scholarly journals Role of Leptin in Inflammation and Vice Versa

2020 ◽  
Vol 21 (16) ◽  
pp. 5887 ◽  
Author(s):  
Antonio Pérez-Pérez ◽  
Flora Sánchez-Jiménez ◽  
Teresa Vilariño-García ◽  
Víctor Sánchez-Margalet

Inflammation is an essential immune response for the maintenance of tissue homeostasis. In a general sense, acute and chronic inflammation are different types of adaptive response that are called into action when other homeostatic mechanisms are insufficient. Although considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and tissue injury, the causes and mechanisms of systemic chronic inflammation are much less known. The pathogenic capacity of this type of inflammation is puzzling and represents a common link of the multifactorial diseases, such as cardiovascular diseases and type 2 diabetes. In recent years, interest has been raised by the discovery of novel mediators of inflammation, such as microRNAs and adipokines, with different effects on target tissues. In the present review, we discuss the data emerged from research of leptin in obesity as an inflammatory mediator sustaining multifactorial diseases and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses. On the other direction, chronic inflammation, either from autoimmune or infectious diseases, or impaired microbiota (dysbiosis) may impair the leptin response inducing resistance to the weight control, and therefore it may be a cause of obesity. Thus, we are reviewing the published data regarding the role of leptin in inflammation, and the other way around, the role of inflammation on the development of leptin resistance and obesity

2021 ◽  
pp. 101269022110186
Author(s):  
Véronique Boudreault ◽  
Marie-Pierre Gagnon-Girouard ◽  
Noémie Carbonneau ◽  
Sophie Labossière ◽  
Catherine Bégin ◽  
...  

The use of extreme weight-control behaviors is prevalent among adolescent athletes and may result from individual and sport-specific factors. Weight-related maltreatment from coaches and parents, and conformity to sport ethic norms have recently been linked to the use of extreme weight-control behaviors. This study aims to investigate the role of sport ethic norms and weight-related maltreatment from coaches and parents in the use of extreme weight-control behaviors among adolescent athletes. A sample of 999 French-Canadian athletes aged 14–17 years competing in a variety of sports completed an online survey assessing extreme weight-control behaviors, weight-related maltreatment from coaches and parents, and conformity to sport ethic norms. A total of 16.9% of the adolescent athletes reported having adopted extreme weight-control behaviors during their athletic careers. Extreme weight-control behaviors were significantly more prevalent among girls (19.75% vs 9.7% in boys) and weight-class-sport athletes (44%). In addition, 7.4% of the sample experienced at least one type of weight-related maltreatment by coaches or parents. Sex, weight-related neglect by coaches and parents, and weight-related psychological violence by coaches explained 24.4% of extreme weight-control behaviors variance. Indeed, participants who engaged in extreme weight-control behaviors experienced significantly more violence than the other participants did. In contrast, no differences were observed between people who engaged in extreme weight-control behaviors and those who did not due to conformity to sport ethic norms.


Author(s):  
MEDEA JGARKAVA ◽  
RUSUDAN RUKHADZE ◽  
NINO KARANADZE ◽  
IA PANTSULAIA

The risk of developing of the diseases such as Alzheimer's disease, atherosclerosis, osteoporosis, arthritis, type 2 diabetes and cancer increases with age. This is why these diseases are also referred to as age-related diseases. There is evidence that the development of age-related diseases significantly contributes to the so-called. Immune aging, in particular, age-related changes in the immune system, one of the manifestations of which is a low level systemic chronic inflammation. The term "inflammatory aging" (Inflamm-aging) well describes the close relationship between low-grade chronic inflammation and aging. At the present stage of the development of medicine, the mechanisms associated with the development of age-related, low-level, chronic inflammatory processes and the ways of their evaluation require further in-depth, multidisciplinary studies. Clearly, inflammatory aging is a predictor of many age-related disease development and high risk of death. Clinical studies have confirmed the view that inhibition of certain mediators of inflammation may reduce the incidence of age-related diseases. However, similar studies focusing on anti-inflammatory drugs are few in number and the results are ambiguous. Further fundamental and translational studies in this direction hope that in the future we will be able to regulate inflammatory processes in a way that ensures a healthy and long-lasting aging of the population.


