Department of Clinical and Experimental Medicine, University of Catania, Via S. Sofia 78, 95123, Catania, Italy.
Department of Experimental and Clinical Medicine, "Magna Graecia" University, Catanzaro, Italy.
J Endocrinol Invest. 2021 Jul;44(7):1547-1550. doi: 10.1007/s40618-020-01445-9. Epub 2020 Oct 14.
Preliminary clinical evidence suggests that metformin has TSH lowering effects in patients with T2DM and hypothyroidism or in those with TSH serum levels in the upper normal value. Also, metformin may exert a protective role against thyroid nodules growth in patients without insulin-resistance. The cross-talk between tyrosine kinase receptors and the G protein-coupled receptors (which the TSHR belongs to) has been already shown and IRS1 may represent the hub link between TSHR and IR pathways. By influencing IRS1 phosphorylation pattern, metformin may sensitize TSHR to TSH, thus explaining the findings of clinical studies. However, the existence of this molecular pathway must be confirmed through proper studies and further prospective randomized placebo-controlled studies are needed to confirm this hypothesis.
初步临床证据表明，二甲双胍可降低 T2DM 伴甲状腺功能减退或 TSH 血清水平在上限正常的患者的 TSH 水平。此外，二甲双胍可能对无胰岛素抵抗的患者的甲状腺结节生长发挥保护作用。已经证明了酪氨酸激酶受体和 G 蛋白偶联受体（TSHR 属于该受体）之间的串扰，并且 IRS1 可能代表 TSHR 和 IR 途径之间的枢纽联系。通过影响 IRS1 的磷酸化模式，二甲双胍可能使 TSHR 对 TSH 敏感，从而解释了临床研究的结果。然而，必须通过适当的研究来证实这种分子途径的存在，并且需要进一步的前瞻性随机安慰剂对照研究来验证这一假设。
