scholarly journals The Role of Physical Exercise Intesity to Irisin Levels on Overweight and Obese

2021 ◽  
Vol 57 (4) ◽  
pp. 357
Author(s):  
Ido Nur Abdulloh ◽  
Sugiharto Sugiharto ◽  
Purwo Sri Rejeki
Keyword(s):  
Physical Exercise ◽  
Uncoupling Protein ◽  
Pharmacological Therapy ◽  
Mitogen Activated Protein Kinase ◽  
Amino Acid Residues ◽  
Mitogen Activated Protein ◽  
Fibronectin Type Iii ◽  
Obese Subjects ◽  
Fibronectin Type Iii Domain ◽  
The Right

Highlight:The differences in intensity physical exercise mechanisms associated with increased irisin secretion in overweight and obese subjects were determined.The secretion of irisin in the right intensity blood on obesity can be reduced because the calories were balanced. Abstract:Physical exercise is a non-pharmacological therapy that can secrete various types of myokines to treat obesity problems. One of the myokines that play a role is irisin. Irisin is a polypeptide hormone with 112 amino acid residues that are synthesized in skeletal muscle after the proteolytic precursor cleavage of fibronectin type III domain-containing protein 5 (FNDC5). The release of irisin in the blood circulation will stimulate the browning process in white fat tissue by inducing the expression of uncoupling protein-1 (UCP-1) through signaling p38 mitogen-activated protein kinase (p38-MAPK) to increase energy expenditure, thermogenesis and reduce fat accumulation. This study described the differences in intensity of physical exercise mechanisms associated with the increased irisin secretion in overweight and obese subjects. This study was designed as a literature review that involved studies from research journals in the last 10 years concerning humans from some databases, such as Science Direct, PubMed, and Google Scholar. This study also discussed the relationship between the intensity of physical exercise and the synthesis, secretion, circulation, and regulation of irisin in preventing obesity.

scholarly journals MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets

2008 ◽  
Vol 115 (7) ◽  
pp. 203-218 ◽  
Author(s):  
Anthony J. Muslin
Keyword(s):  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Mapk Pathway ◽  
Science Research ◽  
Pharmacological Therapy ◽  
Model Systems ◽  
Mitogen Activated Protein Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Intracellular MAPK (mitogen-activated protein kinase) signalling cascades probably play an important role in the pathogenesis of cardiac and vascular disease. A substantial amount of basic science research has defined many of the details of MAPK pathway organization and activation, but the role of individual signalling proteins in the pathogenesis of various cardiovascular diseases is still being elucidated. In the present review, the role of the MAPKs ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPK in cardiac hypertrophy, cardiac remodelling after myocardial infarction, atherosclerosis and vascular restenosis will be examined, with attention paid to genetically modified murine model systems and to the use of pharmacological inhibitors of protein kinases. Despite the complexities of this field of research, attractive targets for pharmacological therapy are emerging.

scholarly journals Pengaruh Irisin pada Pencoklatan Lemak Putih

2021 ◽  
Vol 10 (2) ◽  
pp. 396-401
Author(s):  
Natalia Danayati
Keyword(s):  
Protein Kinase ◽  
Uncoupling Protein ◽  
Mitogen Activated Protein Kinase ◽  
Uncoupling Protein 1 ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Pendahuluan: Irisin merupakan miokin baru yang menghubungkan aktivitas fisik yang berhubungan dengan peningkatan kinerja metabolisme dan berkaitanan dengan pencoklatan jaringan adiposa putih menjadi coklat. Tujuan: Mengetahui pengaruh irisin pada pencoklatan lemak putih. Metode: Menggunakan studi literatur dari sumber ilmiah dengan meringkas dari publikasi dan membandingkan hasil yang disajikan. Hasil: Irisin yang disekresikan dari otot, akan menstimulasi ekspresi dari uncoupling protein 1 (UCP1) dalam adiposit yang menyebabkan pencoklatan jaringan adiposa putih melalui p38 mitogen-activated protein kinase (MAPK) dan melalui extracellular-signal regulated kinase (ERK). Kesimpulan: Irisin yang disekresikan otot rangka akan mengekspresikan UPC-1 di jaringan adiposa yang menyebabkan jaringan adiposa putih menjadi coklat dan peningkatan aktivitas thermogenesis.

scholarly journals p38 Mitogen-Activated Protein Kinase Is the Central Regulator of Cyclic AMP-Dependent Transcription of the Brown Fat Uncoupling Protein 1 Gene

2004 ◽  
Vol 24 (7) ◽  
pp. 3057-3067 ◽  
Author(s):  
Wenhong Cao ◽  
Kiefer W. Daniel ◽  
Jacques Robidoux ◽  
Pere Puigserver ◽  
Alexander V. Medvedev ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
P38 Mapk ◽  
Uncoupling Protein ◽  
Brown Fat ◽  
Mitogen Activated Protein Kinase ◽  
Uncoupling Protein 1 ◽  
Response Element ◽  
Mitogen Activated Protein

