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[Insulin resistance and evolution].

J M Fernández-Real Lemos1

  • 1Unidad de Diabetes, Endocrinología y Nutrición (UDEN), Hospital Universitario de Girona Dr. Josep Trueta, Girona, España. endocrino@htrueta.scs.es

Nutricion Hospitalaria
|April 4, 2002
PubMed
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[Adipsia and hypernatremia as the first manifestation of hypothalamic astrocytoma. Report of a case and review of the literature].

Anales de medicina interna (Madrid, Spain : 1984)·2000
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The immune system, through cytokines like tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6), can cause insulin resistance. This adaptation, beneficial in the past, now contributes to type 2 diabetes and atherosclerosis in modern environments.

Area of Science:

  • Immunology and Metabolism
  • Genetics and Chronic Disease

Context:

  • Infections and injuries activate the immune system, inducing metabolic changes.
  • Tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) play key roles in inflammation and infection response.
  • Gene polymorphisms in TNF-alpha and IL-6 are linked to insulin resistance and chronic infection mortality.

Purpose:

  • To explore the metabolic effects of immune system activation, particularly TNF-alpha and IL-6.
  • To investigate the association between immune system gene variants, insulin resistance, and body fat.
  • To understand how evolutionary immune adaptations may contribute to modern chronic diseases.

Summary:

  • Immune system activation leads to metabolic changes, including insulin resistance, by influencing TNF-alpha and IL-6.

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  • Specific gene polymorphisms of TNF-alpha and IL-6 correlate with insulin resistance, body fat, and mortality in chronic infections.
  • While beneficial for ancestral survival (e.g., intermittent fasting, infection control), these immune responses now contribute to type 2 diabetes and atherosclerosis in Westernized environments.

    • Impact:

    • Highlights the dual role of immune system adaptations in evolutionary and modern contexts.
    • Suggests a genetic predisposition to metabolic diseases in individuals with specific cytokine gene profiles.
    • Underscores the mismatch between ancient genetic adaptations and contemporary lifestyles, leading to chronic disease development.