Insulin as an anti-inflammatory and antiatherosclerotic hormone.
Fasting hyperinsulinemia is associated with an increased risk of atherosclerotic complications, namely heart attack and stroke, which has led to the concept that insulin may promote atherosclerosis despite the absence of any evidence that insulin is atherogenic either in humans or in experimental models. Recent evidence shows that insulin exerts vasodilatory, antiplatelet, and anti-inflammatory effects at the cellular level in vitro and in humans in vivo. Because atherosclerosis is an inflammatory process, insulin is probably antiatherosclerotic in the long-term. Recent data on experimental atherosclerosis in mice show that (a) insulin administration reduces the number and the size of atherosclerotic lesions in apolipoprotein E null mice; and (b) in insulin receptor substrate-2 null mice, the interruption in insulin signal transduction results in enhanced atherogenicity. The use of a low dose of insulin infusion in patients with acute myocardial infarction (AMI) has been shown to markedly improve clinical outcomes both in diabetic and nondiabetic patients. The authors' most recent data show that a low-dose infusion of insulin in patients with AMI induces a reduction in inflammation (C-reactive protein and serum amyloid A) and oxidative stress and may have a role in myocardial protection. The authors conclude that insulin is both anti-inflammatory and antiatherogenic and may be of use in the treatment of cardiovascular inflammatory conditions, including AMI.
Division of Endocrinology, Diabetes and Metabolism, State University of New York, Kaleida Health Buffalo, New York, USA. pdandona@kaleidahealth.org
Paresh
P
Dandona
Ahmad
A
Aljada
Sandeep
S
Dhindsa
Rajesh
R
Garg
D001161:Arteriosclerosis / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy* / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology* / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology; D009203:Myocardial Infarction / Q000188:drug therapy; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D007004:Hypoglycemic Agents; D007328:Insulin; D014409:Tumor Necrosis Factor-alpha