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Insight Into Mouse Models of Hyperthyroidism
Hyperthyroidism is characterized by an increase in the synthesis and secretion of thyroid hormones in the thyroid gland, and the most common cause of overproduction of thyroid hormones is Graves’ disease (GD). Long-term disease models of hyperthyroidism have been established. In general, methods to induce GD include transfection of fibroblasts, injecting plasmids or adenovirus containing thyroid stimulating hormone receptor (TSHR) or TSHR subunit, and exogenous artificial thyroid hormone supplementation. Fortunately, in mouse studies, novel treatments for GD and Graves’ orbitopathy (GO) were discovered. It has been rep...
Source: Frontiers in Endocrinology - June 22, 2022 Category: Endocrinology Source Type: research

Lipocalin-2: a role in hepatic gluconeogenesis via AMP-activated protein kinase (AMPK)
ConclusionThe present study demonstrates that LCN2 regulates insulin sensitivity and glucose metabolism through inhibiting AMPK activity, and regulating FoxO1 and its downstream genes PEPCK/G6P, which regulate hepatic gluconeogenesis.
Source: Journal of Endocrinological Investigation - January 9, 2021 Category: Endocrinology Source Type: research

Cellular prion protein regulates the differentiation and function of adipocytes through autophagy flux
In this study, we investigated whether normal cellular prion protein (PrP<C>) is involved in the modulation of autophagy and affects adipogenic differentiation in vivo and in vitro. Surprisingly, autophagy flux signals were activated in the adipose tissue of prion protein-deficient mice and PrP<C>-deleted 3T3-L1 adipocytes. The activation of autophagy flux mediated by PrP<C> deletion was confirmed in the adipose tissue via transmission electron microscopy. Adipocyte differentiation factors were highly induced in prion protein-deficient adipose tissue and 3T3-L1 adipocytes. In addition, deletion of prion protein...
Source: Molecular and Cellular Endocrinology - December 2, 2018 Category: Endocrinology Source Type: research

Estrogen signaling increases nuclear receptor subfamily 4 group A member 1 expression and energy production in skeletal muscle cells.
Authors: Nagai S, Ikeda K, Horie-Inoue K, Takeda S, Inoue S Abstract Estrogen deficiency has been known to associate with musculoskeletal diseases in women, based on the clinical observations of frequent susceptibility to osteoporosis and sarcopenia among postmenopausal women. In skeletal muscles, estrogen has been assumed to play physiological roles in maintaining muscle mass and strength, although its precise molecular mechanism remains to be elucidated. We have previously shown that estrogen regulates energy metabolism through the downregulation of mitochondrial uncoupling protein 3 (UCP3) in skeletal muscles, w...
Source: Endocrine Journal - October 20, 2018 Category: Endocrinology Tags: Endocr J Source Type: research

CIDEC Gene Silencing Alleviates Pulmonary Vascular Remodeling in a Type 2 Diabetic Rat Model
ConclusionsCIDEC/AMPK signaling pathway could be a potential therapeutic candidate against pulmonary vascular diseases in type 2 diabetes.This article is protected by copyright. All rights reserved.
Source: Journal of Diabetes Investigation - September 1, 2017 Category: Endocrinology Authors: Dong ‐xin Sui, Hui‐min Zhou, Feng Wang, Ming Zhong, Wei Zhang, Yun Ti Tags: Original Article Source Type: research

Hypoxia-inducible lipid droplet-associated (HILPDA) is not a direct physiological regulator of lipolysis in adipose tissue.
Abstract Triglycerides are stored in specialized organelles called lipid droplets. Numerous proteins have been shown to be physically associated with lipid droplets and govern their function. Previously, hypoxia-inducible lipid droplet-associated (HILPDA) was localized to lipid droplets and was suggested to inhibit triglyceride lipolysis in hepatocytes. We confirm the partial localization of HILPDA to lipid droplets and show that HILPDA is highly abundant in adipose tissue, where its expression is controlled by the peroxisome proliferator-activated receptor γ and by β-adrenergic stimulation. Levels of HILPDA mar...
Source: Endocrinology - March 17, 2017 Category: Endocrinology Authors: Dijk W, Mattijssen F, de la Rosa Rodriguez M, Loza Valdes A, Loft A, Mandrup S, Kalkhoven E, Qi L, Borst JW, Kersten S Tags: Endocrinology Source Type: research

