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 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 Rheumatic Diseases and Obesity: Adipocytokines as Potential Comorbidity Biomarkers for Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Rossana Scrivo ◽  
Massimiliano Vasile ◽  
Ulf Müller-Ladner ◽  
Elena Neumann ◽  
Guido Valesini
Keyword(s):  
Cardiovascular Risk ◽  
Current Knowledge ◽  
Weight Bearing ◽  
Joint Damage ◽  
Positive Association ◽  
Experimental Models ◽  
Low Grade ◽  
Multifactorial Diseases ◽  
Systemic Factors ◽  
Low Grade Inflammation

Inflammation has been recognized as a common trait in the pathogenesis of multifactorial diseases including obesity, where a low-grade inflammation has been established and may be responsible for the cardiovascular risk related to the disease. Obesity has also been associated with the increased incidence and a worse outcome of rheumatoid arthritis (RA) and osteoarthritis (OA). RA is characterized by systemic inflammation, which is thought to play a key role in accelerated atherosclerosis and in the increased incidence of cardiovascular disease, an important comorbidity in patients with RA. The inflammatory process underlying the cardiovascular risk both in obesity and RA may be mediated by adipocytokines, a heterogeneous group of soluble proteins mainly secreted by the adipocytes. Many adipocytokines are mainly produced by white adipose tissue. Adipocytokines may also be involved in the pathogenesis of OA since a positive association with obesity has been found for weight-bearing and nonweight-bearing joints, suggesting that, in addition to local overload, systemic factors may contribute to joint damage. In this review we summarize the current knowledge on experimental models and clinical studies in which adipocytokines were examined in obesity, RA, and OA and discuss the potential of adipocytokines as comorbidity biomarkers for cardiovascular risk.

scholarly journals Leukocyte Adhesion Molecules in Diabetic Retinopathy

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Kousuke Noda ◽  
Shintaro Nakao ◽  
Susumu Ishida ◽  
Tatsuro Ishibashi
Keyword(s):  
Diabetic Retinopathy ◽  
Adhesion Molecules ◽  
Leukocyte Adhesion ◽  
Microvascular Complications ◽  
Systemic Disease ◽  
Low Grade ◽  
Adhesion Molecule Expression ◽  
Adhesive Interactions ◽  
Low Grade Inflammation ◽  
Leukocyte Adhesion Molecules

Diabetes is a systemic disease that causes a number of metabolic and physiologic abnormalities. One of the major microvascular complications of diabetes is diabetic retinopathy (DR), a leading cause of blindness in people over age 50. The mechanisms underlying the development of DR are not fully understood; however, extensive studies have recently implicated chronic, low-grade inflammation in the pathophysiology of DR. During inflammation leukocytes undergo sequential adhesive interactions with endothelial cells to migrate into the inflamed tissues, a process known as the “leukocyte recruitment cascade” which is orchestrated by precise adhesion molecule expression on the cell surface of leukocytes and the endothelium. This paper summarizes the recent clinical and preclinical works on the roles of leukocyte adhesion molecules in DR.

scholarly journals Recent Advances in Adipose Tissue Dysfunction and Its Role in the Pathogenesis of Non-Alcoholic Fatty Liver Disease

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3300
Author(s):  
Xiaoxiao Wang ◽  
Huiying Rao ◽  
Feng Liu ◽  
Lai Wei ◽  
Honggui Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Current Knowledge ◽  
Low Grade ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver ◽  
Adipose Tissue Dysfunction ◽  
Adipose Dysfunction

Obesity is a serious ongoing health problem that significantly increases the incidence of nonalcoholic fatty liver disease (NAFLD). During obesity, adipose tissue dysfunction is obvious and characterized by increased fat deposition (adiposity) and chronic low-grade inflammation. The latter has been implicated to critically promote the development and progression of NAFLD, whose advanced form non-alcoholic steatohepatitis (NASH) is considered one of the most common causes of terminal liver diseases. This review summarizes the current knowledge on obesity-related adipose dysfunction and its roles in the pathogenesis of hepatic steatosis and inflammation, as well as liver fibrosis. A better understanding of the crosstalk between adipose tissue and liver under obesity is essential for the development of new and improved preventive and/or therapeutic approaches for managing NAFLD.

scholarly journals Osteopontin: The Molecular Bridge between Fat and Cardiac–Renal Disorders

