scholarly journals Minireview: Peripheral Nesfatin-1 in Regulation of the Gut Activity–15 Years since the Discovery

Animals ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 101
Author(s):  
Katarzyna Kras ◽  
Siemowit Muszyński ◽  
Ewa Tomaszewska ◽  
Marcin B. Arciszewski
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Intestinal Barrier ◽  
Inhibitory Effect ◽  
Scientific Interest ◽  
Therapeutic Approaches ◽  
Current State ◽  
Apoptotic Effects ◽  
G Protein Coupled ◽  
Peripheral Actions

Nesfatin-1, discovered in 2006, is an anorexigenic molecule derived from the precursor protein NEFA/nucleobindin2. It is generally postulated that this molecule acts through a specific G protein-coupled receptor, as yet unidentified. Research conducted over the last 15 years has revealed both central and peripheral actions of nesfatin-1. Given its major central role, studies determining its inhibitory effect on food intake seem to be of major scientific interest. However, in recent years a number of experiments have found that peripheral organs, including those of the gastrointestinal tract (GIT), may also be a source (possibly even the predominant source) of nesfatin-1. This mini-review aimed to summarize the current state of knowledge regarding the expression and immunoreactivity of nesfatin-1 and its possible involvement (both physiological and pathological) in the mammalian GIT. Research thus far has shown very promising abilities of nesfatin-1 to restore the balance between pro-oxidants and antioxidants, to interplay with the gut microbiota, and to alter the structure of the intestinal barrier. This necessitates more extensive research on the peripheral actions of this molecule. More in-depth knowledge of such mechanisms (especially those leading to anti-inflammatory and anti-apoptotic effects) is important for a better understanding of the involvement of nefatin-1 in GIT pathophysiological conditions and/or for future therapeutic approaches.

Roux-en-Y Gastrointestinal Bypass Promotes Activation of TGR5 and Peptide YY

2020 ◽  
Vol 20 (8) ◽  
pp. 1262-1267
Author(s):  
Haojun Yang ◽  
Hanyang Liu ◽  
YuWen Jiao ◽  
Jun Qian
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
The Body ◽  
Wild Type ◽  
L Cells ◽  
Body Weights ◽  
Gastrointestinal Bypass ◽  
G Protein Coupled

Background: G protein-coupled bile acid receptor (TGR5) is involved in a number of metabolic diseases. The aim of this study was to identify the role of TGR5 after Roux-en-Y gastric bypass (GBP). Methods: Wild type and TGR5 knockout mice (tgr5-/-) were fed a high-fat diet (HFD) to establish the obesity model. GBP was performed. The changes in body weight and food intake were measured. The levels of TGR5 and peptide YY (PYY) were evaluated by RT-PCR, Western blot, and ELISA. Moreover, the L-cells were separated from wild type and tgr5-/- mice. The levels of PYY in L-cells were evaluated by ELISA. Results: The body weights were significantly decreased after GBP in wild type mice (p<0.05), but not tgr5-/- mice (p>0.05). Food intake was reduced after GBP in wild type mice, but also not significantly affected in tgr5-/- mice (p>0.05). The levels of PYY were significantly increased after GBP compared with the sham group (p<0.05); however, in tgr5-/- mice the expression of PYY was not significantly affected (p>0.05). After INT-777 stimulation in L-cells obtained from murine intestines, the levels of PYY were significantly increased in L-cells tgr5+/+ (p<0.05). Conclusion: Our study suggests that GBP up-regulated the expression of TGR5 in murine intestines, and increased the levels of PYY, which further reduced food intake and decreased the body weight.

scholarly journals Limosilactobacillus fermentum CECT5716: Mechanisms and Therapeutic Insights

