scholarly journals Discovery of a possible role of asprosin in ovarian follicular function

2021 ◽  
Vol 66 (1) ◽  
pp. 35-44
Author(s):  
Excel Rio S Maylem ◽  
Leon J Spicer ◽  
Isadora Batalha ◽  
Luis F Schutz
Keyword(s):  
Gene Expression Analysis ◽  
Polycystic Ovarian Syndrome ◽  
Developmental Regulation ◽  
Mrna Abundance ◽  
Hormone Regulation ◽  
Fibrillin 1 ◽  
Ovarian Syndrome ◽  
Receptor Family

Asprosin is a novel fasting-induced protein encoded by fibrillin-1 (FBN1) gene, produced when FBN1 is cleaved by the enzyme furin, and is associated with insulin resistance and polycystic ovarian syndrome in humans. To characterize mRNA abundance of FBN1, FURIN, and the presumed asprosin receptor, olfactory receptor family 4 subfamily M member 1 (OR4M1) in granulosa (GC) and theca cells (TC), and identify hormones regulating FBN1 mRNA expression, GC and TC from small (1–5 mm; SM) and large (>8 mm; LG) follicles were collected from ovaries of heifers obtained at an abattoir and used for real-time PCR gene expression analysis or in vitro evaluation of hormone regulation and asprosin effects. SMTC had 151-fold greater (P < 0.05) FBN1 mRNA abundance than SMGC, and LGTC had 50-fold greater FBN1 mRNA than LGGC. In contrast, OR4M1 mRNA was 81-fold greater in SMGC than LGGC and did not differ from SMTC, but LGTC had 9-fold greater OR4M1 mRNA than LGGC. FURIN mRNA was 2.6-fold greater in SMTC than SMGC, but did not differ among follicular sizes. In cultured TC, leptin, insulin, LH, IGF1 and steroids did not affect FBN1 mRNA, but TGFB1 increased (P < 0.05) FBN1 mRNA by 2.2-fold; EGF and FGFs increased FBN1 mRNA by 1.3- to 1.5-fold. Asprosin enhanced LH-induced TC androstenedione production, reduced IGF1-induced TC proliferation, and had no effect on progesterone production. Developmental regulation of FBN1, FURIN and OR4M1 along with direct effects of asprosin on TC suggests that asprosin may be a novel regulator of ovarian follicular function.

scholarly journals D-Chiro-Inositol Improves Sperm Mitochondrial Membrane Potential: In Vitro Evidence

2020 ◽  
Vol 9 (5) ◽  
pp. 1373 ◽  
Author(s):  
Rosita A. Condorelli ◽  
Federica Barbagallo ◽  
Aldo E. Calogero ◽  
Rossella Cannarella ◽  
Andrea Crafa ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Sperm Motility ◽  
Mitochondrial Membrane ◽  
Polycystic Ovarian Syndrome ◽  
Biologically Active ◽  
Ovarian Syndrome

The use of inositols in endocrinological clinical practice is increasingly widespread. Most of the existing evidence concerns myoinositol (MYO), the most abundant form in nature, especially in women with polycystic ovarian syndrome. We have previously shown that MYO increases sperm motility in patients with asthenozoospermia by the increase of sperm mitochondrial membrane potential (MMP), a biofunctional sperm parameter closely associated to sperm motility. The aim of this study was to evaluate the effects of D-chiro-inositol (DCI), another biologically active isoform of inositols, on sperm MMP, as data on this matter has never been released so far. To accomplish this, semen samples from 15 patients with asthenozoospermia and 15 healthy normozoospermic men were incubated with increasing concentrations of DCI (0, 75, and 750 µg/mL) or phosphate buffer saline for 30 min. Incubation with DCI significantly improved sperm MMP at lower concentrations, and with shorter incubation length than those used in our similar MYO studies. In conclusion, these findings indicate that DCI positively impacts on sperm mitochondrial function in vitro. Studies aimed at assessing the role of DCI in the treatment of asthenozoospermia in-vivo are warranted.

