title: Comparison of the effects of hypolipidemic treatment on monocyte proinflammatory cytokine release in men and women with type 2 diabetes and atherogenic dyslipidemia.
abstract: BACKGROUND
  Statins and fibrates reduce monocyte release of proinflammatory cytokines, but it remains unknown whether this effect is sex dependent.
  
  
  METHODS
  We retrospectively analysed age-, weight-, and lipid-matched populations of type 2 diabetic patients of both sexes, who, because of atherogenic dyslipidaemia, were treated with simvastatin (40 mg daily), fenofibrate (200 mg daily), or simvastatin plus fenofibrate. Monocyte release of tumour necrosis factor α (TNF-α), inteleukin-1β, interleukin-6, and monocyte chemoattractant protein-1 (MCP-1), as well as circulating levels of high-sensitivity C-reactive protein (hsCRP) and free fatty acids (FFA) were assessed separately for men and women before and after 12 weeks of treatment.
  
  
  RESULTS
  Baseline monocyte release of TNF-α, interleukin-1β, interleukin-6, and MCP-1, as well as plasma hsCRP and FFA levels were comparable in both sexes. Simvastatin, fenofibrate, and simvastatin/fenofibrate combination therapy reduced monocyte release of TNF-α, inteleukin-1β, interleukin-6, and MCP-1, with no difference between the treatment groups. The impact of simvastatin and fenofibrate administered alone on monocyte cytokine release and systemic inflammation did not differ between the men and women. The effect of simvastatin/fenofibrate combination therapy on monocyte release of interleukin-6 and MCP-1 was more pronounced in the male population. The impact of simvastatin administered together with fenofibrate on TNF-α, interleukin-1β, and hsCRP was also stronger in the men than in the women, but the difference did not reach the level of significance.
  
  
  CONCLUSIONS
  The obtained results suggest that sex differences determine the strength of the monocyte-suppressing effect of simvastatin/ /fenofibrate combination therapy in type 2 diabetic patients with atherogenic dyslipidaemia.
authors.affiliation: Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland. r.krysiak@interia.pl.
authors.forename: Robert
authors.initials: R
authors.lastname: Krysiak
authors.forename: Anna
authors.initials: A
authors.lastname: Gdula-Dymek
authors.forename: Bogdan
authors.initials: B
authors.lastname: Marek
authors.forename: Bogusław
authors.initials: B
authors.lastname: Okopień
mesh_terms: D050197:Atherosclerosis; D002097:C-Reactive Protein / Q000032:analysis; D016207:Cytokines / Q000097:blood* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D050171:Dyslipidemias / Q000150:complications* / Q000188:drug therapy; D005260:Female; D011345:Fenofibrate / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D012737:Sex Factors; D019821:Simvastatin / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D016207:Cytokines; D000960:Hypolipidemic Agents; D002097:C-Reactive Protein; D019821:Simvastatin; D011345:Fenofibrate