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Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Coculture Analysis of Extracellular Protein Interactions Affecting Insulin Secretion by Pancreatic Beta Cells

Published on: June 15, 2013

Mosaic analysis of insulin receptor function.

Tadahiro Kitamura¹, Yukari Kitamura, Jun Nakae

¹Department of Medicine, College of Physicians & Surgeons of Columbia University, New York, New York 10032, USA.

The Journal of Clinical Investigation

|January 15, 2004

Summary

This summary is machine-generated.

Insulin receptor (Insr) ablation in mice revealed that insulin promotes growth independently of its metabolic effects. The extent of Insr loss directly correlates with growth retardation, highlighting receptor number

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Area of Science:

Endocrinology
Molecular Biology
Genetics

Background:

Insulin is known to regulate both metabolism and growth.
The precise mechanism by which insulin influences growth, and whether this is solely dependent on its metabolic actions, remains unclear.
Previous studies using insulin receptor (Insr) knockout models were limited by early postnatal lethality.

Purpose of the Study:

To investigate whether insulin-dependent growth is a direct effect or a consequence of insulin's metabolic actions.
To elucidate the role of the insulin receptor in mediating insulin's growth-promoting effects.
To understand the relationship between insulin receptor expression levels and the specificity of insulin action.

Main Methods:

Generation of mice with variable cellular mosaicism for null insulin receptor (Insr) alleles.
Assessment of growth, metabolic parameters (lipoatrophy, hypoglycemia, diabetes), and gene expression in Insr-deficient mice.
Analysis of hepatic insulin-like growth factor binding protein-1 (IGFBP-1) expression.

Main Results:

Mice with approximately 80% Insr ablation exhibited severe growth retardation, lipoatrophy, and hypoglycemia, mimicking human leprechaunism.
Mice with 98% Insr ablation showed similar growth retardation and lipoatrophy but developed diabetes without beta-cell hyperplasia.
Growth retardation in these models was strongly correlated with a significant increase in hepatic IGFBP-1 expression.

Conclusions:

Insulin regulates growth through mechanisms independent of its metabolic functions.
The degree of insulin receptor (Insr) deficiency is a critical determinant of insulin's specific actions.
These findings underscore the importance of the insulin receptor in mediating insulin's distinct roles in growth and metabolism.