5 replies to this topic

[\SHINE/]

Metab Syndr Relat Disord (2004) 2: 137-42.

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone.

P Dandona, A Aljada, A O'Donnell, S Dhindsa, R Garg

Fasting hyperinsulinemia is associated with an increased risk of atherosclerotic complications of heart attack and stroke. This has resulted in the concept that insulin may promote atherosclerosis in spite of the absence of any evidence that insulin is atherogenic either in the human or in experimental models. Recent evidence shows that insulin exerts vasodilatory, anti-platelet and anti-inflammatory effects at the cellular level in vitro and in the human in vivo. Since atherosclerosis is a chronic inflammatory process of the arterial wall, insulin may be potentially anti-atherosclerotic in the long term. More recent data on experimental atherosclerosis in the mouse shows that (1) insulin administration reduces the number and the size of atherosclerotic lesions in apo E null mice and (2) in IRS-2 null mice, the interruption in insulin signal transduction results in enhanced atherogenicity. Finally, the use of a low dose of insulin infusion in patients with acute myocardial infarction has been shown to markedly improve clinical outcomes, both in diabetic and nondiabetic patients. Our own most recent data show that a low dose infusion of insulin in patients with acute myocardial infarction induces a reduction in inflammation (C-reactive protein and serum amyloid A) and oxidative stress, and promotes fibrinolysis. We conclude that insulin is anti-inflammatory and potentially antiatherogenic and may be of use in the treatment of cardiovascular inflammatory conditions

[JMS162]

That's interesting, I've noticed igf has anti-inflammatory properties as well, which I guess isn't surprising since they're so similar. Whenever I'm on it, the tendonitus in my shoulder doesn't bother me near as much.

[ajdos]

Besides the anit aterio-inflammation I wonder if it benefits connective tissue in a similar manner?

[DragonRider]

I wonder if it benefits connective tissue in a similar manner?

Good question. I'd like to know also.

[\SHINE/]

Besides the anit aterio-inflammation I wonder if it benefits connective tissue in a similar manner?

Good question, as IGF in a couple of studies in vivo showed to help collagen and ligaments it's quite possible insulin could do so as well. (i've been looking into this as well)

peace.

[MissKBuff]

Yes, believe it or not, I've actually heard this before.

Metabolism Department, The University of Texas Medical Branch, Galveston, and Shriners Hospitals for Children-Galveston Burns Hospital, 77550, USA. rwolfe@sbi.utmb.edu

The anabolic nature of insulin on muscle protein has been recognized since the initial clinical use of insulin therapy in type 1 diabetes about sixty years ago, but the exact mechanism whereby insulin effects muscle protein metabolism in human subjects remains unclear. In particular, the effect of insulin on muscle protein synthesis has been debated. In vitro studies document a stimulatory effect of insulin on muscle protein synthesis, but in vivo results are conflicting. Everything from decreased muscle protein synthesis to increased muscle protein synthesis in response to insulin has been reported. A recent publication suggests that the response of muscle protein synthesis to insulin is dose dependent, and that only supraphysiological dose of insulin stimulate muscle protein synthesis. On the other hand, some studies show a stimulatory effect of insulin in low doses. It is possible to form a more coherent picture of the effect of insulin if the results from various experiments are expressed in the context of the availability of amino acids. In general, insulin stimulated muscle protein synthesis in studies in which intramuscular amino acid availability was maintained or increased regardless of the dose of insulin. In contrast, insulin was ineffective in stimulating muscle protein synthesis when amino acid availability was allowed to drop, irrespective of the dose of insulin. Thus, whereas insulin has a potential stimulatory effect on human muscle protein synthesis, an adequate availability of amino acids is required for that potential to be expressed in an actual increase in the synthetic rate.

PMID: 10642086 [PubMed - indexed for MEDLINE]

This next one doesn't have much to do with insulin, but it's interesting none the less:

Connective tissue growth factor (CTGF) is expressed in atherosclerotic plaques. It is generally recognized that CTGF contributes to atherosclerosis by stimulating vascular smooth muscle cell (VSMC) proliferation and extracellular matrix production during the development of atherosclerosis. Recent studies indicate that CTGF may also contribute to plaque destabilization as it induces apoptosis and stimulates MMP-2 expression in VSMCs. Thiazolidinediones (TZDs), a new class of insulin sensitizing drugs for type 2 diabetes, inhibit atherosclerosis. However, their effect on CTGF expression in atherosclerotic plaques remains unknown. In this study, male LDL receptor-deficient mice were fed high-fat diet for 4 months to induce the formation of atherosclerotic plaques and then given the high-fat diet with or without pioglitazone for the next 3 months. At the end of the 7-month study, CTGF expression in aortic atherosclerotic lesions was examined. Results showed that CTGF expression was increased in mice fed the high-fat diet by seven-fold as compared to that in mice fed normal chow, but the treatment with pioglitazone significantly inhibited the high-fat diet-induced CTGF expression. To verify these in vivo observations, in vitro studies using human aortic SMC were conducted. Quantitative real-time PCR and Western blot showed that pioglitazone inhibited TGF-β-stimulated CTGF expression. In conclusion, the present study has demonstrated that pioglitazone inhibits CTGF expression in mouse advanced atherosclerotic plaques and in cultured human SMCs, and hence unveiled a possible mechanism potentially involved in the inhibition of atherosclerosis by TZD.