The association between normal thyroid function and diabetic kidney disease (DKD) has gained increasing attention. The present study evaluated the relationship between normal thyroid hormone levels and DKD in type 2 diabetes mellitus (T2DM) patients. A total of 862 type 2 diabetes patients were enrolled in this cross-sectional study in Xi’an, Shaanxi Province, China. The subjects were evaluated for anthropometric measurements, thyroid function and DKD. Of 862 patients, 246 (28.5%) suffered from DKD, and the prevalence of DKD did not differ between men and women. The prevalence of DKD showed a significantly decreasing trend across the quartiles based on free triiodothyronine (FT3) levels (41.1%, 30.6%, 23.8%, and 18.9%, P < 0.001). In comparison with all participants categorized in the first FT3 quartile group (FT3-Q1) (<4.380), the adjusted odds ratio of DKD in the second FT3 quartile group (FT3-Q2), the third FT3 quartile group (FT3-Q3), and the fourth FT3 quartile group (FT3-Q4) were 0.655(95%CI: 0.406–1.057), 0.493(95%CI: 0.299–0.813), 0.406(0.237–0.697) (P < 0.05). Also, similar results were observed in men. Conversely, none of the FT3 groups was associated with DKD in women. The present study showed that FT3 within normal range was negatively correlated with DKD in T2DM patients.

The relationship between normal thyroid function and type 2 diabetes mellitus (T2DM) has been a particular focus for concern. The present study determined the relationship between thyroid hormone levels and the prevalence of diabetic retinopathy (DR) in T2DM patients. A cross-sectional study (n = 633) was performed in Xi’an, Shaanxi Province, China. Subjects were evaluated for anthropometric measurements, thyroid function, and diabetic retinopathy. Logistic regression models were used to assess the relationships between thyroid hormones and DR. Of 633 patients, 243 (38.4%) patients suffered from DR. The prevalence of DR showed a significantly decreasing trend across the quartiles based on free triiodothyronine (FT3) (FT3 quartile 1 group [FT3-Q1] <4.35 pmol/L, FT3 quartile 2 group [FT3-Q2] 4.35–4.70 pmol/L, FT3 quartile 3 group [FT3-Q3] 4.70–5.08 pmol/L, and FT3 quartile 4 group [FT3-Q4] ≥5.08 pmol/L) (56.7%, 42.5%, 33.1%, 23.8%, P<0.001). In comparison with all participants categorized in FT3-Q1, the multivariable adjusted odds ratios (95% confidence interval) of DR in FT3-Q2, FT3-Q3, and FT3-Q4 were 0.587 (0.340–1.012), 0.458 (0.258–0.813), and 0.368 (0.201–0.673), (P=0.055, P=0.008, P=0.001), respectively. FT3 levels within the normal range are negatively associated with DR in euthyroid patients with type 2 diabetes. Further studies should be aimed at clarifying the relationship between thyroid hormones and T2DM.

This randomised clinical trial suggests that PDT with ALA of 10% concentration offers better efficacy and safety than 5% or 20% concentration for generalised recalcitrant facial verruca plana.

a number of studies have reported that diabetic retinopathy (dr) is the major cause of blindness. Berberine (BBr) is a bioactive constituent that displays effects on blood glucose; however, the mechanism underlying the role of BBr during the development of dr is not completely understood. in the present study, a rat model of dr was successfully established. The eye tissues were removed and subsequently assessed by hematoxylin and eosin staining and the Tunel assay. The catalase, malondialdehyde, reactive oxygen species, glutathione and superoxide dismutase contents of the eye tissues were measured. Müller cells were chosen for further in vitro experiments. cell apoptosis was examined by annexin V-FiTc apoptosis detection and Hoechst staining, and the mitochondrial membrane potential was assessed by Jc-1 mitochondrial membrane potential detection. BBr decreased ganglion cell layer, cell apoptosis, reduced diabetic-induced oxidative stress and deactivated the nF-κB signaling pathway in the rat model of dr. High glucose enhanced oxidative stress and induced mitochondria-dependent cell apoptosis in Müller cells by activating the nF-κB signaling pathway. BBr reversed the high glucose-induced effects by decreasing the phosphorylation of iκB, inhibiting nF-κB nuclear translocation and deactivating the nF-κB signaling pathway. The results suggested that BBr protected against dr by inhibiting oxidative stress and cell apoptosis via deactivation of the nF-κB signaling pathway; therefore, suggesting that BBr may serve as a promising therapeutic agent for dr.