Carey · Diabetes 2006 · Controlled human physiological infusion study and in vitro cell culture experiment · n=?

Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase.

Cited 896 times in the scientific literature.

Level 3 - non-randomized controlled study

Controlled human physiological intervention study with in vitro mechanistic experiments; randomization not reported in abstract.

PubMed 17003332 · doi:10.2337/db05-1404 · record verified 2026-08-29

What was done

Healthy humans received an acute interleukin-6 (IL-6) infusion during a hyperinsulinemic-euglycemic clamp to assess in vivo glucose disposal and endogenous glucose production suppression. Cultured L6 myotubes were treated with IL-6 to evaluate fatty acid oxidation, basal and insulin-stimulated glucose uptake, GLUT4 translocation, and AMP-activated protein kinase (AMPK) activation. L6 myotubes infected with a dominant-negative AMPK alpha-subunit were used to test if AMPK activation mediated these cellular metabolic actions.

What was found

In healthy humans, acute IL-6 infusion increased insulin-stimulated glucose disposal without altering endogenous glucose production suppression. In L6 myotubes, IL-6 increased fatty acid oxidation, basal and insulin-stimulated glucose uptake, GLUT4 translocation to the plasma membrane, and rapidly increased AMPK activation. In dominant-negative AMPK-infected cells, these metabolic effects were abrogated. The abstract reports no numerical values, doses, or statistical metrics.

Why it matters

This study shows that acute IL-6 enhances insulin sensitivity and glucose disposal in healthy humans in vivo and identifies an AMPK-dependent mechanism for IL-6-mediated glucose uptake and lipid oxidation in skeletal muscle.

Limits

The abstract omits human sample size, participant characteristics, IL-6 dosing details, and quantitative effect sizes. Findings reflect acute IL-6 exposure in healthy individuals and cannot be assumed to apply to chronic inflammatory states or diabetic populations. Mechanistic pathways were tested in rodent myotubes rather than human tissue.

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