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Modulation of gene expression profiles by hyperosmolarity and insulin.

Christine Schäfer¹, Thor Gehrmann, Lisa Richter

¹Heinrich-Heine-University, Clinic for Gastroenterology, Hepatology, and Infectiology, Düsseldorf, Germany.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology

|September 1, 2007

Summary

Cell hydration, altered by hyperosmolarity, differentially impacts insulin sensitivity in gene expression. This study reveals how osmotic stress affects insulin

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Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

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Area of Science:

Cellular Biology
Metabolic Regulation
Molecular Endocrinology

Background:

Cell hydration is crucial for cell function and insulin sensitivity.
Hyperosmolarity significantly influences metabolic pathways.
Understanding osmotic effects on insulin signaling is key.

Purpose of the Study:

To investigate how hyperosmolarity modulates insulin's effects on gene expression in rat hepatoma cells.
To identify specific genes and pathways affected by osmotic stress and insulin.

Main Methods:

Utilized cDNA/oligonucleotide arrays, Northern, and Western blot analyses.
Examined gene and protein expression in H4IIE rat hepatoma cells under varying osmotic conditions and insulin stimulation.
Assessed osmosensitive expression of key proteins like Igfbp1, Mrp5, and cyclin D1.

Main Results:

Hyperosmolarity altered insulin sensitivity for numerous genes, including those involved in transport, signaling, and metabolism.
Established osmosensitive expression of insulin-like growth factor binding protein 1 (Igfbp1), multidrug resistance protein 5 (Mrp5), and cyclin D1 (Ccnd1) at mRNA and protein levels.
Observed blunted insulin responses for genes like betaine homocysteine-S-methyl transferase and increased responses for Mrp5 and cyclin D1 under hyperosmotic conditions.
Noted interference with cyclin D1 mRNA translation, leading to decreased protein levels despite increased mRNA under hyperosmolarity.
Identified several insulin-regulated genes whose expression was largely insensitive to hyperosmolarity.

Conclusions:

Hyperosmolarity differentially modulates insulin sensitivity at the gene expression level.
Osmotic stress impacts cellular processes by altering the response of specific genes to insulin.
Findings highlight the complex interplay between cell hydration status and metabolic regulation by insulin.