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May 1, 1997Diabetes

Insulin Stimulates Nitric Oxide Synthesis in Human Platelets and, Through Nitric Oxide, Increases Platelet Concentrations of Both Guanosine-3′, 5′-Cyclic Monophosphate and Adenosine-3′, 5′-Cyclic Monophosphate

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Population

Human platelets

Design

Preclinical

Authors

MTMariella TrovatiUniversity of CagliariGAGiovanni AnfossiUniversity of TurinPMPaola MassuccoOspedale San Luigi Gonzaga

Discussion

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Implication

Insulin may inhibit platelet aggregation via NO in vitro; leaves open clinical antithrombotic relevance in diabetes.

Key Points

  • To determine whether insulin stimulates nitric oxide synthesis in human platelets and whether this pathway increases concentrations of both cGMP and cAMP.
  • Measured nitric oxide production in isolated human platelets via citrulline synthesis from L-arginine after insulin incubation.
  • Evaluated platelet cGMP and cAMP levels across time intervals (2–120 min) and in the presence of adenylate cyclase agonists Iloprost and forskolin.
  • Inhibited nitric oxide synthase using N(G)-monomethyl-L-arginine to establish pathway dependency.
  • Insulin dose-dependently increased nitric oxide production (n=4, P=0.015) and increased cAMP from 39.8 ± 1.4 to 121.3 ± 12.6 pmol/10^9 platelets at 1,920 pmol/l after 8 min (n=16, P=0.0001).
  • Insulin amplified the cAMP-raising actions of Iloprost and forskolin (n=5, P=0.0001) as well as their anti-aggregating effects (n=6 and n=8, P=0.0001).
  • Inhibition of nitric oxide synthase with N(G)-monomethyl-L-arginine completely blunted the insulin-mediated increases in basal cGMP and cAMP (n=4) and agonist-induced cAMP responses (n=5).

Structured PICO

P
Population
Human platelets
I
Intervention
Insulin (dose-dependent, e.g., 1,920 pmol/l)
O
Outcome
Nitric oxide (NO) synthesis (evaluated as citrulline synthesis from L-arginine), cGMP, and cAMP concentrationssurrogate

Insulin exerts a platelet anti-aggregating effect by increasing nitric oxide synthesis, which in turn enhances both cGMP and cAMP levels.

Cite This Study

Trovati et al. (1997) studied this question.

synapsesocial.com/papers/6a731d4f64decaab472c162fhttps://doi.org/10.2337/diab.46.5.742
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Insulin Increases Guanosine-3′ ,5′-Cyclic Monophosphate in Human Platelets: A Mechanism Involved in the Insulin Anti-Aggregating Effect1994 · 56 citations
  2. 2Platelet Resistance to Nitrates in Obesity and Obese NIDDM, and Normal Platelet Sensitivity to Both Insulin and Nitrates in Lean NIDDM1998 · 107 citations
  3. 3Insulin Directly Reduces Platelet Sensitivity to Aggregating Agents: Studies In Vitro and In Vivo1988 · 121 citations
  4. 4Inhaled NO inhibits platelet aggregation and elevates plasma but not intraplatelet cGMP in healthy human volunteers2003 · 46 citations
  5. 5Impaired synthesis and action of antiaggregating cyclic nucleotides in platelets from obese subjects: possible role in platelet hyperactivation in obesity2004 · 57 citations