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 1016
Author(s):  
María Jesús Rodríguez-Sojo ◽  
Antonio Jesús Ruiz-Malagón ◽  
María Elena Rodríguez-Cabezas ◽  
Julio Gálvez ◽  
Alba Rodríguez-Nogales
Keyword(s):  
Competitive Exclusion ◽  
Intestinal Barrier ◽  
Mechanisms Of Action ◽  
Intestinal Barrier Function ◽  
Therapeutic Approaches ◽  
Beneficial Effects ◽  
Host Health ◽  
Inflammatory Processes ◽  
Immunomodulatory Properties ◽  
Immunological Alterations

Probiotics microorganisms exert their health-associated activities through some of the following general actions: competitive exclusion, enhancement of intestinal barrier function, production of bacteriocins, improvement of altered microbiota, and modulation of the immune response. Among them, Limosilactobacillus fermentum CECT5716 has become one of the most promising probiotics and it has been described to possess potential beneficial effects on inflammatory processes and immunological alterations. Different studies, preclinical and clinical trials, have evidenced its anti-inflammatory and immunomodulatory properties and elucidated the precise mechanisms of action involved in its beneficial effects. Therefore, the aim of this review is to provide an updated overview of the effect on host health, mechanisms, and future therapeutic approaches.

scholarly journals 337 Metabolic Foundations of Microbiota-Host Interactions

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 69-69
Author(s):  
Dylan Dodd
Keyword(s):  
Gastrointestinal Tract ◽  
Gut Microbiota ◽  
Small Molecules ◽  
Recent Work ◽  
Mechanistic Studies ◽  
Therapeutic Approaches ◽  
Dense Population ◽  
Metabolic Potential ◽  
Host Interactions ◽  
New Therapeutic Approaches

Abstract The gastrointestinal tract of mammals is home to a dense population of microbes which influence host physiology and health. One of the most concrete ways that the gut microbiota impacts host biology is through the production of hundreds of chemically diverse small molecules. These molecules are absorbed into the bloodstream, where they reach concentrations similar to those achieved by pharmaceuticals and bind host receptors leading to changes in cellular and organ physiology. Here I will summarize recent work from our group and others that show how microbially sourced metabolites alter health and physiology of the host. I will also discuss how mechanistic studies of small molecules from the microbiota are enabling new therapeutic approaches to harness the metabolic potential of the gut microbiota.

scholarly journals The inhibitory effect of Gβγ and Gβ isoform specificity on ENaC activity

2013 ◽  
Vol 305 (9) ◽  
pp. F1365-F1373 ◽  
Author(s):  
Ling Yu ◽  
Otor Al-Khalili ◽  
Billie Jeanne Duke ◽  
James D. Stockand ◽  
Douglas C. Eaton ◽  
...  
Keyword(s):  
Single Channel ◽  
Inhibitory Effect ◽  
G Protein Coupled Receptors ◽  
Open Probability ◽  
A6 Cells ◽  
Kinase C ◽  
Downstream Effectors ◽  
Isoform Specificity ◽  
Low Levels ◽  
G Protein Coupled

Epithelial Na+ channel (ENaC) activity, which determines the rate of renal Na+ reabsorption, can be regulated by G protein-coupled receptors. Regulation of ENaC by Gα-mediated downstream effectors has been studied extensively, but the effect of Gβγ dimers on ENaC is unclear. A6 cells endogenously contain high levels of Gβ1 but low levels of Gβ3, Gβ4, and Gβ5 were detected by Q-PCR. We tested Gγ2 combined individually with Gβ1 through Gβ5 expressed in A6 cells, after which we recorded single-channel ENaC activity. Among the five β and γ2 combinations, β1γ2 strongly inhibits ENaC activity by reducing both ENaC channel number ( N) and open probability ( Po) compared with control cells. In contrast, the other four β-isoforms combined with γ2 have no significant effect on ENaC activity. By using various inhibitors to probe Gβ1γ2 effects on ENaC regulation, we found that Gβ1γ2-mediated ENaC inhibition involved activation of phospholipase C-β and its enzymatic products that induce protein kinase C and ERK1/2 signaling pathways.

