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Olmesartan ameliorates insulin sensitivity by modulating tumor necrosis factor-alpha and cyclic AMP in skeletal

Koichi Yamaguchi1, Nobuyuki Ura, Hideyuki Murakami

  • 1Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.

Hypertension Research : Official Journal of the Japanese Society of Hypertension
|January 20, 2006
PubMed

Insights

High tumor necrosis factor-alpha (TNF-a) in skeletal muscle is linked to insulin resistance. This study found that cyclic adenosine monophosphate (cAMP) inversely affects TNF-a, suggesting a new therapeutic target.

Area of Science:

  • Metabolism and Endocrinology
  • Molecular Biology
  • Physiology

Background:

  • Tumor necrosis factor-alpha (TNF-a) in skeletal muscle is a key factor in insulin resistance.
  • The renin-angiotensin system and cyclic adenosine monophosphate (cAMP) are implicated in TNF-a regulation.

Purpose of the Study:

  • To investigate the relationship between cAMP and TNF-a in skeletal muscle.
  • To explore the role of the renin-angiotensin system in this interaction.

Main Methods:

  • Rats were fed a normal or fructose-rich diet for 6 weeks.
  • Angiotensin II type 1 receptor antagonist (olmesartan) was administered to fructose-fed rats.
  • Levels of TNF-a and cAMP in soleus muscle were measured.

Main Results:

  • Fructose-fed rats showed higher TNF-a and lower cAMP levels in skeletal muscle.
  • Olmesartan treatment increased cAMP and decreased TNF-a in fructose-fed rats.
  • A negative correlation between cAMP and TNF-a was observed; a cAMP analogue reduced TNF-a.

Conclusions:

  • Suppressed cAMP levels may contribute to increased TNF-a and insulin resistance.
  • Angiotensin II may regulate TNF-a in skeletal muscle via modulation of cAMP pathways.
  • Targeting cAMP could be a strategy for managing insulin resistance.

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