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Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets

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Published on: June 25, 2012

Glucose enhances rat islet function via stimulating CART expression.

Wan Xu¹, Yuqing Zhang¹, Mengyao Bai¹

¹Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, China.

Biochemical and Biophysical Research Communications

|November 9, 2016

Summary

This summary is machine-generated.

Cocaine- and amphetamine-regulated transcript (CART) peptide is upregulated in type-2 diabetes models. This study shows CART enhances glucose-stimulated insulin secretion, suggesting a role in pancreatic beta-cell function.

Keywords:

Cocaine- and amphetamine-regulated transcript Glucose Islet function Type 2 diabetes

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Area of Science:

Endocrinology
Molecular Biology
Metabolic Research

Background:

Cocaine- and amphetamine-regulated transcript (CART) is an anorexigenic peptide found in the nervous and endocrine systems.
CART is upregulated in pancreatic beta-cells in rodent models of type-2 diabetes.
The role of CART in glucose-potentiated insulin secretion is not well understood.

Purpose of the Study:

To investigate the role of CART in glucose-potentiated insulin secretion.
To determine the regulation of CART expression by glucose and related signaling pathways.
To assess the impact of CART on pancreatic beta-cell function.

Main Methods:

Quantitative analysis of CART mRNA expression in rat islets.
Stimulation of islets with glucose, glucokinase agonist (GKA50), and GLP-1 analogue (exendin-4).
Inhibition of cAMP-dependent signaling pathways (PKA, CREB) and assessment of CART mRNA.
Overexpression of CART to evaluate its effect on insulin secretion.

Main Results:

Glucose time- and dose-dependently increased CART mRNA expression in rat islets.
GKA50 and exendin-4 also enhanced CART mRNA levels.
PKA inhibition and CREB inactivation suppressed forskolin-stimulated CART mRNA expression.
CART overexpression amplified glucose- and forskolin-stimulated insulin secretion and improved dexamethasone-impaired secretion.

Conclusions:

Islet-derived CART is involved in high glucose-potentiated pancreatic beta-cell function.
CART expression is regulated by glucose and cAMP-dependent pathways.
CART plays a significant role in modulating insulin secretion.