ABSTRACT It is well established that catecholamine-stimulated thermogenesis in brown fat requires β-adrenergic elevations in cyclic AMP (cAMP) to increase expression of the uncoupling protein 1 (UCP1) gene. However, little is known about the downstream components of the signaling cascade or the relevant transcription factor targets thereof. Here we demonstrate that cAMP- and protein kinase A-dependent activation of p38 mitogen-activated protein kinase (MAPK) in brown adipocytes is an indispensable step in the transcription of the UCP1 gene in mice. By phosphorylating activating transcription factor 2 (ATF-2) and peroxisome proliferator-activated receptor gamma (PPARγ) coativator 1α (PGC-1α), members of two distinct nuclear factor families, p38 MAPK controls the expression of the UCP1 gene through their respective interactions with a cAMP response element and a PPAR response element that both reside within a critical enhancer motif of the UCP1 gene. Activation of ATF-2 by p38 MAPK additionally serves as the cAMP sensor that increases expression of the PGC-1α gene itself in brown adipose tissue. In conclusion, our findings illustrate that by orchestrating the activity of multiple transcription factors, p38 MAPK is a central mediator of the cAMP signaling mechanism of brown fat that promotes thermogenesis.

Pressing the right buttons: signaling in lymphangiogenesis

Blood ◽  
2014 ◽  
Vol 123 (17) ◽  
pp. 2614-2624 ◽  
Author(s):  
Sanja Coso ◽  
Esther Bovay ◽  
Tatiana V. Petrova
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Lymphatic Vessels ◽  
Transforming Growth Factor Β ◽  
Mitogen Activated Protein Kinase ◽  
Vegf Receptor ◽  
Morphogenetic Protein ◽  
Mitogen Activated Protein ◽  
Lymphatic Vasculature ◽  
The Right

Abstract Lymphatic vasculature is increasingly recognized as an important factor both in the regulation of normal tissue homeostasis and immune response and in many diseases, such as inflammation, cancer, obesity, and hypertension. In the last few years, in addition to the central role of vascular endothelial growth factor (VEGF)-C/VEGF receptor-3 signaling in lymphangiogenesis, significant new insights were obtained about Notch, transforming growth factor β/bone morphogenetic protein, Ras, mitogen-activated protein kinase, phosphatidylinositol 3 kinase, and Ca2+/calcineurin signaling pathways in the control of growth and remodeling of lymphatic vessels. An emerging picture of lymphangiogenic signaling is complex and in many ways distinct from the regulation of angiogenesis. This complexity provides new challenges, but also new opportunities for selective therapeutic targeting of lymphatic vasculature.

scholarly journals Irisin Is Regulated by CAR in Liver and Is a Mediator of Hepatic Glucose and Lipid Metabolism

2016 ◽  
Vol 30 (5) ◽  
pp. 533-542 ◽  
Author(s):  
Li Mo ◽  
Jing Shen ◽  
Qinhui Liu ◽  
Yuwei Zhang ◽  
Jiangying Kuang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Uncoupling Protein ◽  
Constitutive Androstane Receptor ◽  
Physiological Role ◽  
Glucose And Lipid Metabolism ◽  
Diet Induced Obesity ◽  
Fibronectin Type Iii ◽  
Glucose And Lipid Homeostasis ◽  
Fibronectin Type Iii Domain ◽  
Amp Activated Protein Kinase

Abstract Irisin, a hormone proteolytically processed from fibronectin type III domain-containing protein 5 (FNDC5), has been reported to induce the browning of sc adipocytes by increasing the level of uncoupling protein 1. In this study, we showed that activation of the nuclear receptor constitutive androstane receptor induced FNDC5 mRNA expression in the liver and increased the circulating level of irisin in mice. FNDC5/irisin is a direct transcriptional target of constitutive androstane receptor. Hepatic-released irisin functioned as a paracrine/autocrine factor that inhibited lipogenesis and gluconeogenesis via the Adenosine 5′-monophosphate (AMP)-activated protein kinase pathway. Adenovirus-overexpressed irisin improved hepatic steatosis and insulin resistance in genetic-induced obese mice. Irisin transgenic mice were also protected against high-fat diet-induced obesity and insulin resistance. In conclusion, our results reveal a novel pathway in regulating FNDC5/irisin expression and identify a physiological role for this hepatic hormone in glucose and lipid homeostasis.

Auricular acupuncture induces FNDC5/irisin and attenuates obese inflammation in mice

2020 ◽  
Vol 38 (4) ◽  
pp. 264-271
Author(s):  
Yi Lu ◽  
Guohua Li
Keyword(s):  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Control Diet ◽  
Auricular Acupuncture ◽  
Acupuncture Points ◽  
Brown Adipose ◽  
Fibronectin Type Iii ◽  
Fibronectin Type Iii Domain ◽  
Factor Α ◽  
Old Mice

