Aiceles Veronica, Gombar Flavia Meireles, Cavalcante Fernanda da Silveira, Ramos Cristiane da Fonte
Laboratory of Morphometry, Metabolism and Cardiovascular Disease, Biomedical Centre, Institute of Biology, State University of Rio de Janeiro, Brazil.
Horm Metab Res. 2019 May;51(5):330-335. doi: 10.1055/a-0876-6007. Epub 2019 Apr 3.
The goal of this study is to investigate whether congenital hypothyroidism induced by MMI during gestation (G) or gestation plus lactation (GL) would affect the leptin action upon body weight control on hypothalamus. Six to eight pups per group were killed at 90 days of age. For statistical analysis one-way ANOVA followed by the Holm-Sìdak post hoc test was used. Hypothyroidism resulted in a significant increase in leptin serum levels in G 20% and GL 25% (p<0.04). There was a significant expression decrease of OBR in G 45% and GL 63%; pSTAT3 in G 56% and GL 51%; pERK in G 50% and GL 48%; POMC in G 41% and GL 46% (p<0.04), while a significant increase was assigned to SOCS3 in G 52% and GL 170% (p<0.04) protein expression. We can conclude that hypothyroxinemia condition in rats on adulthood results in impairment of the leptin signaling pathway via ObRb-STAT3 in the hypothalamus, which is likely to be involved in the leptin resistance.
本研究的目的是调查孕期（G）或孕期加哺乳期（GL）由甲巯咪唑诱导的先天性甲状腺功能减退是否会影响瘦素在下丘脑对体重控制的作用。每组6至8只幼崽在90日龄时处死。统计分析采用单因素方差分析，随后进行Holm-Sìdak事后检验。甲状腺功能减退导致G组瘦素血清水平显著升高20%，GL组升高25%（p<0.04）。G组OBR表达显著降低45%，GL组降低63%；G组pSTAT3降低56%，GL组降低51%；G组pERK降低50%，GL组降低48%；G组POMC降低41%，GL组降低46%（p<0.04），而G组SOCS3蛋白表达显著升高52%，GL组升高170%（p<0.04）。我们可以得出结论，成年大鼠甲状腺素血症状态会导致下丘脑通过ObRb-STAT3的瘦素信号通路受损，这可能与瘦素抵抗有关。
