Shalev and colleagues at the University of Alabama at Birmingham now report the effects
of knocking out TXNIP in α cells.
In a mouse model of streptomycin-induced diabetes, α cell knockout, while not as significant as β-cell TXNIP knockout, improved diabetes-related hyperglycemia and hyperglucagonemia
.
Alpha cell knockout mice, known as aTKO, had normal glucose homeostasis without significant abnormalities
when fed normal foods.
In knockout mice, there was no change in the structure of the aTKO island and no change
in the number of alpha cells.
Of the five recently reported proteins involved in α cell glucagon expression, only one, Grp78, has significantly altered
expression in aTKO islets.
Therefore, down-regulating α-cell TXNIP appears to inhibit α-cell glucagon secretion, which in turn may help explain the improvement
in hyperglucagonemia and hyperglycemia observed in diabetic aTKO mice.
Shalev, director of the UAB Comprehensive Diabetes Center and professor in the Department of Endocrinology, Diabetes and Metabolic Medicine, said: "Interestingly, we recently found that inhibiting the pharmacological effects of TXNIP with a small molecule inhibitor also leads to a decrease
in alpha cell glucagon secretion in different diabetic mouse models in vitro and in vivo alphac1-6 cells.
Co-authored the paper with Shalev, "α Cell TXNIP Deficiency Improves Diabetes-Related Hyperglycemia and Hyperglucagonemia," published in the journal Endocrinology including Brian Lu, Junqin Chen, Guanlan Xu, Truman B.
Support from the National Institutes of Health grant DK078752 and the Human Islet Research Network DK120379
.