Objective: To investigate whether auricular acupuncture (AA) attenuates bodyweight and obese inflammation through the release of irisin from muscle tissue in mice. Methods: Sixty 4-week-old mice were fed a high fat diet (HFD) for 4 weeks. These animals were divided into six groups that remained untreated (HFD) or underwent electrical AA (HFD+EAA), sham EAA (HFD+SEAA), adrenalectomy (HFD+AD), adrenalectomy and EAA (HFD+AD+EAA), or adrenalectomy and injection of recombinant lentivirus expressing fibronectin type III domain-containing protein 5 (rFNDC) (HFD+AD+rFNDC) in the ninth week. The EAA and SEAA were performed at two traditional auricular acupuncture points daily for 4 weeks. An additional 10 mice fed a control diet were included as a normal control (NC) group. At the end of the study, norepinephrine (NE) in the serum, tumour necrosis factor α (TNFα) and interleukin 1β (IL-1β) in the serum and white adipose tissue, irisin in the serum and muscle, uncoupling protein-1 (UCP-1) in the brown adipose tissue (BAT), and FNDC5 in the muscle, were analysed. Results: The AD+EAA group exhibited better control of bodyweight and inflammation compared with the AD+SEAA and untreated HFD model groups (P<0.05), especially regarding the increased expression of NE, FNDC5, irisin and UCP-1 (P<0.05). After adrenalectomy, mice receiving EAA had less NE, FNDC5, irisin and UCP-1 as well as greater expression of inflammatory cytokines and bodyweight. However, lentiviral overexpression of rFNDC successfully reversed this situation in the AD mice and mimicked the effects of EAA on bodyweight, inflammation and expression of FNDC5, irisin and UCP-1, although it did not impact NE. Conclusions: EAA promoted NE release from the adrenal gland leading to further expression of FNDC5, irisin and UCP-1, which contributed to weight management and inflammatory inhibition.

A Thrombopoietin Receptor Mutant Deficient in Jak-STAT Activation Mediates Proliferation But Not Differentiation in UT-7 Cells

Blood ◽  
1999 ◽  
Vol 94 (8) ◽  
pp. 2676-2685 ◽  
Author(s):  
Marion Dorsch ◽  
Nika N. Danial ◽  
Paul B. Rothman ◽  
Stephen P. Goff
Keyword(s):  
Human Cell Line ◽  
Mitogen Activated Protein Kinase ◽  
Amino Acid Residues ◽  
Signal Transducers ◽  
Cellular Processes ◽  
Proliferation And Differentiation ◽  
Signaling Events ◽  
Mitogen Activated Protein ◽  
Hematopoietic Precursor ◽  
Receptor Mutant

Thrombopoietin (TPO) stimulates proliferation and differentiation of cells of the megakaryocytic lineage. It exerts its function by binding and activating c-mpl, a member of the hematopoietic receptor superfamily. Upon binding of TPO to its receptor, numerous signaling events are triggered. These include activation of the Jak-STAT (signal transducers and activators of transcription) pathway, mitogen-activated protein kinase (MAPK), Tec, and phospatidylinositol (PI) 3-kinase and phosphorylation of Shc and Vav. The contribution of different signaling pathways to the induction of specific cellular processes such as proliferation and differentiation is incompletely understood. We have previously described a mutant of c-mpl that fails to activate the Jak-STAT pathway but nevertheless retains its ability to mediate proliferation and activation of most signaling events in the murine hematopoietic precursor cell lines BAF/3 and 32D. We confirm here the ability of this mutant to mediate proliferation in the absence of Jak-STAT activation in the human cell line UT-7 and further show that this mutant fails to mediate TPO-induced megakaryocytic differentiation. Comparison of the signaling capacity of this mutant in UT-7 and BAF/3 cells shows considerable cell-type–specific differences. Whereas in BAF/3 cells the mutant still mediates activation of Shc, MAPK, Vav, and PI 3-kinase at levels comparable to the wild-type receptor, these events are strongly diminished in UT-7 cells expressing the mutant. Furthermore, we show that the C-terminal 25 amino acid residues of the receptor mutant are crucial for the mitogenic response in UT-7 cells.

scholarly journals Mitogen-Activated Protein Kinase in Pfiesteria piscicida and Its Growth Rate-Related Expression

2003 ◽  
Vol 69 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Senjie Lin ◽  
Huan Zhang
Keyword(s):  
Growth Rate ◽  
Amino Acid ◽  
Protein Kinase ◽  
Mitogen Activated Protein Kinase ◽  
Amino Acid Residues ◽  
Amino Acid Similarity ◽  
Reverse Transcription Pcr ◽  
Pfiesteria Piscicida ◽  
Mitogen Activated Protein ◽  
Salinity Shock

ABSTRACT A full-length cDNA (1,434 bp) of mitogen-activated protein kinase (MAPK), a key molecule of a signal transduction cascade, was isolated from the estuarine heterotrophic dinoflagellate Pfiesteria piscicida. This cDNA (Ppmapk1) encoded a protein (PpMAPK1) of 428 amino acid residues that shared about 30 to 40% amino acid similarity with MAPKs in other organisms. Phylogenetic analysis indicated that PpMAPK1 was tightly clustered with MAPK3 in protozoans. Using reverse transcription-PCR, expression of this gene was evaluated for P. piscicida cultures grown under different conditions. While salinity shock, heat shock, starvation, and a subsequent encounter with prey did not appear to affect expression of this gene, Ppmapk1 expression level was correlated with growth rate, suggesting involvement of this gene in the regulation of cell proliferation in the organism.

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