scholarly journals Intraportal Infusion of Ghrelin Could Inhibit Glucose-Stimulated GLP-1 Secretion by Enteric Neural Net in Wistar Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Xiyao Zhang ◽  
Wensong Li ◽  
Ping Li ◽  
Manli Chang ◽  
Xu Huang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Portal Vein ◽  
Wistar Rat ◽  
Inhibitory Effect ◽  
Neural Net ◽  
Incretin Effect ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Intraportal Infusion

As a regulator of food intake and energy metabolism, the role of ghrelin in glucose metabolism is still not fully understood. In this study, we determined the in vivo effect of ghrelin on incretin effect. We demonstrated that ghrelin inhibited the glucose-stimulated release of glucagon-like peptide-1 (GLP-1) when infused into the portal vein of Wistar rat. Hepatic vagotomy diminished the inhibitory effect of ghrelin on glucose-stimulated GLP-1 secretion. In addition, phentolamine, a nonselective α receptor antagonist, could recover the decrease of GLP-1 release induced by ghrelin infusion. Pralmorelin (an artificial growth hormone release peptide) infusion into the portal vein could also inhibit the glucose-stimulated release of GLP-1. And growth hormone secretagogue receptor antagonist, [D-lys3]-GHRP-6, infusion showed comparable increases of glucose stimulated GLP-1 release compared to ghrelin infusion into the portal vein. The data showed that intraportal infusion of ghrelin exerted an inhibitory effect on GLP-1 secretion through growth hormone secretagogue receptor 1α (GHS1α receptor), which indicated that the downregulation of ghrelin secretion after food intake was necessary for incretin effect. Furthermore, our results suggested that the enteric neural net involved hepatic vagal nerve and sympathetic nerve mediated inhibition effect of ghrelin on incretin effect.

scholarly journals GPR40 reduces food intake and body weight through GLP-1

2017 ◽  
Vol 313 (1) ◽  
pp. E37-E47 ◽  
Author(s):  
Judith N. Gorski ◽  
Michele J. Pachanski ◽  
Joel Mane ◽  
Christopher W. Plummer ◽  
Sarah Souza ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Partial Agonist ◽  
Glucose Lowering ◽  
Partial Agonists ◽  
Lower Glucose ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion ◽  
G Protein Coupled

G protein-coupled receptor 40 (GPR40) partial agonists lower glucose through the potentiation of glucose-stimulated insulin secretion, which is believed to provide significant glucose lowering without the weight gain or hypoglycemic risk associated with exogenous insulin or glucose-independent insulin secretagogues. The class of small-molecule GPR40 modulators, known as AgoPAMs (agonist also capable of acting as positive allosteric modulators), differentiate from partial agonists, binding to a distinct site and functioning as full agonists to stimulate the secretion of both insulin and glucagon-like peptide-1 (GLP-1). Here we show that GPR40 AgoPAMs significantly increase active GLP-1 levels and reduce acute and chronic food intake and body weight in diet-induced obese (DIO) mice. These effects of AgoPAM treatment on food intake are novel and required both GPR40 and GLP-1 receptor signaling pathways, as demonstrated in GPR40 and GLP-1 receptor-null mice. Furthermore, weight loss associated with GPR40 AgoPAMs was accompanied by a significant reduction in gastric motility in these DIO mice. Chronic treatment with a GPR40 AgoPAM, in combination with a dipeptidyl peptidase IV inhibitor, synergistically decreased food intake and body weight in the mouse. The effect of GPR40 AgoPAMs on GLP-1 secretion was recapitulated in lean, healthy rhesus macaque demonstrating that the putative mechanism mediating weight loss translates to higher species. Together, our data indicate effects of AgoPAMs that go beyond glucose lowering previously observed with GPR40 partial agonist treatment with additional potential for weight loss.