scholarly journals PSIV-5 Developmental and hormonal regulation of gene expression of fibrillin-1 (FBN1) and the asprosin receptor, olfactory receptor family 4 subfamily M member 1 (OR4M1), in bovine ovarian cells

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 283-284
Author(s):  
Excel Rio Maylem ◽  
Leon Spicer ◽  
Isadora Batalha ◽  
Luis Schutz
Keyword(s):  
Gene Expression ◽  
Hormonal Regulation ◽  
Regulation Of Gene Expression ◽  
Cell Types ◽  
Mrna Abundance ◽  
Hormone Regulation ◽  
Polycystic Ovaries ◽  
Fbn1 Gene ◽  
Fibrillin 1

Abstract Asprosin is a novel fasting-induced protein associated with insulin resistance and polycystic ovaries in humans. It is encoded by FBN1 gene and produced when FBN1 is cleaved by the enzyme furin. In cattle, the role of asprosin is unknown. To characterize mRNA abundance of FBN1, furin, and the asprosin receptor, OR4M1, in granulosa (GC) and theca cells (TC), and identify hormones regulating FBN1 mRNA expression, GC and TC from small (&lt; 6 mm; SM) and large (&gt;5 mm; LG) follicles were collected from heifers at an abattoir and used for real-time gene expression analysis or in vitro evaluation of hormone regulation. SMTC had 151-fold greater (P &lt; 0.05) FBN1 mRNA abundance than SMGC, and LGTC had 50-fold greater (P &lt; 0.05) FBN1 mRNA than LGGC. In contrast, OR4M1 mRNA abundance was significantly greater (by 81-fold) in SMGC than LGGC and did not differ from SMTC, but LGTC had 9-fold greater (P &lt; 0.05) OR4M1 mRNA abundance than LGGC. Furin mRNA was significantly greater (by 2.6-fold) in SMGC than SMTC but did not differ between LGTC and LGGC. In SMGC, leptin, insulin, GH, FSH, EGF, and steroids had no effect (P &gt;0.10) on FBN1 mRNA abundance. In contrast, TGFB1, WNT3A and FGF9 increased (P &lt; 0.05) and IGF1 significantly decreased SMGC FBN1 mRNA abundance. In LGTC, leptin, insulin, LH, IGF1 and steroids did not significantly affect FBN1 mRNA, but TGFB1, WNT3A, EGF, FGF2 and FGF9 increased (P&lt; 0.05) FBN1 mRNA abundance. Altogether, FBN1 mRNA was more highly expressed in TC than GC and was stimulated by TGFB1, WNT3A and FGF9 in both cell types. Developmental and hormonal regulation of FBN1, furin and OR4M1 along with a greater expression of OR4M1 mRNA in GC than TC suggests that asprosin may be acting as a paracrine regulator of ovarian follicular function in cattle.

scholarly journals Expression of chemerin and its receptors in rat testes and its action on testosterone secretion

2013 ◽  
Vol 220 (2) ◽  
pp. 155-163 ◽  
Author(s):  
Lei Li ◽  
Ping Ma ◽  
Chen Huang ◽  
Yongjun Liu ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Leydig Cells ◽  
Polycystic Ovarian Syndrome ◽  
The Novel ◽  
Developmentally Regulated ◽  
Dehydrogenase Gene ◽  
Gene And Protein Expression ◽  
G Protein Coupled ◽  
Ovarian Syndrome

The novel adipokine chemerin plays a role in the regulation of lipid and carbohydrate metabolism, and recent reports of elevated chemerin levels in polycystic ovarian syndrome and preeclampsia have pointed to an emerging role of chemerin in reproduction. We hypothesised that chemerin, like other adipokines, may function to regulate male gonadal steroidogenesis. In this study, we show that chemerin and its three receptors chemokine-like receptor 1 (CMKLR1), G-protein-coupled receptor 1 (GPR1) and chemokine (C-C motif) receptor-like 2 were expressed in male reproductive tracts, liver and white adipose tissue. CMKLR1 and GPR1 proteins were localised specifically in the Leydig cells of human and rat testes by immunohistochemistry. The expression ofchemerinand its receptors in rat testes was developmentally regulated and highly expressed in Leydig cells.In vitrotreatment with chemerin suppressed the human chorionic gonadotropin (hCG)-induced testosterone production from primary Leydig cells, which was accompanied by the inhibition of 3β-hydroxysteroid dehydrogenase gene and protein expression. The hCG-activated p44/42 MAPK (Erk1/2) pathway in Leydig cells was also inhibited by chemerin cotreatment. Together, these data suggest that chemerin is a novel regulator of male gonadal steroidogenesis.

