The Crosstalk between Gut Inflammation and Gastrointestinal Disorders During Acute Pancreatitis

Guo, Zhiliang; Wang, Pu; Yi, Zhihui; Huang, Zhiyin; Tang, Chengwei

doi:10.2174/13816128113199990414

Cited by 32 publications

(29 citation statements)

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“…With the glutamine-derived cytosolic acetyl CoA, HIF-1 and protein kinase B (AKT) activation has been shown to up-regulate fatty acid synthase (FAS) for acetyl CoA to fatty acid conversion. Hypoxia has been demonstrated to enhance fatty acid synthesis via the sterol regulatory-element binding protein (SREBP)-1, which is a transcriptional regulator for the FAS gene, in multiple types of cancer [68,69]. SREBP-1 induction follows activation of HIF-1 by the phosphorylation of AKT [69].…”

Section: Molecular Connections Between Hypoxia and Cancer Cell Metmentioning

confidence: 99%

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Justus

Sanderlin

Yang

2015

IJMS

123

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Cancer cells preferentially utilize glycolysis, instead of oxidative phosphorylation, for metabolism even in the presence of oxygen. This phenomenon of aerobic glycolysis, referred to as the “Warburg effect”, commonly exists in a variety of tumors. Recent studies further demonstrate that both genetic factors such as oncogenes and tumor suppressors and microenvironmental factors such as spatial hypoxia and acidosis can regulate the glycolytic metabolism of cancer cells. Reciprocally, altered cancer cell metabolism can modulate the tumor microenvironment which plays important roles in cancer cell somatic evolution, metastasis, and therapeutic response. In this article, we review the progression of current understandings on the molecular interaction between cancer cell metabolism and the tumor microenvironment. In addition, we discuss the implications of these interactions in cancer therapy and chemoprevention.

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Section: Molecular Connections Between Hypoxia and Cancer Cell Metmentioning

confidence: 99%

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Justus

Sanderlin

Yang

2015

IJMS

123

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“…Intestinal ischemia-reperfusion significantly contributes to small intestinal injury during SAP [27, 28] by inducing gut mucosal injury and affecting gut muscular layer to impair gut motility, which is frequently seen in SAP [14], and the reduced intestinal motility significantly contributes to disrupted intestinal microflora and BT [14]. …”

Section: Introductionmentioning

confidence: 99%

“…SAP induces significant small intestinal injury [27, 28], and the failure of gut barrier is associated with BT [27], which is evident in SAP [6, 24, 25]. SAP patients have significantly increased serum LPS level, which is likely derived from the gut lumen or from translocated intestinal bacteria [38].…”

Section: Introductionmentioning

confidence: 99%

HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis

Yang

Tenhunen

Tønnessen

2017

International Journal of Inflammation

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Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokines significantly contribute to gut mucosal injury and intestinal bacterial translocation (BT) during SAP. Circulating HMGB1 level is significantly increased in SAP patients and HMGB1 is an important factor that mediates (at least partly) gut BT during SAP. Gut BT plays a critical role in triggering/inducing systemic inflammation/sepsis in critical illness, and profound systemic inflammatory response syndrome (SIRS) can lead to multiple organ dysfunction syndrome (MODS) during SAP, and systemic inflammation with multiorgan dysfunction is the cause of death in experimental SAP. Therefore, HMGB1 is an important factor that links gut BT and systemic inflammation. Furthermore, HMGB1 significantly contributes to multiple organ injuries. The SAP patients also have significantly increased circulating histones and cell-free DNAs levels, which can reflect the disease severity and contribute to multiple organ injuries in SAP. Hepatic Kupffer cells (KCs) are the predominant source of circulating inflammatory cytokines in SAP, and new evidence indicates that hepatocyte is another important source of circulating HMGB1 in SAP; therefore, treating the liver injury is important in SAP.

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“…[28,29] Violation of the enterohepatic barrier as one of the pathological manifestations of enteric insufficiency leads to the emergence of an additional source of endotoxicosis, which closes the vicious circle and causes the occurrence of irreversible lesions of various organs and systems. [30] Strengths and limitations: Experimental research designs are repeatable, and therefore, results can be checked and verified. Findings usually cannot be generalized to the study population or community because of small amount of animals in experimental groups.…”

Section: Discussionmentioning

confidence: 99%

The influence of carrageenan on markers of endogenous intoxication in rats

Marushchak¹,

Krynytska²,

Kopanytsia³

et al. 2017

Natl J Physiol Pharm Pharmacol

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Background:The growth of the world population and the need to increase food production led to the widespread use of food additives. One of such additives is carrageenan. Potentially negative health effects of carrageenans prompt us to question safety of their widespread use. Aims and Objectives: In this study, we defined the effect of carrageenan (E407) consumption on the main markers of endogenous intoxication in rats. Materials and Methods: Experimental studies were conducted on 72 non-linear, female, white rats weighing 150-180 g. The experimental animals had free access to 0.5% carrageenan solution in drinking water. Control group of animals received pure water. Syndrome of endogenous intoxication was evaluated using measurements of low, medium, and high molecular weight substances in blood plasma, red blood cell suspension, and urine. Results: Our results indicate shift of the markers of intoxication syndrome toward mainly catabolic substances. The results obtained after 1 week of the experiment correspond with phase of partial compensation, characterized by increased concentrations of low and middle molecular weight substances in red blood cells and plasma. After 2 weeks and up to 1 month of the experiment, the predominantly catabolic markers of endogenous intoxication continue to increase in erythrocytes and plasma, indicating a shift to the phase of partial decompensation to systems and organs of detoxification. Conclusion: The consumption of carrageenan with drinking water in concentration of 0.5% was associated with the development of excessive levels of low and middle molecular weight substances with reduced ability of kidneys to excrete toxic products.

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The Crosstalk between Gut Inflammation and Gastrointestinal Disorders During Acute Pancreatitis

Cited by 32 publications

References 0 publications

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

Molecular Connections between Cancer Cell Metabolism and the Tumor Microenvironment

HMGB1 and Histones Play a Significant Role in Inducing Systemic Inflammation and Multiple Organ Dysfunctions in Severe Acute Pancreatitis

The influence of carrageenan on markers of endogenous intoxication in rats

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