scholarly journals A System-Level Mechanism of Anmyungambi Decoction for Obesity: A Network Pharmacological Approach

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1881
Author(s):  
Dongyeop Jang ◽  
Hayeong Jeong ◽  
Chang-Eop Kim ◽  
Jungtae Leem
Keyword(s):  
Signaling Pathway ◽  
Leptin Receptor ◽  
Tumor Necrosis Factor Receptor ◽  
Type Ii Diabetes Mellitus ◽  
System Level ◽  
Low Grade ◽  
Nonalcoholic Fatty Liver ◽  
Systemic Inflammatory Disease ◽  
Related Proteins ◽  
Necrosis Factor

Obesity is a low-grade systemic inflammatory disease involving adipocytokines. As though Anmyungambi decoction (AMGB) showed significant improvement on obesity in a clinical trial, the molecular mechanism of AMGB in obesity remains unknown. Therefore, we explored the potential mechanisms of action of AMGB on obesity through network pharmacological approaches. We revealed that targets of AMGB are significantly associated with obesity-related and adipocyte-elevated genes. Evodiamine, berberine, genipin, palmitic acid, genistein, and quercetin were shown to regulate adipocytokine signaling pathway proteins which mainly involved tumor necrosis factor receptor 1, leptin receptor. In terms of the regulatory pathway of lipolysis in adipocytes, norephedrine, pseudoephedrine, quercetin, and limonin were shown to affect adrenergic receptor-beta, protein kinase A, etc. We also found that AMGB has the potentials to enhance the insulin signaling pathway thereby preventing type II diabetes mellitus. Additionally, AMGB was discovered to be able to control not only insulin-related proteins but also inflammatory mediators and apoptotic regulators and caspases, hence reducing hepatocyte injury in nonalcoholic fatty liver disease. Our findings help develop a better understanding of how AMGB controls obesity.

scholarly journals Tumor necrosis factor receptor 1 gain-of-function mutation aggravates nonalcoholic fatty liver disease but does not cause insulin resistance in a murine model*

Hepatology ◽  
2013 ◽  
Vol 57 (2) ◽  
pp. 566-576 ◽  
Author(s):  
Marcela Aparicio-Vergara ◽  
Pascal P.H. Hommelberg ◽  
Marijke Schreurs ◽  
Nanda Gruben ◽  
Rinke Stienstra ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Tumor Necrosis Factor ◽  
Fatty Liver ◽  
Murine Model ◽  
Fatty Liver Disease ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Nonalcoholic Fatty Liver ◽  
Necrosis Factor

scholarly journals NAFLD and Infection, a Nuanced Relationship

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Abimbola Adenote ◽  
Igor Dumic ◽  
Cristian Madrid ◽  
Christopher Barusya ◽  
Charles W. Nordstrom ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Systemic Disease ◽  
Type Ii Diabetes Mellitus ◽  
Low Grade ◽  
Extrahepatic Manifestations ◽  
Nonalcoholic Fatty Liver ◽  
Multiple Organs ◽  
Clostridioides Difficile ◽  
Low Grade Inflammation ◽  
Ovarian Syndrome

The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased significantly over the last few decades mirroring the increase in obesity and type II diabetes mellitus. NAFLD has become one of the most common indications for liver transplantation. The deleterious effects of NAFLD are not isolated to the liver only, for it has been recognized as a systemic disease affecting multiple organs through protracted low-grade inflammation mediated by the metabolic activity of excessive fat tissue. Extrahepatic manifestations of NAFLD such as cardiovascular disease, polycystic ovarian syndrome, chronic kidney disease, and hypothyroidism have been well described in the literature. In recent years, it has become evident that patients suffering from NAFLD might be at higher risk of developing various infections. The proposed mechanism for this association includes links through hyperglycemia, insulin resistance, alterations in innate immunity, obesity, and vitamin D deficiency. Additionally, a risk independent of these factors mediated by alterations in gut microbiota might contribute to a higher burden of infections in these individuals. In this narrative review, we synthetize current knowledge on several infections including urinary tract infection, pneumonia, Helicobacter pylori, coronavirus disease 2019, and Clostridioides difficile as they relate to NAFLD. Additionally, we explore NAFLD’s association with hidradenitis suppurativa.

scholarly journals Dendritic cell maturation in the corneal epithelium with onset of type 2 diabetes is associated with tumor necrosis factor receptor superfamily member 9

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Neil S. Lagali ◽  
Reza A. Badian ◽  
Xu Liu ◽  
Tobias R. Feldreich ◽  
Johan Ärnlöv ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Dendritic Cell ◽  
Tumor Necrosis Factor ◽  
Corneal Epithelium ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Low Grade ◽  
Antigen Presenting ◽  
Necrosis Factor

