scholarly journals Postprandial effects on electrolyte homeostasis in the kidney

2019 ◽  
Vol 317 (6) ◽  
pp. F1405-F1408 ◽  
Author(s):  
Christine A. Klemens ◽  
Michael W. Brands ◽  
Alexander Staruschenko
Keyword(s):  
Insulin Signaling ◽  
Present Review ◽  
Volume Loss ◽  
Electrolyte Homeostasis ◽  
Important Regulator ◽  
Osmotic Load

Insulin is known to be an important regulator of a number of different channels and transporters in the kidney, but its role in the kidney to prevent Na+ and volume loss during the osmotic load after a meal has only recently been validated. With increasing numbers of people suffering from diabetes and hypertension, furthering our understanding of insulin signaling and renal Na+ handling in both normal and diseased states is essential for improving patient treatments and outcomes. The present review is focused on postprandial effects on Na+ reabsorption in the kidney and the role of the epithelial Na+ channels as an important channel contributing to insulin-mediated Na+ reclamation.

scholarly journals Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice

2015 ◽  
Vol 55 (3) ◽  
pp. 231-243 ◽  
Author(s):  
Bo Zhou ◽  
Huixia Li ◽  
Jiali Liu ◽  
Lin Xu ◽  
Qinyue Guo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Mammalian Target Of Rapamycin ◽  
Tumor Necrosis Factor Receptor ◽  
Mitochondrial Activity ◽  
Causative Role ◽  
Important Regulator

Progranulin (PGRN) has recently emerged as an important regulator for insulin resistance. However, the direct effect of PGRN in vivo and the underlying role of progranulin in adipose insulin resistance involving the autophagy mechanism is not fully understood. In this study, mice treated with PGRN for 21 days exhibited the impaired glucose tolerance and insulin sensitivity, remarkable adipose autophagy as well as attenuated insulin signaling via inhibition of mammalian target of rapamycin (mTOR) pathway. Furthermore, blockade of tumor necrosis factor receptor 1 (TNFR1) by TNFR1BP-Fc injection resulted in the restoration of impaired insulin sensitivity and insulin signaling induced by PGRN. Consistent with these findings in vivo, PGRN treatment induced defective insulin signaling, abnormal autophagic and mitochondrial activity in cultured adipocytes, while such effects were nullified by the blockade of TNFR1. In addition, PGRN-deficient adipocytes were more refractory to tunicamycin- or dexamethasone-induced insulin resistance, indicating the causative role of the TNFR1 pathway in the action of PGRN. Collectively, our findings support the notion that PGRN is a key regulator of insulin resistance and that PGRN may mediate its effects, at least in part, by inducing autophagy via the TNFR1-dependent mechanism.

Osteoporosis Entwined with Cardiovascular Disease: The Implication of Osteoprotegerin and Example of Statins

2020 ◽  
Vol 27 ◽  
Author(s):  
Maria V. Deligiorgi ◽  
Mihalis I. Panayiotidis ◽  
Gerasimos Siasos ◽  
Dimitrios T. Trafalis
Keyword(s):  
Cardiovascular Disease ◽  
Physicochemical Characteristics ◽  
Dual Role ◽  
Present Review ◽  
Vascular Cells ◽  
Molecular Fingerprint ◽  
Missing Link ◽  
Epidemiological Factors ◽  
Outstanding Issue

: Beyond being epiphenomenon of shared epidemiological factors, the integration of osteoporosis (OP) with cardiovascular disease (CVD)− termed "calcification paradox"− reflects a continuum of aberrant cardiometabolic status. The present review provides background knowledge on "calcification paradox", focusing on the endocrine aspect of vasculature orchestrated by the osteoblastic molecular fingerprint of vascular cells, acquired via imbalance among established modulators of mineralization. Osteoprotegerin (OPG)–the well-established osteoprotective cytokine−has recently been shown to exert a vessel-modifying role. Prompted by this notion, the present review interrogates OPG as the potential missing link between OP and CVD. However, so far, the confirmation of this hypothesis is hindered by the equivocal role of OPG in CVD, being both proatherosclerotic and antiatherosclerotic. Further research is needed to illuminate whether OPG could be biomarker of the "calcification paradox". Moreover, the present review brings into prominence the dual role of statins−cardioprotective and osteoprotective− as potential illustration of the integration of CVD with OP. Considering that the statins-induced modulation of OPG is central to the statins-driven osteoprotective signalling, statins could be suggested as illustration of the role of OPG in the bone/vessels crosstalk, if further studies consolidate the contribution of OPG to the cardioprotective role of statins. Another outstanding issue that merits further evaluation is the inconsistency of the osteoprotective role of statins. Further understanding of the varying bone-modifying role of statins, likely attributed to the unique profile of different classes of statins defined by distinct physicochemical characteristics, may yield tangible benefits for treating simultaneously OP and CVD.