2020 ◽  
Vol 21 (15) ◽  
pp. 5568
Author(s):  
Elena Vianello ◽  
Marta Kalousová ◽  
Elena Dozio ◽  
Lorenza Tacchini ◽  
Tomáš Zima ◽  
...  
Keyword(s):  
Molecular Interactions ◽  
Visceral Fat ◽  
Current Knowledge ◽  
Common Factor ◽  
Cell Types ◽  
The Body ◽  
Matricellular Protein ◽  
Low Grade ◽  
Renal Disorders ◽  
Low Grade Inflammation

Osteopontin (OPN) is a multifaceted matricellular protein, with well-recognized roles in both the physiological and pathological processes in the body. OPN is expressed in the main organs and cell types, in which it induces different biological actions. During physiological conditioning, OPN acts as both an intracellular protein and soluble excreted cytokine, regulating tissue remodeling and immune-infiltrate in adipose tissue the heart and the kidney. In contrast, the increased expression of OPN has been correlated with the severity of the cardiovascular and renal outcomes associated with obesity. Indeed, OPN expression is at the “cross roads” of visceral fat extension, cardiovascular diseases (CVDs) and renal disorders, in which OPN orchestrates the molecular interactions, leading to chronic low-grade inflammation. The common factor associated with OPN overexpression in adipose, cardiac and renal tissues seems attributable to the concomitant increase in visceral fat size and the increase in infiltrated OPN+ macrophages. This review underlines the current knowledge on the molecular interactions between obesity and the cardiac–renal disorders ruled by OPN.

scholarly journals Periodontitis, Low-Grade Inflammation and Systemic Health: A Scoping Review

Medicina ◽  
2020 ◽  
Vol 56 (6) ◽  
pp. 272
Author(s):  
Gennaro Cecoro ◽  
Marco Annunziata ◽  
Morena Tina Iuorio ◽  
Livia Nastri ◽  
Luigi Guida
Keyword(s):  
Scoping Review ◽  
Current Knowledge ◽  
Inflammatory Factors ◽  
Cochrane Library ◽  
Low Grade ◽  
Eligibility Criteria ◽  
Hand Search ◽  
Scoping Reviews ◽  
Systemic Health ◽  
Low Grade Inflammation

Background and objectives: Periodontitis is a multifactorial chronic inflammatory infectious disease in which an infection is necessary, but not sufficient, for development of the condition. Individual susceptibility strictly linked to the immune and inflammatory response of the organism must also be present. Low-grade inflammation (LGI) is a systemic status of chronic sub-clinical production of inflammatory factors. This condition represents a risk factor for many chronic diseases including diabetes, cardiovascular disease, cerebrovascular disease, neurodegenerative disease and cancer. This scoping review aims to clarify, summarize and disseminate current knowledge on the possible link between periodontitis, LGI and systemic health. Materials and Methods: PRISMA Extension for Scoping Reviews guidelines were followed. An ad-hoc created keyword string was used to search the electronic databases of PubMed/Medline, Embase, The Cochrane Library and ClinicalTrials.gov. A hand search of specialized journals and their reference lists was also performed. Results: 14 studies that respected eligibility criteria were selected and analyzed. There is emerging evidence of strong links between periodontitis, LGI and systemic health. On the one hand, periodontitis influences the systemic status of LGI and on the other hand, the systemic production of inflammatory factors affects periodontitis with a bidirectional connection. Conclusions: LGI and the subsequent onset of a systemic inflammatory phenotype can be considered the common substrate of many chronic inflammatory diseases including periodontitis, with multiple mutual connections between them. Understanding of the biological principles and mechanisms underlying such a complex interrelationship could lead to significant improvements in the field of personalized diagnostics and therapeutic protocols.

scholarly journals Current and Evolving Concepts on the Pathogenesis of Diverticular Disease

2019 ◽  
Vol 28 ◽  
pp. 225-235 ◽  
Author(s):  
Antonio Tursi
Keyword(s):  
Diverticular Disease ◽  
Current Knowledge ◽  
Acute Diverticulitis ◽  
Colonic Motility ◽  
Human Colon ◽  
Recurrent Abdominal Pain ◽  
Low Grade ◽  
Host Immune Responses ◽  
Low Grade Inflammation

Background & Aims: Diverticulosis of the colon is the most common anatomic alteration of the human colon, and it is characterized by the out-pouching of the colonic mucosa and submucosa through the muscular layer. Recurrent abdominal pain is experienced by about 20% of patients with diverticulosis, and inflammation of diverticula may lead to acute diverticulitis. In the past few years, several studies have investigated the factors predisposing or triggering diverticular disease (DD) occurrence. Moreover, new physiopathological knowledge has been acquired. The aim of this study was to review current knowledge regarding the pathogenesis of DD. Methods: A search of PubMed and EMBASE database was performed to identify articles relevant to the pathogenesis of DD. Results: Several papers have shown that genetic predisposition, environmental factors, and colonic dysmotility are implicated in the pathogenesis of DD. More recent studies have associated specific host immune responses, gut microbiota imbalance and therefore low-grade inflammation as contributors to symptom occurrence in DD and diverticulitis. Conclusions: Current and evolving evidence highlighted the role of genetic susceptibility, environment, colonic motility, visceral sensitivity, immune response, and microbiota in the pathogenesis of this disease. Further studies are required to identify potential targets for medical or surgical decision-making.

