-
1.
Inflammation in Obesity-Related Complications in Children: The Protective Effect of Diet and Its Potential Role as a Therapeutic Agent.
Calcaterra, V, Regalbuto, C, Porri, D, Pelizzo, G, Mazzon, E, Vinci, F, Zuccotti, G, Fabiano, V, Cena, H
Biomolecules. 2020;(9)
Abstract
Obesity is a growing health problem in both children and adults, impairing physical and mental state and impacting health care system costs in both developed and developing countries. It is well-known that individuals with excessive weight gain frequently develop obesity-related complications, which are mainly known as Non-Communicable Diseases (NCDs), including cardiovascular disease, type 2 diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver disease, hypertension, hyperlipidemia and many other risk factors proven to be associated with chronic inflammation, causing disability and reduced life expectancy. This review aims to present and discuss complications related to inflammation in pediatric obesity, the critical role of nutrition and diet in obesity-comorbidity prevention and treatment, and the impact of lifestyle. Appropriate early dietary intervention for the management of pediatric overweight and obesity is recommended for overall healthy growth and prevention of comorbidities in adulthood.
-
2.
High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions.
Zhang, DM, Jiao, RQ, Kong, LD
Nutrients. 2017;(4)
Abstract
High dietary fructose is a major contributor to insulin resistance and metabolic syndrome, disturbing tissue and organ functions. Fructose is mainly absorbed into systemic circulation by glucose transporter 2 (GLUT2) and GLUT5, and metabolized in liver to produce glucose, lactate, triglyceride (TG), free fatty acid (FFA), uric acid (UA) and methylglyoxal (MG). Its extrahepatic absorption and metabolism also take place. High levels of these metabolites are the direct dangerous factors. During fructose metabolism, ATP depletion occurs and induces oxidative stress and inflammatory response, disturbing functions of local tissues and organs to overproduce inflammatory cytokine, adiponectin, leptin and endotoxin, which act as indirect dangerous factors. Fructose and its metabolites directly and/or indirectly cause oxidative stress, chronic inflammation, endothelial dysfunction, autophagy and increased intestinal permeability, and then further aggravate the metabolic syndrome with tissue and organ dysfunctions. Therefore, this review addresses fructose-induced metabolic syndrome, and the disturbance effects of direct and/or indirect dangerous factors on the functions of liver, adipose, pancreas islet, skeletal muscle, kidney, heart, brain and small intestine. It is important to find the potential correlations between direct and/or indirect risk factors and healthy problems under excess dietary fructose consumption.
-
3.
The role of chemerin in human disease.
Stojek, M
Postepy higieny i medycyny doswiadczalnej (Online). 2017;(0):110-117
Abstract
Adipose tissue is not merely a storage depot of triacylglycerols but also a major endocrine organ. Its cells, including adipocytes, synthesize and secrete a range of biologically active molecules termed adipokines. Adipokines that display the properties of cytokines are often called adipocytokines. In recent years there has been increasing interest in a new adipokine called chemerin. Chemerin is a protein synthesized mostly by the adipose tissue and the liver as inactive pre‑pro‑chemerin. After the intracellular hydrolytic cutting off of the 20‑amino‑acid N‑terminal polypeptide, it is secreted into the bloodstream as inactive pro‑chemerin. Biologically active chemerin is then derived from pro‑chemerin after cleavage of the C‑terminal fragment by serum proteases involved in inflammation, coagulation and fibrinolysis. Proteolytic cleavage leads to formation of several chemerin‑derived peptides, both biologically active (often with opposing functions) and inactive. Within the last decade, there has been a growing number of publications regarding the role of chemerin in human disease. It seems to be implicated in the inflammatory response, metabolic syndrome, cardiovascular disease and alimentary tract disorders. The article presents the most recent information on the role of chemerin in human disease, and specifically alimentary tract disorders. The available evidence suggests that chemerin is an important link between adipose tissue mass, metabolic processes, the immune system and inflammation, and therefore plays a major role in human pathophysiology.
-
4.
Amylin in vasodilation, energy expenditure and inflammation.
