Lipid biosynthesis enzyme Agpat5 in AgRP-neurons is required for insulin-induced hypoglycemia sensing and glucagon secretion

September 27, 2022
Nat Commun
https://pubmed.ncbi.nlm.nih.gov/36180454

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36180454

Research summary

This study explores how Agpat5 in AgRP neurons regulates the counterregulatory response to hypoglycemia. Conditional deletion of Agpat5 in AgRP neurons impaired glucose-sensing neuronal activity and reduced glucagon secretion in response to insulin-induced hypoglycemia. This reveals Agpat5’s key role in glucose homeostasis through central neuronal pathways.

Key outcome of the study

Agpat5 deletion in AgRP neurons disrupts the neuronal response to hypoglycemia and blunts glucagon secretion, emphasizing its role in neuroendocrine regulation of blood glucose.

Mouse model

Conditional Agpat5 Knockout mouse model developed by genOway, using Flex technology for Cre-dependent gene inactivation. The model includes an IRES-linked reporter allowing for traceable expression.

TARGET:
Agpat5
1-acylglycerol-3-phosphate O-acyltransferase 5

Keywords

Hypoglycemia, Glucagon secretion, AgRP neurons, Neuroendocrinology, Glucose regulation

Technical specifications

Conditional Knockout, Flex technology, IRES reporter, Cre-dependent inactivation, Neuron-specific targeting

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