Insulin receptors in virus-induced diabetes mellitus in mice

Area of Science:

• Virology
• Immunology
• Metabolic Diseases

Background:

• Encephalomyocarditis virus (EMCV) is known to cause various diseases in mammals.
• Viral infections can trigger metabolic dysfunctions, including alterations in glucose homeostasis.
• Insulin resistance is a key factor in the development of diabetes mellitus.

Purpose of the Study:

• To investigate the impact of EMCV infection on insulin receptor dynamics in mice.
• To determine the relationship between viral load, glucose metabolism, and insulin receptor expression.
• To elucidate the role of insulin receptor alterations in virus-induced diabetes.

Main Methods:

• DBA/2 mice were infected with the M variant of EMCV.
• Quantitative estimations of insulin receptors on liver cell membranes were performed.
• Fasting plasma insulin concentration and 125-I insulin binding to receptors were measured.
• Changes in receptor number and affinity were assessed over time.

Main Results:

• EMCV infection caused impaired glucose metabolism starting on day 3, lasting for 5 months.
• Fasting plasma insulin levels decreased significantly by day 14.
• Specific binding of 125-I insulin to liver cell membrane receptors decreased significantly by day 3.
• Insulin receptor number declined by day 1, significantly by day 3, and normalized by day 7.
• Reduced receptor affinity was observed in infected mice, with greater impact in males.

Conclusions:

• Alterations in insulin receptors are a significant factor in the initial impairment of glucose metabolism during EMCV infection.
• These findings suggest a mechanism for virus-induced diabetes involving direct effects on insulin signaling pathways.
• The study highlights the potential for viral agents to induce metabolic disorders resembling type 2 diabetes.