scholarly journals Immune regulation of islet homeostasis and adaptation

2020 ◽  
Author(s):  
Jinglong Guo ◽  
Wenxian Fu
Keyword(s):  
Immune Cells ◽  
Cell Function ◽  
Normal Function ◽  
Low Grade ◽  
Multiple Organs ◽  
Monocytes And Macrophages ◽  
Β Cell Function ◽  
Islet Inflammation ◽  
And Function ◽  
Low Grade Inflammation

Abstract The islet of Langerhans produces endocrine hormones to regulate glucose homeostasis. The normal function of the islet relies on the homeostatic regulations of cellular composition and cell–cell interactions within the islet microenvironment. Immune cells populate the islet during embryonic development and participate in islet organogenesis and function. In obesity, a low-grade inflammation manifests in multiple organs, including pancreatic islets. Obesity-associated islet inflammation is evident in both animal models and humans, characterized by the accumulation of immune cells and elevated production of inflammatory cytokines/chemokines and metabolic mediators. Myeloid lineage cells (monocytes and macrophages) are the dominant types of immune cells in islet inflammation during the development of obesity and type 2 diabetes mellitus (T2DM). In this review, we will discuss the role of the immune system in islet homeostasis and inflammation and summarize recent findings of the cellular and molecular factors that alter islet microenvironment and β cell function in obesity and T2DM.

scholarly journals Association of Adipose Tissue and Adipokines with Development of Obesity-Induced Liver Cancer

2021 ◽  
Vol 22 (4) ◽  
pp. 2163
Author(s):  
Yetirajam Rajesh ◽  
Devanand Sarkar
Keyword(s):  
Adipose Tissue ◽  
Cancer Progression ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Metabolic Complications ◽  
Endocrine Organ ◽  
Nonalcoholic Fatty Liver ◽  
Underlying Mechanisms ◽  
Low Grade Inflammation ◽  
Excessive Accumulation

Obesity is rapidly dispersing all around the world and is closely associated with a high risk of metabolic diseases such as insulin resistance, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD), leading to carcinogenesis, especially hepatocellular carcinoma (HCC). It results from an imbalance between food intake and energy expenditure, leading to an excessive accumulation of adipose tissue (AT). Adipocytes play a substantial role in the tumor microenvironment through the secretion of several adipokines, affecting cancer progression, metastasis, and chemoresistance via diverse signaling pathways. AT is considered an endocrine organ owing to its ability to secrete adipokines, such as leptin, adiponectin, resistin, and a plethora of inflammatory cytokines, which modulate insulin sensitivity and trigger chronic low-grade inflammation in different organs. Even though the precise mechanisms are still unfolding, it is now established that the dysregulated secretion of adipokines by AT contributes to the development of obesity-related metabolic disorders. This review focuses on several obesity-associated adipokines and their impact on obesity-related metabolic diseases, subsequent metabolic complications, and progression to HCC, as well as their role as potential therapeutic targets. The field is rapidly developing, and further research is still required to fully understand the underlying mechanisms for the metabolic actions of adipokines and their role in obesity-associated HCC.

scholarly journals The Role of MIF in Type 1 and Type 2 Diabetes Mellitus

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Yuriko I. Sánchez-Zamora ◽  
Miriam Rodriguez-Sosa
Keyword(s):  
Diabetes Mellitus ◽  
Macrophage Migration Inhibitory Factor ◽  
Inflammatory Responses ◽  
Current Knowledge ◽  
Low Grade ◽  
Clinical Environment ◽  
Low Grade Inflammation

Autoimmunity and chronic low-grade inflammation are hallmarks of diabetes mellitus type one (T1DM) and type two (T2DM), respectively. Both processes are orchestrated by inflammatory cytokines, including the macrophage migration inhibitory factor (MIF). To date, MIF has been implicated in both types of diabetes; therefore, understanding the role of MIF could affect our understanding of the autoimmune or inflammatory responses that influence diabetic pathology. This review highlights our current knowledge about the involvement of MIF in both types of diabetes in the clinical environment and in experimental disease models.

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