Although pancreatic α-cells play a vital role in maintaining metabolic homeostasis, little is known about their involvement in regulating maternal metabolic responses to pregnancy. For a study, researchers sought to determine if pancreatic α-cells responded to pregnancy and their role in maternal metabolic adaption. The findings using C57BL/6 revealed that pregnancy increased α-cell mass by boosting α-cell proliferation, which was related to a temporary elevation in maternal serum glucagon levels in early pregnancy. During pregnancy, maternal pancreatic GLP-1 content rose considerably. They ablated the α-cells (α-null) before and during pregnancy using the inducible Cre/loxp method while keeping enteroendocrine L-cells and serum GLP-1 levels normal. In contrast to an enhanced GTT before pregnancy, α-null dams had a markedly impaired GTT and considerably higher blood glucose concentrations in the fed state. Glucagon receptor antagonism, on the other hand, did not affect maternal glucose metabolism, showing that glucagon receptor signaling is unnecessary in maternal glucose homeostasis.
The GLP-1 receptor agonist, on the other hand, increased insulin production and glucose metabolism in -null dams. Furthermore, the GLP-1 receptor antagonist Exendin (9-39) inhibited pregnancy-induced insulin secretion, while GLP-1 restored glucose-induced insulin secretion in cultured islets from -null dams. The findings showed that α-cells played an important role in regulating maternal metabolic adaption during pregnancy by increasing insulin output.