Calpain-10 Activity Underlies Angiotensin II-induced Aldosterone Production in an Adrenal Glomerulosa Cell Model.
Abstract Aldosterone is a steroid hormone important in the regulation of blood pressure. Aberrant production of aldosterone results in the development and progression of diseases including hypertension and congestive heart failure; therefore, a complete understanding of aldosterone production is important for developing more effective treatments. Angiotensin II (AngII) regulates steroidogenesis, in part through its ability to increase intracellular calcium levels. Calcium can activate calpains, proteases classified as typical or atypical based on the presence or absence of penta-EF-hands, that are involved in vari...
Source: Endocrinology - April 2, 2015 Category: Endocrinology Authors: Seremwe M, Schnellmann RG, Bollag WB Tags: Endocrinology Source Type: research

Dexamethasone downregulates caveolin-1 causing muscle atrophy via inhibited insulin signaling
In this study, we report a new pathway in which glucocorticoids reduce the levels of upstream insulin signaling components by downregulating the transcription of the gene encoding caveolin-1 (CAV1), a scaffolding protein present in the caveolar membrane. Treatment with the glucocorticoid dexamethasone (DEX) decreased CAV1 protein and Cav1 mRNA expression, with a concomitant reduction in insulin receptor alpha (IRα) and IR substrate 1 (IRS1) levels in C2C12 myotubes. On the basis of the results of promoter analysis using deletion mutants and site-directed mutagenesis a negative glucocorticoid-response element in the r...
Source: Journal of Endocrinology - March 19, 2015 Category: Endocrinology Authors: Son, Y. H., Lee, S.-J., Lee, K.-B., Lee, J.-H., Jeong, E. M., Chung, S. G., Park, S.-C., Kim, I.-G. Tags: Research Source Type: research

GATA4 is a key regulator of steroidogenesis and glycolysis in mouse Leydig cells.
Abstract Transcription factor GATA4 is expressed in somatic cells of the mammalian testis. Gene targeting studies in mice have shown that GATA4 is essential for proper differentiation and function of Sertoli cells. The role of GATA4 in Leydig cell development, however, remains controversial because targeted mutagenesis experiments in mice have not shown a consistent phenotype, possibly due to context-dependent effects or compensatory responses. We therefore undertook a reductionist approach to study the function of GATA4 in Leydig cells. Using microarray analysis and quantitative RT-PCR, we identified a set of gen...
Source: Endocrinology - February 10, 2015 Category: Endocrinology Authors: Schrade A, Kyrönlahti A, Akinrinade O, Pihlajoki M, Häkkinen M, Fischer S, Alastalo TP, Velagapudi V, Toppari J, Wilson DB, Heikinheimo M Tags: Endocrinology Source Type: research

SUMOylation protects against IL-1{beta}-induced apoptosis in INS-1 832/13 cells and human islets
We examined insulin secretion, intracellular Ca2+ responses, induction of endoplasmic reticulum stress markers and inducible nitric oxide synthase (iNOS) expression, and apoptosis by TUNEL and caspase 3 cleavage. Surprisingly, upregulation of SENP1 reduces insulin secretion and impairs intracellular Ca2+ handling. This secretory dysfunction is due to SENP1-induced cell death. Indeed, the detrimental effect of SENP1 on secretory function is diminished when two mediators of β-cell death, iNOS and NF-B, are pharmacologically inhibited. Conversely, enhanced SUMOylation protects against IL-1β-induced cell death. This ...
Source: AJP: Endocrinology and Metabolism - October 15, 2014 Category: Endocrinology Authors: Hajmrle, C., Ferdaoussi, M., Plummer, G., Spigelman, A. F., Lai, K., Manning Fox, J. E., MacDonald, P. E. Tags: Articles Source Type: research

Orphan nuclear receptor Nur77 mediates fasting-induced hepatic fibroblast growth factor 21 expression.
In conclusion, this study shows that Nur77 mediates fasting-induced hepatic FGF21 expression, and suggests an alternative mechanism via which hepatic FGF21 transcription is mediated under fasting conditions. PMID: 24885573 [PubMed - as supplied by publisher]
Source: Endocrinology - June 2, 2014 Category: Endocrinology Authors: Min AK, Bae KH, Jung YA, Choi YK, Kim MJ, Kim JH, Jeon JH, Kim JG, Lee IK, Park KG Tags: Endocrinology Source Type: research