scholarly journals Effect of Fermented Feed on the Microbial Population of the Gastrointestinal Tracts of Pigs

2001 ◽  
Vol 67 (7) ◽  
pp. 3071-3076 ◽  
Author(s):  
Ren� L. van Winsen ◽  
Bert A. P. Urlings ◽  
Len J. A. Lipman ◽  
Jos M. A. Snijders ◽  
David Keuzenkamp ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Significant Positive Correlation ◽  
Stomach Contents ◽  
Significant Negative Correlation ◽  
Inhibitory Effect ◽  
Positive Correlation ◽  
Fermented Feed ◽  
The Family ◽  
Colon And Rectum

ABSTRACT An in vivo experiment was performed with pigs to study the inhibitory effect of fermented feed on the bacterial population of the gastrointestinal tract. Results demonstrated a significant positive correlation between pH and lactobacilli in the stomach contents of pigs in dry feed as well as in the stomach contents of pigs fed fermented feed. Furthermore, a significant positive correlation between the pH and the numbers of bacteria in the familyEnterobacteriaceae in the contents of the stomach of pigs fed dry feed was found. In the stomach contents of pigs fed fermented feed, a significant negative correlation was found between the concentration of the undissociated form of lactic acid and the numbers of Enterobacteriaceae. The numbers ofEnterobacteriaceae in the contents of the stomach, ileum, cecum, colon, and rectum of pigs fed fermented feed were significantly lower compared with the contents of the stomach, ileum, caecum, colon, and rectum of pigs fed dry feed. The numbers of total lactobacilli were significantly higher in the stomach contents of pigs fed fermented feed and in the ileum contents of one pig group fed fermented feed compared with the contents of pigs fed dry feed. However, the influence of lactobacilli on numbers of Enterobacteriaceae could not be demonstrated. It was concluded that fermented feed influences the bacterial ecology of the gastrointestinal tract and reduces the levels of Enterobacteriaceae in the different parts of the gastrointestinal tract.

scholarly journals SARS-CoV-2 and Acute Cerebrovascular Events: An Overview

2021 ◽  
Vol 10 (15) ◽  
pp. 3349
Author(s):  
Mehdi Ghasemi ◽  
Raffaella Pizzolato Umeton ◽  
Kiandokht Keyhanian ◽  
Babak Mohit ◽  
Nasrin Rahimian ◽  
...  
Keyword(s):  
Functional Outcomes ◽  
Case Reports ◽  
Critical Role ◽  
Epidemiological Studies ◽  
Therapeutic Approaches ◽  
Angiotensin Converting Enzyme 2 ◽  
Cerebrovascular Complications ◽  
Current State ◽  
Cerebrovascular Events ◽  
Brain Homeostasis

Since the coronavirus disease 2019 (COVID-19) pandemic, due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, accumulating evidence indicates that SARS-CoV-2 infection may be associated with various neurological manifestations, including acute cerebrovascular events (i.e., stroke and cerebral venous thrombosis). These events can occur prior to, during and even after the onset of COVID-19’s general symptoms. Although the mechanisms underlying the cerebrovascular complications in patients with COVID-19 are yet to be fully elucidated, the hypercoagulability state, inflammation and altered angiotensin-converting enzyme 2 (ACE-2) signaling in association with SARS-CoV-2 may play key roles. ACE-2 plays a critical role in preserving heart and brain homeostasis. In this review, we discuss the current state of knowledge of the possible mechanisms underlying the acute cerebrovascular events in patients with COVID-19, and we review the current epidemiological studies and case reports of neurovascular complications in association with SARS-CoV-2, as well as the relevant therapeutic approaches that have been considered worldwide. As the number of published COVID-19 cases with cerebrovascular events is growing, prospective studies would help gather more valuable insights into the pathophysiology of cerebrovascular events, effective therapies, and the factors predicting poor functional outcomes related to such events in COVID-19 patients.

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