scholarly journals Troglitazone, an Insulin-Sensitizing Thiazolidinedione, Represses Combined Stimulation by LH and Insulin of de Novo Androgen Biosynthesis by Thecal Cells in Vitro

2002 ◽  
Vol 87 (3) ◽  
pp. 1129-1133 ◽  
Author(s):  
Johannes D. Veldhuis ◽  
George Zhang ◽  
James C. Garmey
Keyword(s):  
Gene Expression ◽  
Polycystic Ovarian Syndrome ◽  
De Novo ◽  
Drug Concentrations ◽  
Thecal Cells ◽  
Cyp17 Gene ◽  
Pparγ Agonist ◽  
Ovarian Syndrome ◽  
Prostaglandin J2

Polycystic ovarian syndrome (anovulatory hyperandrogenism) is marked by adolescent onset of systemic hyperinsulinism, oligoovulation, hirsutism, excessive LH and androgen secretion, and variable reduction in fertility. Insulin and LH are believed to act in concert to promote ovarian androgen hypersecretion in this disorder. Administration of troglitazone, an insulin-sensitizing agent and putative PPARγ agonist, can decrease hyperinsulinism, suppress T production, and ameliorate oligoovulation in some women with this endocrinopathy. The present study tests the hypothesis that troglitazone directly inhibits de novo androgen biosynthesis stimulated jointly by LH and insulin in primary cultures of (porcine) thecal cells. We show that troglitazone dose-dependently antagonizes LH/insulin’s combined stimulation of androstenedione and T production by thecal cells in vitro. Consistent steroidogenic inhibition of 80–95% was achieved at drug concentrations of 3–6.8 μm (P &lt; 0.001). Exposure of thecal cells to the thiazolidinedione derivative also blocked bihormonally stimulated accumulation of CYP17 (cytochrome P450 17 α-hydroxylase/C17–20 lyase) gene expression, as reflected by decreased accumulation of cognate heterogeneous nuclear RNA and mRNA (by 30–65%; P &lt; 0.05). Moreover, troglitazone suppressed LH/insulin-induced phosphorylation of the 52-kDa immunoprecipitated CYP17 enzyme by 88% (P &lt; 0.001). A putative natural agonist of PPARγ nuclear transcription, 15-deoxy-δ-12,14-prostaglandin J2, also inhibited LH/insulin-driven androstenedione biosynthesis and CYP17 gene expression in thecal cells. In conclusion, a synthetic thiazolidinedione (troglitazone) and a natural ligand of PPARγ (15-deoxy-δ-12,14-prostaglandin J2) effectively impede the concerted stimulation by LH and insulin of in vitro thecal cell androgen production, CYP17 gene expression, and CYP17 protein phosphorylation. This ensemble of inhibitory actions on LH/insulin-stimulated steroidogenesis offers a plausible mechanistic basis for at least part of the observed clinical efficacy of troglitazone in mitigating androgen excess in women with polycystic ovarian syndrome.

scholarly journals Adnexal Torsion during Pregnancy after Oocyte In Vitro Maturation and Intracytoplasmic Sperm Injection Cycle

2010 ◽  
Vol 2010 ◽  
pp. 1-3 ◽  
Author(s):  
Simone Giulini ◽  
Giulia Dante ◽  
Susanna Xella ◽  
Antonio La Marca ◽  
Tiziana Marsella ◽  
...  
Keyword(s):  
In Vitro Maturation ◽  
Polycystic Ovarian Syndrome ◽  
Polycystic Ovary ◽  
Adnexal Torsion ◽  
Term Pregnancy ◽  
Ovary Syndrome ◽  
Clinical Disorder ◽  
Injection Cycle ◽  
Ovarian Syndrome

