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Indy mutants: live long and prosper.

Stewart Frankel¹, Blanka Rogina

¹Department of Biology, University of Hartford West Hartford, CT, USA.

Frontiers in Genetics

|February 25, 2012

Summary

This summary is machine-generated.

Reduced Indy gene expression extends lifespan and mimics caloric restriction effects in flies and mice. This suggests INDY is a potential drug target for metabolic disorders like obesity and type 2 diabetes.

Keywords:

Indy caloric restriction

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Area of Science:

Metabolic regulation
Aging research
Genetics

Background:

The Indy gene encodes a transporter crucial for the Krebs cycle.
Reduced Indy expression in flies and worms increases lifespan.
Indy homologs are expressed in tissues vital for intermediary metabolism.

Purpose of the Study:

To investigate the hypothesis that decreased INDY activity mimics caloric restriction (CR).
To explore INDY as a potential therapeutic target for metabolic diseases.

Main Methods:

Comparative studies of Indy mutant flies and C. elegans homologs.
Analysis of physiological similarities between Indy mutant flies on high-calorie diets and control flies on CR.
Examination of mIndy knockout mice, focusing on hepatic mitochondrial biogenesis, lipid metabolism, and insulin sensitivity.

Main Results:

Indy mutant flies exhibit traits similar to CR, including increased activity, reduced weight, and improved insulin signaling.
mIndy knockout mice show enhanced hepatic mitochondrial biogenesis, increased lipid oxidation, and reduced lipogenesis.
mIndy(-/-) mice are protected against diet-induced adiposity and insulin resistance.

Conclusions:

Decreased INDY activity effectively simulates caloric restriction.
The INDY transporter is a promising drug target for metabolic syndrome, type 2 diabetes, and obesity.