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Studies have also examined its potential influence on angiogenesis, fibroblast signaling, and nitric oxide related pathways

We have taken three previously suggested mechanisms of crosstalk for the actions of insulin to explain the observed behaviour in the experimental data: 1) an anti-lipolytic effect of insulin via protein kinase B (PKB) and PDE3B [3, 13] action-1, 2) a positive lipolytic effect of insulin via PDE3B at high concentrations of insulin [3] action-2, and 3) an anti-lipolytic effect of insulin via -adrenergic receptors [4] action-3

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Notably, some of the beneficial effects observed with L