AbstractType 2 diabetes mellitus is characterized by a low-grade inflammation; however, mechanisms leading to this inflammation in specific tissues are not well understood. The eye can be affected by diabetes; thus, we hypothesized that inflammatory changes in the eye may parallel the inflammation that develops with diabetes. Here, we developed a non-invasive means to monitor the status of inflammatory dendritic cell (DC) subsets in the corneal epithelium as a potential biomarker for the onset of inflammation in type 2 diabetes. In an age-matched cohort of 81 individuals with normal and impaired glucose tolerance and type 2 diabetes, DCs were quantified from wide-area maps of the corneal epithelial sub-basal plexus, obtained using clinical in vivo confocal microscopy (IVCM). With the onset of diabetes, the proportion of mature, antigen-presenting DCs increased and became organized in clusters. Out of 92 plasma proteins analysed in the cohort, tumor necrosis factor receptor super family member 9 (TNFRSF9) was associated with the observed maturation of DCs from an immature to mature antigen-presenting phenotype. A low-grade ocular surface inflammation observed in this study, where resident immature dendritic cells are transformed into mature antigen-presenting cells in the corneal epithelium, is a process putatively associated with TNFRSF9 signalling and may occur early in the development of type 2 diabetes. IVCM enables this process to be monitored non-invasively in the eye.

scholarly journals Temporary Blockade of the Tumor Necrosis Factor Receptor Signaling Pathway Impedes the Spread of Scrapie to the Brain

2002 ◽  
Vol 76 (10) ◽  
pp. 5131-5139 ◽  
Author(s):  
Neil A. Mabbott ◽  
Gillian McGovern ◽  
Martin Jeffrey ◽  
Moira E. Bruce
Keyword(s):  
Tumor Necrosis Factor ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Transmissible Spongiform Encephalopathies ◽  
Lymphoid Tissues ◽  
Necrosis Factor Alpha ◽  
Spongiform Encephalopathies ◽  
Similar Treatment ◽  
Necrosis Factor

ABSTRACT Although the transmissible spongiform encephalopathies (TSEs) are neurodegenerative diseases, their agents usually replicate and accumulate in lymphoid tissues long before infection spreads to the central nervous system (CNS). Studies of a mouse scrapie model have shown that mature follicular dendritic cells (FDCs), which express the host prion protein (PrPc), are critical for replication of infection in lymphoid tissues. In the absence of mature FDCs, the spread of infection to the CNS is significantly impaired. Tumor necrosis factor alpha (TNF-α) secretion by lymphocytes is important for maintaining FDC networks, and signaling is mediated through TNF receptor 1 (TNFR-1) expressed on FDCs and/or their precursors. A treatment that blocks TNFR signaling leads to the temporary dedifferentiation of mature FDCs, raising the hypothesis that a similar treatment would significantly delay the peripheral pathogenesis of scrapie. Here, specific neutralization of the TNFR signaling pathway was achieved through treatment with a fusion protein consisting of two soluble human TNFR (huTNFR) (p80) domains linked to the Fc portion of human immunoglobulin G1 (huTNFR:Fc). A single treatment of mice with huTNFR:Fc before or shortly after intraperitoneal injection with the ME7 scrapie strain significantly delayed the onset of disease in the CNS and reduced the early accumulation of disease-specific PrP in the spleen. These effects coincided with a temporary dedifferentiation of mature FDCs within 5 days of huTNFR:Fc treatment. We conclude that treatments that specifically inhibit the TNFR signaling pathway may present an opportunity for early intervention in peripherally transmitted TSEs.

scholarly journals Insulin resistance in patients with psoriasis

2021 ◽  
Vol 17 (7) ◽  
pp. 570-574
Author(s):  
I.V. Pankiv
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Psoriatic Arthritis ◽  
Systemic Inflammation ◽  
Polycystic Ovary ◽  
Developed Countries ◽  
Low Grade ◽  
Nonalcoholic Fatty Liver ◽  
Systemic Inflammatory Disease

Psoriasis is a chronic systemic inflammatory disease accompanied by an activation of skin dendritic cells with accumulation in the inflammatory foci of interleukin-23 and activated Th-1 lymphocytes (Th-17, Th-22). In recent years, there has been a large number of evidence linking psoriasis with other inflammatory diseases, including obesity, diabetes mellitus, atherosclerosis, hypertension, nonalcoholic fatty liver disease, polycystic ovary syndrome, benign prostatic hyperplasia, etc. All of these conditions are associated with systemic inflammation and insulin resistance induced by it. Psoriasis is the most common chronic dermatosis and affects 1–2 % of the population in developed countries. Psoriasis as a chronic immune-mediated inflammatory skin disease is often associated with metabolic syndrome and its components such as obesity, hypertension, insulin resistance and dyslipidemia. The risk of developing metabolic syndrome in patients with psoriasis is 40 % higher than in the general population. Psoriasis and metabo­lic syndrome share some pathogenic mechanisms such as chronic low-grade systemic inflammation and an increased level of pro-inflammatory cytokines. Systemic inflammation causes obesity, cardiovascular diseases, diabetes mellitus type 2. These conditions increase the risk of mortality among patients with psoriasis. There is a positive correlation between the severity of psoriasis and metabolic syndrome, which is manifested by a severe rash, reduction of the remission and higher risk of psoriatic arthritis development. The carriers of the risk allele of FTO gene are characterized by a more severe psoriasis, the presence of psoriatic arthritis and increased body mass index. A review of the literature focuses on the relationship between insulin resistance and the pathogenesis of psoriasis.

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