ACTA ENDOCRINOLOGICA (BUC)

The International Journal of Romanian Society of Endocrinology / Registered in 1938

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Year Volume Issue First page
10.4183/aeb.
Author
Title
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  • General Endocrinology

    Zhao LF, Iwasaki Y, Han BL, Wang J, Zhang Y, Han J, Liu GY, Jiang X

    Triiodothyronine Activates Glycerol-3-Phosphate Acyltransferase 3 via AGGTCA-Like-Direct-Repeat-4 Type Thyroid Hormone Response Element

    Acta Endo (Buc) 2020 16(2): 129-135 doi: 10.4183/aeb.2020.129

    Abstract
    Background. Thyroid hormone participates in lipid metabolism regulation. However, the effects on triacyleride or triacylglycerol metabolism are complex and not fully clarified yet. In this study, we try to identify novel thyroid hormone-targeting lipogenic metabolic genes and analyze their molecular regulative mechanism. Method. Thirty-five promoters of twenty-nine human lipogenic regulative enzyme genes were constructed into pXP1 luciferase reporter plasmid (PFK2/FBP2-luc) and transfected into HeGP2 cells, respectively. Gene expression induced by triiodothyronine (T3) was detected by luciferase assay. The T3-activated gene promoter was then analyzed by sequence analysis, deletion and mutation, and electrophoretic mobility shift assay (EMSA). Results. After 10 nM T3 stimulation for 36 h, phosphogluconate dehydrogenase, malic enzyme, Glycerol- 3-phosphate acyltransferase (GPAT) 3, and 1-acylglycerol-3- phosphate O-acyltransferase (AGPAT) 2 were significantly activated, respectively. A AGGTCA-like-direct-repeat-4 consensus thyroid hormone response element (DR4-TRE)- like sequence was found in the GPAT3 promoter, which was then verified to be necessary for T3-induced GPAT3 activation by gene deletion and mutation analysis. EMSA further identified that T3-thyroid receptor (TR) α-retinoid-X receptor (RXR) complex directly bound on the GPAT3 promoter. Conclusion. Triiodothyronine could activate the GPAT3 through DR4-TRE-like sequence binding to participate in lipogenic regulation. AGPAT2 may be another thyroid hormone target enzyme.
  • Perspectives

    Jiang L, Wei R, Diao J, Ding H, Wang W, Ao R

    Proteomics of Tear in Inactive Thyroid-Associated Ophthalmopathy

    Acta Endo (Buc) 2021 17(3): 291-303 doi: 10.4183/aeb.2021.291

    Abstract
    Background. Thyroid-associated ophthalmopathy (TAO), one of the most common orbital diseases in adults, seriously reduces patients’ quality of life. Although human tear proteomics identified many abnormal expressed proteins and proposed several pathogeneses of TAO, most of these studies focused on the active stage or mixed types in TAO. In this study we identified significantly changed proteins and preliminary revealed the potential signalling pathways and mechanisms of TAO with the late, inactive stage. Patients and Methods. Tears from TAO patients (n=6) with a CAS score < 3 and 6 control healthy subject were collected. The pooled tears were further fractionated using high pH reversed-phase chromatography, then submitted to LC-MS/MS and subsequent bioinformatic analysis. Results. Proteomic profiling identified 107 significantly changed proteins between the inactive stage of TAO patients and healthy cases. Among these proteins, 62 were upregulated, and 45 were downregulated in TAO cases compared to healthy individuals. Enrichment analysis revealed that the immune system, cell cycle, metabolism (carbohydrate metabolism and metabolism of cofactors and vitamins), protein synthesis and degradation might play a vital role in the progress of inactive TAO. The present investigation represents the first proteomic tear study of TAO patients in the inactive stage. Conclusion. The results shed light on the differences between inactive TAO patients and healthy cases, thus enabling us to understand better the molecular mechanisms and potential targets for the treatment of inactive TAO.
  • General Endocrinology

    Yang G, Chen S, Ding P, Jiang G, Fu C, Hu G, Feng X, Zhu W

    Pioglitazone Improves Insulin Sensitivity in Insulinresistant KKAy Mice: Involvement of a PPAR?-Dependent Signaling Pathway

    Acta Endo (Buc) 2013 9(4): 515-524 doi: 10.4183/aeb.2013.515

    Abstract
    Aim. To explore the effects and underlying mechanisms of pioglitazone (pio) on insulin sensitivity in insulin-resistant KKAy mice. Methods. Sixteen eight-week-old male KKAy mice were randomly assigned to two groups based on body weight: an insulin resistance model group and a pioglitazone treatment group (hereafter referred to as the pio-group). Eight male C57BL/6J mice were used as an insulin resistance control group. Mice in all three groups were fed an AIN-93G diet, and pio was added to the diet in the pio-group. After twelve weeks of treatment, blood glucose, serum insulin, glucose tolerance, and insulin tolerance were measured. ELISA was used to determine adiponectin and leptin in serum. A real time PCR assay was used to detect the mRNA of adiponectin and leptin in epididymal adipose tissue. A Western blot assay was used to analyze protein expression and/ or phosphorylation levels of peroxisome proliferator activated receptor γ (PPARγ), insulin receptor substrate 1 (IRS1), and protein kinase B (PKB/AKT) in the liver and epididymal adipose tissue.Results. The results showed that Pio treatment may effectively reduce levels of blood glucose and serum insulin, improve insulin tolerance and glucose tolerance, increase serum adiponectin, decrease serum leptin, and enhance mRNA expression of adiponectin in epididymal adipose tissue. Furthermore, with pio treatment, protein expression of PPARγ and phosphorylation levels of IRS1 and AKT were increased in the liver and epididymal adipose tissue. Conclusion. These results suggested that Pio intervention may ameliorate insulin resistance and improve insulin sensitivity in KKAy mice, which may be due to an increase of PPARγ and further activation of the insulin signaling transduction pathway (IRS1 and AKT) in the liver and epididymal adipose tissue of KKAy mice.