Yang, F
Frontiers in bioscience (Landmark edition). 2014;(6):936-44
Abstract
Metabolic syndrome significantly increases the incidence of atherosclerosis-related diseases including coronary artery disease, stroke, and type 2 diabetes. Recent progress has demonstrated that amylin, or islet amyloid polypeptide, is circulating multifunctional hormone and neuropeptide, which is co-secreted with insulin into the bloodstream by pancreatic beta cells and plays a very important role in regulating feeding, energy homeostasis and inflammation. Recent FDA approval of amylin analog pramlintide as a new drug for treating type 1 and 2 diabetes positions amylin in the spotlight. In this analytical review, I summarize the recent progress on amylin studies in the following sections: 1) introduction to the molecular features of amylin; 2) amylin's amyloidogenic and proinflammatory effects; 3) a satiety hormone and new drug in increasing energy expenditure; and 4) a vasodilator inducing hypotension and tachycardia; and 5) a neuropeptide in depolarizing cholinergic neurons via closure of potassium channels. Continued improvement of our understanding on this multifunctional hormone would lead to future development of pramlintide as novel therapies for other inflammatory, hematological, metabolic, neurological and vascular diseases.
-
5.
Inflammasomes.
de Zoete, MR, Palm, NW, Zhu, S, Flavell, RA
Cold Spring Harbor perspectives in biology. 2014;(12):a016287
-
-
Free full text
-
Abstract
Inflammasomes are large cytosolic multiprotein complexes that assemble in response to detection of infection- or stress-associated stimuli and lead to the activation of caspase-1-mediated inflammatory responses, including cleavage and unconventional secretion of the leaderless proinflammatory cytokines IL-1β and IL-18, and initiation of an inflammatory form of cell death referred to as pyroptosis. Inflammasome activation can be induced by a wide variety of microbial pathogens and generally mediates host defense through activation of rapid inflammatory responses and restriction of pathogen replication. In addition to its role in defense against pathogens, recent studies have suggested that the inflammasome is also a critical regulator of the commensal microbiota in the intestine. Finally, inflammasomes have been widely implicated in the development and progression of various chronic diseases, such as gout, atherosclerosis, and metabolic syndrome. In this perspective, we discuss the role of inflammasomes in infectious and noninfectious inflammation and highlight areas of interest for future studies of inflammasomes in host defense and chronic disease.
-
6.
Hematological disorders following gastric bypass surgery: emerging concepts of the interplay between nutritional deficiency and inflammation.
Chen, M, Krishnamurthy, A, Mohamed, AR, Green, R
BioMed research international. 2013;:205467
Abstract
Obesity and the associated metabolic syndrome are among the most common and detrimental metabolic diseases of the modern era, affecting over 50% of the adult population in the United States. Surgeries designed to promote weight loss, known as bariatric surgery, typically involve a gastric bypass procedure and have shown high success rates for treating morbid obesity. However, following gastric bypass surgery, many patients develop chronic anemia, most commonly due to iron deficiency. Deficiencies of vitamins B1, B12, folate, A, K, D, and E and copper have also been reported after surgery. Copper deficiency can cause hematological abnormalities with or without neurological complications. Despite oral supplementation and normal serum concentrations of iron, copper, folate, and vitamin B12, some patients present with persistent anemia after surgery. The evaluation of hematologic disorders after gastric bypass surgery must take into account issues unique to the postsurgery setting that influence the development of anemia and other cytopenias. In this paper, the clinical characteristics and differential diagnosis of the hematological disorders associated with gastric bypass surgery are reviewed, and the underlying molecular mechanisms are discussed.
-
7.
Impact of metabolic syndrome on re-stenosis development: role of drug-eluting stents.
Goyal, SN, Bharti, S, Krishnamurthy, B, Agrawal, Y, Ojha, SK, Arya, DS
Diabetes & vascular disease research. 2012;(3):177-88
Abstract
Metabolic syndrome (MetS) is defined as a cluster of numerous cardiovascular risk factors, which encompasses obesity, dyslipidaemia, insulin resistance and hypertension. Patients with MetS are more prone to developing cardiovascular events than other patients. To date, several approaches such as physical exercise, dietary control and invasive and non-invasive therapeutic interventions for dyslipidaemia, hypertension and insulin resistance have been used to manage MetS. However, there is a progressive elevation in the incidence of fatal and non-fatal cardiovascular events due to the increased prevalence of obesity and diabetes. Percutaneous coronary intervention has emerged over the last few years as an effective revascularisation strategy for those with coronary artery disease, in parallel with the development of effective anti-platelet medications and newer drug-eluting stents. In recent years, considerable research efforts have been undertaken to elucidate the pathophysiology of re-stenosis and develop strategies to prevent re-stenosis following percutaneous transluminal coronary angioplasty and stent implantation. Although the rate of stent re-stenosis and target-lesion revascularisation has been reduced, there is little information in the literature on the outcome of MetS in the pathophysiology of re-stenosis. In this review article, we summarise the recent development and progress on re-stenosis and the role of drug-eluting stents, particularly in MetS.
