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Open access

Beibei Zhu, Yan Han, Fen Deng, Kun Huang, Shuangqin Yan, Jiahu Hao, Peng Zhu, and Fangbiao Tao

Objectives: Compared with other thyroid markers, fewer studies explored the associations between triiodothyronine (T3) and T3/free thyroxine (fT4) and glucose abnormality during pregnancy. Thus, we aimed to: (1) examine the associations of T3 and T3/fT4 with glucose metabolism indicators; and (2) evaluate, in the first trimester, the performance of the two markers as predictors of gestational diabetes mellitus (GDM) risk.

Methods: Longitudinal data from 2723 individuals, consisting of three repeated measurements of T3 and fT4, from the Man’anshan birth cohort study (MABC), China, were analyzed using a time-specific generalized estimating equation (GEE). The receiver operating characteristic curve (ROC) - area under the curve (AUC) and Hosmer-Lemeshow goodness of fit test were used to assess the discrimination and calibration of prediction models.

Results: T3 and T3/fT4 presented stable associations with the level of fasting glucose, glucose at 1h/2h across pregnancy. T3 and T3/fT4 in both the first and second trimesters were positively associated with the risk of GDM, with the larger magnitude of association observed in the second trimester (Odds ratio (OR) = 2.50, 95%CI = 1.95, 3.21 for T3; OR = 1.09, 95%CI = 1.07, 1.12 for T3/fT4). T3 ((AUC) = 0.726, 95%CI = 0.698, 0.754) and T3/fT4 (AUC = 0.724, 95%CI = 0.696, 0.753) in the first trimester could improve the performance of the predicting model; however, the overall performance is not good.

Conclusion: Significant and stable associations of T3, T3/fT4 and glucose metabolism indicators were documented. Both T3 and T3/fT4 improve the performance of the GDM predictive model.

Open access

Riying Liang, Meijun Wang, Chang Fu, Hua Liang, Hongrong Deng, Ying Tan, Fen Xu, and Mengyin Cai


Obesity is associated with the development and progression of chronic kidney disease. Emerging evidence suggests that glucagon-like peptide-1 receptor agonist could reduce renal damage and albuminuria. Sirtuin 1 (SIRT1) was considered as a crucial regulator in metabolism-related kidney disease. Herein, the role of SIRT1 in liraglutide-ameliorated high-fat diet (HFD)-induced kidney injury was illustrated.


Male C57BL/6 mice were fed HFD for 20 weeks to induce kidney injury that was then treated with liraglutide for 8 weeks to estimate its protective effect on the kidney. Also, the mechanism of the drug in SV40 MES 13 (SV40) mouse mesangial cells was elucidated.


Liraglutide treatment ameliorated HFD-induced metabolic disorders, including hyperglycemia, increasing body weight, and insulin resistance. In addition, kidney weight, urine albumin-to-creatinine, and kidney morphological changes such as vacuolated tubules, glomerulomegaly, thickened glomerular basement membrane, and tubulointerstitial fibrosis were also significantly ameliorated. Furthermore, apoptotic cells and apoptosis markers were downregulated in the kidney of liraglutide-treated mice. In addition, the expression of SIRT1 protein was upregulated, whereas thioredoxin-interacting protein (TXNIP), which serves as a mediator of oxidative stress and apoptosis in metabolism disease, was downregulated by liraglutide. In SV40 cells, the effect of liraglutide on reversing the upregulation of cleaved caspase-3 induced by high glucose (30 mM) was hampered when SIRT1 was knocked down; also, the downregulation of TXNIP by liraglutide was blocked.


Liraglutide might have a beneficial effect on metabolism-related kidney damage by inhibiting apoptosis via activation of SIRT1 and suppression of TXNIP pathway.