scholarly journals FDG-PET/CT for the Management of Post-Chemotherapy Residual Mass in Hodgkin lymphoma

Cancers ◽  
2021 ◽  
Vol 13 (16) ◽  
pp. 3952
Author(s):  
Andrea Gallamini ◽  
Michał Kurlapski ◽  
Jan Maciej Zaucha
Keyword(s):  
Treatment Outcome ◽  
Hodgkin Lymphoma ◽  
Fdg Pet ◽  
Quantitative Methods ◽  
Present Review ◽  
Response To Treatment ◽  
Published Evidence ◽  
Pet Ct ◽  
Fdg Pet Ct

In the present review, the authors report the published evidence on the use of functional imaging with FDG-PET/CT in assessing the final response to treatment in Hodgkin lymphoma. Despite a very high overall Negative Predictive Value of post-chemotherapy PET on treatment outcome ranging from 94% to 86%, according to different treatment intensity, the Positive Predicting Value proved much lower (40–25%). In the present review the Authors discuss the role of PET to guide consolidation RT over a RM after different chemotherapy regimens, both in early and in advanced-stage disease. A particular emphasis is dedicated to the peculiar issue of the qualitative versus semi-quantitative methods for End-of Therapy PET scan interpretation. A short hint will be given on the role of FDG-PET to assess the treatment outcome after immune checkpoint inhibitors.

scholarly journals Role of Insulin in Health and Disease: An Update

2021 ◽  
Vol 22 (12) ◽  
pp. 6403
Author(s):  
Md Saidur Rahman ◽  
Khandkar Shaharina Hossain ◽  
Sharnali Das ◽  
Sushmita Kundu ◽  
Elikanah Olusayo Adegoke ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Basic Research ◽  
Future Research ◽  
Protective Effects ◽  
Glucose Levels ◽  
Physiological Processes ◽  
Blood Glucose Levels ◽  
Wide Range ◽  
Health And Disease

Insulin is a polypeptide hormone mainly secreted by β cells in the islets of Langerhans of the pancreas. The hormone potentially coordinates with glucagon to modulate blood glucose levels; insulin acts via an anabolic pathway, while glucagon performs catabolic functions. Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. The modulation of a wide range of physiological processes by insulin makes its synthesis and levels critical in the onset and progression of several chronic diseases. Although clinical and basic research has made significant progress in understanding the role of insulin in several pathophysiological processes, many aspects of these functions have yet to be elucidated. This review provides an update on insulin secretion and regulation, and its physiological roles and functions in different organs and cells, and implications to overall health. We cast light on recent advances in insulin-signaling targeted therapies, the protective effects of insulin signaling activators against disease, and recommendations and directions for future research.

Annual review of research

2003 ◽  
Vol 36 (3) ◽  
pp. 165-189 ◽  
Author(s):  
Richard Johnstone
Keyword(s):  
Information And Communications Technology ◽  
Present Review ◽  
Annual Review ◽  
Communications Technology ◽  
Pedagogical Practice ◽  
Separate Section ◽  
Important Trend ◽  
The Impact

The present review refers to studies published in 2002 in leading research journals. It focuses in particular on learning, teaching and policy in respect of second, modern foreign or additional languages. The comments offered about particular studies are not intended to summarise them (for that, it is best to refer to the actual abstracts which the present journal publishes). What is on offer is a personal selection made because some aspect of a particular article seemed to be of particular interest or to reflect an important trend, and I have attempted to link such elements together to form a narrative. Compared with previous years, two important themes seemed to gather particular momentum in 2002: first, the role of ‘frequency’ in acquisition; and second, the impact of complex and contradictory global factors on everyday pedagogical practice, thinking and attitudes. As in previous years reference is made to the abstracts. Thus, Tarone (2002: 03-158) refers to an article by Tarone published in 2002 and reflected in the 2003 series of this journal as abstract 158. In previous years I have discussed ICT (information and communications technology) in a separate section of its own but this has now been integrated into other sections, reflecting a process of ‘normalisation’.

scholarly journals The Role of 5-Lipoxygenase and Leukotrienes in Shock and Ischemia-Reperfusion Injury

2007 ◽  
Vol 7 ◽  
pp. 56-74 ◽  
Author(s):  
Antonietta Rossi ◽  
Carlo Pergola ◽  
Salvatore Cuzzocrea ◽  
Lidia Sautebin
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Biological Activities ◽  
Ischemia Reperfusion ◽  
Targeted Disruption ◽  
Pathological Conditions ◽  
Metabolic Products ◽  
Important Regulator ◽  
Multicellular Organisms