-
8.
Inflammatory markers and cardiovascular risk in the metabolic syndrome.
Espinola-Klein, C, Gori, T, Blankenberg, S, Munzel, T
Frontiers in bioscience (Landmark edition). 2011;(5):1663-74
Abstract
Elevated blood glucose, obesity, high blood pressure, elevated triglycerides and low high density lipoprotein (HDL) cholesterol are well accepted risk factors in the development of coronary artery disease. Clustering of at least three of these factors in an individual is defined as metabolic syndrome (MetS). Obesity is a central pathological mechanism in the disease and it is expected that the incidence of this condition will increase dramatically within the next years. The visceral adipose tissue is not only an energy depot but also an endocrine organ which produces a large number of bioactive molecules, the so called adipokines. In the setting of obesity, the over-production of proinflammatory and pro-thrombotic adipokines is associated with insulin resistance. This mechanism represents the pathophysiological basis for the development of MetS. Inflammation has a central role in the pathogenesis of MetS and in mediating its impact on the development of cardiovascular disease. Knowledge of these mechanisms has relevance in the context of preventive and therapeutic strategies.
-
9.
The effects of diet on inflammation: emphasis on the metabolic syndrome.
Giugliano, D, Ceriello, A, Esposito, K
Journal of the American College of Cardiology. 2006;(4):677-85
Abstract
Reducing the incidence of coronary heart disease with diet is possible. The main dietary strategies include adequate omega-3 fatty acids intake, reduction of saturated and trans-fats, and consumption of a diet high in fruits, vegetables, nuts, and whole grains and low in refined grains. Each of these strategies may be associated with lower generation of inflammation. This review examines the epidemiologic and clinical evidence concerning diet and inflammation. Dietary patterns high in refined starches, sugar, and saturated and trans-fatty acids, poor in natural antioxidants and fiber from fruits, vegetables, and whole grains, and poor in omega-3 fatty acids may cause an activation of the innate immune system, most likely by an excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. The whole diet approach seems particularly promising to reduce the inflammation associated with the metabolic syndrome. The choice of healthy sources of carbohydrate, fat, and protein, associated with regular physical activity and avoidance of smoking, is critical to fighting the war against chronic disease. Western dietary patterns warm up inflammation, while prudent dietary patterns cool it down.
-
10.
Metabolic syndrome, inflammation and atherosclerosis.
Paoletti, R, Bolego, C, Poli, A, Cignarella, A
Vascular health and risk management. 2006;(2):145-52
Abstract
The inflammatory component of atherogenesis has been increasingly recognized over the last decade. Inflammation participates in all stages of atherosclerosis, not only during initiation and during evolution of lesions, but also with precipitation of acute thrombotic complications. The metabolic syndrome is associated with increased risk for development of both cardiovascular disease and type-2 diabetes in humans. Central obesity and insulin resistance are thought to represent common underlying factors of the syndrome, which features a chronic low-grade inflammatory state. Diagnosis of the metabolic syndrome occurs using defined threshold values for waist circumference, blood pressure, fasting glucose and dyslipidemia. The metabolic syndrome appears to affect a significant proportion of the population. Therapeutic approaches that reduce the levels of proinflammatory biomarkers and address traditional risk factors are particularly important in preventing cardiovascular disease and, potentially, diabetes. The primary management of metabolic syndrome involves healthy lifestyle promotion through moderate calorie restriction, moderate increase in physical activity and change in dietary composition. Treatment of individual components aims to control atherogenic dyslipidemia using fibrates and statins, elevated blood pressure, and hyperglycemia. While no single treatment for the metabolic syndrome as a whole yet exists, emerging therapies offer potential as future therapeutic approaches.