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Updated: May 30, 2026

Isolation of Human Islets from Partially Pancreatectomized Patients

Isolation of Human Islets from Partially Pancreatectomized Patients

Published on: July 30, 2011

Review on monogenic diabetes.

Andrea K Steck¹, Wiliam E Winter

¹Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, Aurora, Colorado 80045-6511, USA.

Current Opinion in Endocrinology, Diabetes, and Obesity

|August 17, 2011

Summary

This summary is machine-generated.

Monogenic diabetes, caused by single gene mutations, accounts for 1-2% of cases. Genetic discoveries have improved the understanding and treatment of maturity-onset diabetes of the young (MODY) and neonatal diabetes.

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Area of Science:

Endocrinology
Genetics
Metabolic Disorders

Background:

Monogenic diabetes results from mutations affecting beta-cell function, accounting for 1-2% of all diabetes cases.
Key forms include maturity-onset diabetes of the young (MODY) and neonatal diabetes (permanent and transient).

Purpose of the Study:

To provide an updated review of monogenic diabetes subtypes.
To discuss current understanding and management strategies for MODY and neonatal diabetes.

Main Methods:

Literature review of monogenic diabetes.
Analysis of genetic mutations and their clinical impact.

Main Results:

Individuals with youth-onset diabetes lacking autoantibodies should be screened for MODY subtypes (glucokinase-MODY or transcription factor MODY).
Glucokinase-MODY often requires no pharmacologic treatment, while transcription factor MODY may respond to low-dose sulfonylureas.
Permanent neonatal diabetes, diagnosed within the first six months of life, can often be managed with high-dose sulfonylureas.

Conclusions:

Genetic discoveries have significantly enhanced the diagnosis and management of monogenic diabetes.
Personalized treatment approaches based on specific genetic mutations are crucial for optimal patient outcomes.