Backgrounds In recent years, many studies have shown that insulin resistance is related to the occurrence of thyroid cancer, but there are few reports on whether the two are related under the premise that thyroid function is normal and the metabolic components related to insulin resistance are excluded. This study aims to analyze the insulin resistance of patients with differentiated thyroid cancer after excluding the population with abnormal metabolic components, and to study the risk factors of thyroid cancer in this population. Methods 61 subjects diagnosed with differentiated thyroid carcinoma (DTC) formed the DTC group and 262 subjects with benign nodules formed the control group. Body mass index (BMI, kg/m2), waist circumference (WC), lipid profiles, and free T3 (FT3), free T4 (FT4), thyroid-stimulating hormone (TSH), thyroid peroxidase antibody (TPOAb), thyroid globulin antibody (TGAb), alanine transaminase (ALT), aspartate aminotransferase (AST), fasting plasma glucose (FPG), fasting serum insulin and homeostatic model assessment of insulin resistance (HOMA-IR) levels were measured. Results Mean subjects age (P = 0.021), BMI (P = 0.049), WC (P = 0.01), serum insulin concentration (P = 0.006), and HOMA-IR level (P = 0.005) were significantly greater in the DTC group than in the control group. Multivariate binary logistic regression analysis identified advanced age (OR = 1.027 [1.003–1.051], P = 0.029) and an increased HOMA-IR level (OR = 1.572 [1.277–1.935], P < 0.001) as significant risk factors for thyroid cancer. Conclusions IR may increase the risk of thyroid cancer development even in the absence of conditions affecting insulin resistance.
Aims: This cross-sectional study assessed the association of serum dehydroepiandrosterone levels with the risk of diabetic retinopathy in patients with type 2 diabetes mellitus in China. Materials and Methods: Patients with type 2 diabetes mellitus were included in a multivariate logistic regression analysis to assess the association of dehydroepiandrosterone with diabetic retinopathy after adjusting for confounding factors. A restricted cubic spline was also used to model the association of serum dehydroepiandrosterone level with the risk of diabetic retinopathy and to describe the overall dose-response correlation. Additionally, an interaction test was conducted in the multivariate logistic regression analysis to compare the effects of dehydroepiandrosterone on diabetic retinopathy among age, sex, obesity status, hypertension, dyslipidemia, and glycosylated hemoglobin level subgroups. Results: In total, 1,519 patients were included in the final analysis. Low serum dehydroepiandrosterone was significantly associated with diabetic retinopathy in patients with type 2 diabetes mellitus after adjustment for confounding factors (odds ratio [quartile 4 vs quartile 1]: 0.51; 95% confidence interval: 0.32-0.81; P = 0.012 for the trend). Additionally, the restricted cubic spline indicated that the odds of diabetic retinopathy decreased linearly as the dehydroepiandrosterone concentration increased (Poverall = 0.044; P-nonlinear = 0.364). Finally, the subgroup analyses showed that the dehydroepiandrosterone level stably affected diabetic retinopathy (all P for interaction >0.05). Conclusions: Low serum dehydroepiandrosterone levels were significantly associated with diabetic retinopathy in patients with type 2 diabetes mellitus, suggesting that dehydroepiandrosterone contributes to the pathogenesis of diabetic retinopathy.
The endoplasmic reticulum (ER) membrane protein translocon-associated protein-δ (TRAPδ, also known as SSR4) is involved in insulin biosynthesis in pancreatic β cell lines. However, its pathophysiological significance for the maintenance of islet β cell function and glucose homeostasis is unclear. Herein, we generated a mouse line with pancreatic β cell-specific deletion of TRAPδ (TRAPδ βKO), and found that TRAPδ βKO led to decreased circulating insulin in mice fed with either normal chow diet or high fat diet. Multiple independent experiments confirmed that, although TRAPδ deletion decreased insulin content in the islets, it did not affect composition of islet cells, insulin gene expression, insulin/proinsulin ratio, nor the expression and glycosylation of the prohormone enzymes involved in proinsulin processing. These data suggest that TRAPδ does not play a critical role in the transcription of insulin gene and processing of proinsulin. Importantly, untranslocated preproinsulin was significantly increased when the islets were treated with a proteasomal inhibitor, suggesting that TRAPδ deficiency impaired preproinsulin translocation, resulting in a rapid degradation of untranslocated preproinsulin that accounts for the decreased insulin production. Interestingly, the moderate decrease in the circulating insulin level in TRAPδ βKO mice did not cause impaired glucose tolerance and elevated fasting blood glucose, suggesting that compensatory mechanisms may account for maintaining glucose homeostasis. The insulin tolerance tests confirmed improvement of insulin sensitivity accompanied with upregulation of phosphorylated AKT in the peripheral insulin target tissues of TRAPδ βKO mice. Together, these data uncover a critical role of TRAPδ in preproinsulin translocation and insulin biosynthesis. The moderately decreased circulating insulin promotes insulin sensitivity in the insulin target tissues. Disclosure J.Guo: None. Y.Huang: None. M.Liu: None. Y.Yang: None. N.Xu: None. Y.Yang: None. W.Feng: None. Y.Ye: None. X.Li: None. X.Xu: None. J.Cui: None. Funding National Natural Science Foundation of China (81830025, 82220108014, 82270864, 82070854); National Key R&D Program of China (2019YFA0802502, 2022YFE0131400); Tianjin Municipal Health and Health Committee (TJWJ2021ZD00); Tianjin Key Medical Discipline (Specialty) Construction Project (TJYXZDXK-030A)
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