The leukotrienes (LTs) are metabolic products of arachidonic acid via the 5-lipoxygenase (5-LO) pathway. The biological activities of LTs suggest that they are mediators of acute inflammatory and immediate hypersensitivity responses. In particular, the 5-LO activation has been proposed to be an important regulator for pathogenesis in multicellular organisms. The role of LTs in tissue damage, associated with septic and nonseptic shock and ischemia-reperfusion, has been extensively studied by the use of 5-LO inhibitors, receptor antagonists, and mice with a targeted disruption of the 5-LO gene (5-LOKO). In particular, several data indicate that LTs regulate neutrophil trafficking in damaged tissue in shock and ischemia-reperfusion, mainly through the modulation of adhesion molecule expression. This concept may provide new insights into the interpretation of the protective effect of 5-LO inhibition, which may be useful in the therapy of pathological conditions associated with septic and nonseptic shock and ischemia-reperfusion injury.

scholarly journals In Vivo Role of Focal Adhesion Kinase in Regulating Pancreatic  -Cell Mass and Function Through Insulin Signaling, Actin Dynamics, and Granule Trafficking

Diabetes ◽  
2012 ◽  
Vol 61 (7) ◽  
pp. 1708-1718 ◽  
Author(s):  
E. P. Cai ◽  
M. Casimir ◽  
S. A. Schroer ◽  
C. T. Luk ◽  
S. Y. Shi ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Insulin Signaling ◽  
Cell Mass ◽  
Actin Dynamics ◽  
Pancreatic Cell ◽  
And Function

scholarly journals The mechano-sensitive response of β1 integrin promotes SRC-positive late endosome recycling and activation of Yes-associated protein

2020 ◽  
Vol 295 (39) ◽  
pp. 13474-13487
Author(s):  
Marc R. Block ◽  
Molly Brunner ◽  
Théo Ziegelmeyer ◽  
Dominique Lallemand ◽  
Mylène Pezet ◽  
...  
Keyword(s):  
Late Endosome ◽  
Cell Periphery ◽  
Β1 Integrin ◽  
Nonreceptor Tyrosine Kinase ◽  
Cell Contractility ◽  
Late Endosomes ◽  
Important Regulator ◽  
Nuclear Shuttling ◽  
Endosomal System

Yes-associated protein (YAP) signaling has emerged as a crucial pathway in several normal and pathological processes. Although the main upstream effectors that regulate its activity have been extensively studied, the role of the endosomal system has been far less characterized. Here, we identified the late endosomal/lysosomal adaptor MAPK and mTOR activator (LAMTOR) complex as an important regulator of YAP signaling in a preosteoblast cell line. We found that p18/LAMTOR1-mediated peripheral positioning of late endosomes allows delivery of SRC proto-oncogene, nonreceptor tyrosine kinase (SRC) to the plasma membrane and promotes activation of an SRC-dependent signaling cascade that controls YAP nuclear shuttling. Moreover, β1 integrin engagement and mechano-sensitive cues, such as external stiffness and related cell contractility, controlled LAMTOR targeting to the cell periphery and thereby late endosome recycling and had a major impact on YAP signaling. Our findings identify the late endosome recycling pathway as a key mechanism that controls YAP activity and explains YAP mechano-sensitivity.

Morin Exerts Anti-Diabetic Effects in Human HepG2 Cells Via Down-Regulation of miR-29a

2018 ◽  
Vol 127 (09) ◽  
pp. 615-622 ◽  
Author(s):  
Toktam Razavi ◽  
Shideh Montasser Kouhsari ◽  
Khalil Abnous
Keyword(s):  
Insulin Signaling ◽  
High Glucose ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Expression Level ◽  
Inhibitory Effects ◽  
Down Regulation ◽  
Insulin Mimetic ◽  
Important Regulator ◽  
First Time

Abstract Diabetes mellitus is a complex metabolic disease around the world that is characterized by hyperglycemia resulting from impaired insulin secretion, insulin action, or both. MicroRNA-29a is an important regulator of insulin signaling and gluconeogenesis pathways through IRS2, PI3K and PEPCK expressions which up regulates in Diabetes. Morin is a substantial bioflavonoid which has insulin mimetic effect, and interacting with nucleic acids and proteins. In this study HepG2 cells, were exposed to high glucose to induce diabetic condition. We have determined whether high glucose stimulation might promotes miR-29a expression level in HepG2 cells and subsequently evaluated the Morin treatment effects on this state. In HepG2 cells, high glucose increases miR-29a expression level and decreases its target genes, IRS2 and PI3K expression, and increases associated downstream gene in gluconeogenic pathway, PEPCK. Morin treatment down regulates miR-29a expression level and improves insulin signaling and glucose metabolism. To confirm the inhibitory effects of Morin on miR-29a, we have transfected cells with mimic and inhibitor-miR-29a. This study for the first time identifies that Morin improves diabetic condition through down regulation of the miR-29a level, and suggest that this new inhibitor of miR-29a may be a useful biomedicine to treat diabetes.

Sign in / Sign up

Export Citation Format

Share Document