2010 ◽  
Vol 108 (1) ◽  
pp. 155-160 ◽  
Author(s):  
Noémie de Crozé ◽  
Frédérique Maczkowiak ◽  
Anne H. Monsoro-Burq

The neural crest (NC) emerges from combinatorial inductive events occurring within its progenitor domain, the neural border (NB). Several transcription factors act early at the NB, but the initiating molecular events remain elusive. Recent data from basal vertebrates suggest that ap2 might have been critical for NC emergence; however, the role of AP2 factors at the NB remains unclear. We show here that AP2a initiates NB patterning and is sufficient to elicit a NB-like pattern in neuralized ectoderm. In contrast, the other early regulators do not participate in ap2a initiation at the NB, but cooperate to further establish a robust NB pattern. The NC regulatory network uses a multistep cascade of secreted inducers and transcription factors, first at the NB and then within the NC progenitors. Here we report that AP2a acts at two distinct steps of this cascade. As the earliest known NB specifier, AP2a mediates Wnt signals to initiate the NB and activate pax3; as a NC specifier, AP2a regulates further NC development independent of and downstream of NB patterning. Our findings reconcile conflicting observations from various vertebrate organisms. AP2a provides a paradigm for the reiterated use of multifunctional molecules, thereby facilitating emergence of the NC in vertebrates.


2018 ◽  
Vol 19 (11) ◽  
pp. 3652 ◽  
Author(s):  
Nicoletta Nuzziello ◽  
Laura Vilardo ◽  
Paride Pelucchi ◽  
Arianna Consiglio ◽  
Sabino Liuni ◽  
...  

MicroRNAs (miRNAs) and transcription factors (TFs) play key roles in complex multifactorial diseases like multiple sclerosis (MS). Starting from the miRNomic profile previously associated with a cohort of pediatric MS (PedMS) patients, we applied a combined molecular and computational approach in order to verify published data in patients with adult-onset MS (AOMS). Six out of the 13 selected miRNAs (miR-320a, miR-125a-5p, miR-652-3p, miR-185-5p, miR-942-5p, miR-25-3p) were significantly upregulated in PedMS and AOMS patients, suggesting that they may be considered circulating biomarkers distinctive of the disease independently from age. A computational and unbiased miRNA-based screening of target genes not necessarily associated to MS was then performed in order to provide an extensive view of the genetic mechanisms underlying the disease. A comprehensive MS-specific miRNA-TF co-regulatory network was hypothesized; among others, SP1, RELA, NF-κB, TP53, AR, MYC, HDAC1, and STAT3 regulated the transcription of 61 targets. Interestingly, NF-κB and STAT3 cooperatively regulate the expression of immune response genes and control the cross-talk between inflammatory and immune cells. Further functional analysis will be performed on the identified critical hubs. Above all, in our view, this approach supports the need of multidisciplinary strategies for shedding light into the pathogenesis of MS.


2021 ◽  
Vol 9 (F) ◽  
pp. 590-594
Author(s):  
Inna Krynytska ◽  
Mariya Marushchak ◽  
Anna Mykolenko ◽  
Iryna Smachylo ◽  
Olha Sopel ◽  
...  

Researching bronchial asthma (BA)-linked gene polymorphisms can help to clarify heterogeneity of the disease and estimate its severity, which, in turn, will aid in developing an appropriate treatment corresponding to the patient’s unique asthma pathogenesis. The aim of presented review is to analyze the published data on the genetic preconditions of BA and the possible role of different genes polymorphisms in its pathogenesis. We have found that despite the fact that numerous genes are involved in the pathogenesis of BA and their polymorphisms are associated with increased risks for BA, it is important to understand that a combination of factors, both genetic and environmental, triggers BA development and determines its progression. On the other hand, the identification of BA susceptibility genes contributing to asthma pathogenesis and treatment response is the first step toward the development of personalized medicine.


2008 ◽  
Vol 76 (7) ◽  
pp. 2939-2949 ◽  
Author(s):  
Yunuen Hernandez ◽  
Max Shpak ◽  
Trevor T. Duarte ◽  
Tavis L. Mendez ◽  
Rosa A. Maldonado ◽  
...  

