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Mitochondrial dysfunction: The pathological link between psoriasis and insulin resistance?

Alejandra Villarreal-Martinez1, Laura Elia Martinez-de-Villarreal2, Minerva Gomez-Flores1

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Psoriasis patients exhibit altered mitochondrial beta-oxidation, indicated by distinct acylcarnitine profiles, regardless of insulin resistance (IR). This suggests mitochondrial dysfunction is linked to psoriasis and potentially stearoyl CoA desaturase (SCD) activity.

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Area of Science:

  • Metabolic research
  • Mitochondrial biology
  • Dermatology

Background:

  • Psoriasis is linked to insulin resistance (IR), with reported lipid disturbances and altered fatty acid oxidation enzymes.
  • Mitochondrial beta-oxidation is impaired in IR, suggesting a common pathway in both conditions.

Purpose of the Study:

  • To investigate mitochondrial beta-oxidation, intermediary metabolism, and mitochondrial content in psoriasis patients with and without IR.
  • To compare these metabolic parameters with those of healthy controls.

Main Methods:

  • Participant groups: psoriasis with IR (n=26), psoriasis without IR (n=17), and healthy controls (n=17).
  • Analysis included quantification of amino acids and acylcarnitines (AC) via tandem mass spectrometry, urinary organic acids by GC/MS, and mitochondrial DNA (mtDNA) quantification.
  • Disease severity (PASI), BMI, and disease duration were assessed for correlation with ACs.

Main Results:

  • Nine analytes, including phenylalanine and various acylcarnitines (e.g., C0, C3, C5), differed between psoriatic groups.
  • Elevated urine uric acid and hippuric acid were observed in psoriasis patients (p=0.01).
  • Mitochondrial DNA content was higher in psoriasis patients compared to controls, with no difference between IR subgroups.

Conclusions:

  • Psoriasis patients, with or without IR, display distinct acylcarnitine profiles indicative of impaired beta-oxidation.
  • These findings suggest mitochondrial dysfunction and increased stearoyl CoA desaturase (SCD) activity in psoriasis patients.