We report a case of right adnexal torsion during pregnancy after an oocyte in vitro maturation and intracitoplasmic sperm injection cycle in patient with polycystic ovary syndrome. A 31-year-old woman with a typical clinical disorder of polycystic ovarian syndrome was included in an oocyte in vitro maturation program. Right adnexal torsion occurred two days after embryo transfer, and laparoscopy detorsion was successfully performed with preservation of adnexa. The patient had a full-term pregnancy and delivered a healthy infant at 40 weeks of gestation. To our knowledge this is the first report of adnexal torsion after an oocyte in vitro maturation and intracitoplasmic sperm injection program.

scholarly journals Role of insulin sensitising agents in altering PSA level in PCOS

2017 ◽  
Vol 6 (11) ◽  
pp. 4986 ◽  
Author(s):  
Rajashree Panigrahy ◽  
Bratati Singh ◽  
Tapan K. Pattnaik ◽  
Sanjukta Misra
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovarian Syndrome ◽  
Specific Antigen ◽  
Serum Testosterone ◽  
Healthy Controls ◽  
Androgen Excess ◽  
Control Serum ◽  
Ovarian Syndrome ◽  
Significant Concentration

Background: Ovarian androgen production can be promoted by insulin resistance which leads to reproductive abnormalities in Polycystic Ovarian Syndrome (PCOS). A wide variety of female tissues can synthesize and secrete Prostate Specific Antigen (PSA). Androgens may take part a significant role in PSA secretion in PCOS. As insulin resistance stimulates androgen production, the baseline value of PSA may decline by insulin sensitising agents in PCOS. Present study is an attempt to measure the function of PSA as a marker of androgen excess in PCOS and to assess the role of insulin sensitising agent metformin in altering PSA level in PCOS.Methods: The study was undertaken to assess the insulin resistance, testosterone and PSA level in 45 women diagnosed as PCOS and 45 healthy controls. Alteration of insulin resistance, serum testosterone and PSA levels by metformin was also analysed.Results: A significant increase in testosterone, PSA level and insulin resistance was observed in PCOS cases when compared with control (p<0.001). When metformin was given for 4 months, improvement in insulin resistance and testosterone level was found in cases, but PSA values observed no change. Correlation was not found linking insulin resistance with PSA level prior to and after therapy.Conclusions: Serum PSA level could be detected in high significant concentration in PCOS women. Various researches explain that insulin resistance and BMI may perhaps control serum PSA level, but our result demonstrate no effect of insulin sensitising agent on serum PSA value.

scholarly journals LTBP1 promotes fibrillin incorporation into the extracellular matrix

2021 ◽  
Author(s):  
Matthias Przyklenk ◽  
Veronika Georgieva ◽  
Fabian Metzen ◽  
Sebastian Mostert ◽  
Birgit Kobbe ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Protein ◽  
Wide Spectrum ◽  
Extracellular Matrix Protein ◽  
Connective Tissues ◽  
Pathogenic Variants ◽  
Human Pathology ◽  
Fibrillin 1

LTBP1 is a large extracellular matrix protein and an associated ligand of fibrillin-microfibrils. Knowledge of LTBP1 functions is largely limited to its role in targeting and sequestering TGFβ growth factors within the extracellular matrix, thereby regulating their bioavailability. However, the recent description of a wide spectrum of phenotypes in multiple tissues in patients harboring LTBP1 pathogenic variants suggests a multifaceted role of the protein in the homeostasis of connective tissues. To better understand the human pathology caused by LTBP1 deficiency it is important to investigate its functional role in extracellular matrix formation. In this study, we show that LTBP1 coordinates the incorporation of fibrillin-1 and -2 into the extracellular matrix in vitro. We also demonstrate that this function is differentially exerted by the two isoforms, the short and long forms of LTBP1. Thereby our findings uncover a novel TGFβ-independent LTBP1 function potentially contributing to the development of connective tissue disorders.

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