ABSTRACT Although encystation (cyst formation) is important for the survival of Giardia lamblia outside its human host, the molecular events that prompt encystation have not been fully elucidated. Here, we demonstrate that sphingolipids (SLs), which are important for the growth and differentiation of many eukaryotes, play key roles in giardial encystation. Transcriptional analyses showed that only three genes in the SL biosynthesis pathways are expressed and transcribed differentially in nonencysting and encysting Giardia trophozoites. While the putative homologues of giardial serine palmitoyltransferase (gSPT) subunit genes (gspt-1 and -2) are differentially expressed in nonencysting and encysting trophozoites, the giardial ceramide glucosyltransferase 1 gene (gglct-1) is transcribed only in encysting cells. l-Cycloserine, an inhibitor of gSPT, inhibited the endocytosis and endoplasmic reticulum/perinuclear targeting of bodipy-ceramide in trophozoites, and this could be reversed by 3-ketosphinganine. On the other hand, d-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol (PPMP), an inhibitor of glucosylceramide synthesis, blocked karyokinesis and reduced cyst production in culture. PPMP also altered the expression of cyst wall protein transcripts in encysting cells. Phylogenetic analyses revealed that the gspt genes are paralogs derived from an ancestral spt sequence that underwent gene duplication early in eukaryotic history. This ancestral sequence, in turn, was probably derived from prokaryotic aminoacyl transferases. In contrast, gglct-1 is found in both prokaryotes and eukaryotes without any evidence of gene duplication. These studies indicate that SL synthesis genes are involved in key events in giardial biology and could serve as potential targets for developing new therapies against giardiasis.


1999 ◽  
Vol 276 (4) ◽  
pp. G795-G799 ◽  
Author(s):  
Mark J. S. Miller ◽  
Manuel Sandoval

Nitric oxide (NO) synthesis is markedly augmented in states of inflammation, largely due to the expression of inducible nitric oxide synthase (iNOS). Although NO has anti-inflammatory consequences under basal conditions, it remains enigmatic as to why NO displays proinflammatory characteristics in chronic inflammation. Either the anti-inflammatory actions are weak and of little consequence or, alternatively, other factors influence the role of NO in chronic inflammation. We propose that the answer to this enigma lies in the conversion of NO to other higher oxides of nitrogen (NO2, nitrogen dioxide; N2O3, dinitrogen trioxide; and ONOO−, peroxynitrite). Emerging therapeutic strategies may be independent of NO synthesis; e.g., antioxidants have no direct interaction with NO but attenuate the levels and activity of higher nitrogen oxides. Thus, whereas iNOS may be a marker for the proinflammatory actions of NO, the species that mediate tissue injury/dysfunction in inflammation are likely to be nitrogen oxides other than NO.


1995 ◽  
Vol 74 (05) ◽  
pp. 1271-1275 ◽  
Author(s):  
C M A Henkens ◽  
V J J Bom ◽  
W van der Schaaf ◽  
P M Pelsma ◽  
C Th Smit Sibinga ◽  
...  

SummaryWe measured total and free protein S (PS), protein C (PC) and factor X (FX) in 393 healthy blood donors to assess differences in relation to sex, hormonal state and age. All measured proteins were lower in women as compared to men, as were levels in premenopausal women as compared to postmenopausal women. Multiple regression analysis showed that both age and subgroup (men, pre- and postmenopausal women) were of significance for the levels of total and free PS and PC, the subgroup effect being caused by the differences between the premenopausal women and the other groups. This indicates a role of sex-hormones, most likely estrogens, in the regulation of levels of pro- and anticoagulant factors under physiologic conditions. These differences should be taken into account in daily clinical practice and may necessitate different normal ranges for men, pre- and postmenopausal women.


1998 ◽  
pp. 61-62
Author(s):  
N. S. Jurtueva

In the XIV century. centripetal tendencies began to appear in the Moscow principality. Inside the Russian church, several areas were distinguished. Part of the clergy supported the specificobar form. The other understood the need for transformations in society. As a result, this led to a split in the Russian church in the 15th century for "non-possessors" and "Josephites". The former linked the fate of the future with the ideology of hesychasm and its moral transformation, while the latter sought support in alliance with a strong secular power.


Sign in / Sign up

Export Citation Format

Share Document