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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
Published January 2, 2022
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