Insulin signaling in adipose tissue of patients with primary aldosteronism

J Endocrinol Invest. 2011 Feb;34(2):86-9. doi: 10.1007/BF03347035.

Abstract

Objective: We studied phosphorylation of insulin-receptors substrate downstream molecules: 1) in the ex-vivo visceral adipose tissue (VAT) of patients with aldosterone-producing adenoma (APA) (no.=7) and non-functioning adenoma (NFA) (no.=7) undergoing laparoscopic adrenalectomy; 2) in aldosterone-treated sc adipocytes of subjects (no.=5) who requested abdominoplasty.

Patients and methods: Western blotting was used to detect phosphorylation of Akt and extracellular signal-regulated kinase (ERK) 1/2 in VAT from APA and NFA patients, and in subcutaneous adipocytes pre-treated with different aldosterone concentrations. Phosphorylation of Akt and ERK1/2 was similar in VAT of patients with APA and NFA. Pre-treatment in adipocytes with both physiological (1 nM) and pharmacological (10 μM) doses of aldosterone did not affect basal or insulin-induced phosphorylation of Akt and ERK1/2.

Conclusions: Our data give further evidence that insulin signaling in human VAT is not affected by primary aldosterone overproduction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipose Tissue / cytology
  • Adipose Tissue / metabolism*
  • Adrenal Cortex Neoplasms / pathology
  • Adrenal Cortex Neoplasms / physiopathology
  • Adrenal Cortex Neoplasms / surgery
  • Adrenalectomy
  • Adrenocortical Adenoma / pathology
  • Adrenocortical Adenoma / physiopathology
  • Adrenocortical Adenoma / surgery
  • Adult
  • Aged
  • Aldosterone / blood
  • Aldosterone / pharmacology
  • Cells, Cultured
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Humans
  • Hyperaldosteronism / physiopathology*
  • Hyperaldosteronism / surgery
  • Insulin / metabolism*
  • Male
  • Middle Aged
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / physiology*

Substances

  • Insulin
  • Aldosterone
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases