In this review article, Göran Hansson, a pioneer in the study of the role of inflammation in atherosclerosis and coronary artery disease, summarizes new ideas on the. Clinical Pathology Laboratory, Department of Experimental Oncology. Giovanni Paolo II National Cancer Institute, V. Le Orazio Flacco 6. Bari, Italy. 2. Department of Surgery Oncology. Giovanni Paolo II National Cancer Institute, V. NAFLD affects a large proportion of the US population and its incidence and prevalence are increasing to epidemic proportions around the world. Since the beginning of the century, the mammalian sirtuin protein family (comprising SIRT1–SIRT7) has received much attention for its regulatory role, mainly in. Stem-loop sequence hsa-mir-155 Accession: MI0000681: Symbol: HGNC:MIR155: Description: Homo sapiens miR-155 stem-loop: Gene family: MIPF0000157; mir-155: Community. A large number of changes, distant from the site or sites of inflammation and involving many organ systems, may accompany inflammation. In 1930 interest was focused. MiR-155 is a microRNA that in humans is encoded by the MIR155 host gene or MIR155HG. MiR-155 plays a role in various physiological and pathological processes. Le Orazio Flacco 6. Bari, Italy. 3. Department of Medical Oncology, Giovanni Paolo II National Cancer Institute, V. Le Orazio Flacco 6. Bari, Italy. How. Divella R, De Luca R, Abbate I, Naglieri E, Daniele A. Obesity and cancer: the role of adipose tissue and adipo- cytokines- induced chronic inflammation. J Cancer 2. 01. 6; 7(1. Available from. http: //www. Abstract. Adipose tissue in addition to its ability to keep lipids is now recognized as a real organ with both metabolic and endocrine functions. Recent studies demonstrated that in obese animals is established a status of adipocyte hypoxia and in this hypoxic state interaction between adipocytes and stromal vascular cells contribute to tumor development and progression. In several tumors such as breast, colon, liver and prostate, obesity represents a poor predictor of clinical outcomes. Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro- inflammatory factors and a consequent alteration of key signaling mediators which may be an active local player in establishing the peritumoral environment promoting tumor growth and progression. Therefore, adipose tissue hypoxia might contribute to cancer risk in the obese population. To date the precise mechanisms behind this obesity- cancer link is not yet fully understood. In the light of information provided in this review that aims to identify the key mechanisms underlying the link between obesity and cancer we support that inflammatory state specific of obesity may be important in obesity- cancer link. Keywords: adipocytes inflammation, adipocytokine, obesity, cancer. Introduction. Obesity, defined as abnormal excess accumulation of fat in adipose tissue, is a chronic low- grade inflammation. It is associated with a high risk of developing type 2 diabetes, metabolic syndrome cardiovascular disease, and several types of cancer . In tumors of breast, colon, liver and prostate, obesity represents a poor predictor of clinical outcomes. The precise mechanisms underlying this obesity- cancer link are not yet well understood. The definition of overweight and obesity according to WHO is defined by body mass index (BMI, weight/height m. BMI = 2. 5- 2. 9 kg/m. BMI . The adipose tissue in addition to its ability to keep lipids is now recognized as a real organ with both metabolic and endocrine functions . The knowledge about the structural and functional principles of adipose tissue has evolved considerably over the last ten years to get to today's conception of the adipose organ . At the cellular level it shows considerable heterogeneity, being constituted only half from mature adipocytes, and for the rest from preadipocytes, fibroblasts, endothelial cells, nerve cells and macrophages . The adipose tissue is divided in brown adipose (BAT) and in white adipose (WAT). The BAT is only a minimal part of the body, which in an adult is approximately 5. The most important knowledge we have today on the white adipose tissue regarding its role. Recently several studies have clearly demonstrated that the white adipose tissue is a true endocrine organ, a secretory organ metabolically active, and far from being inert tissue . It consists of different cell types and produces a number of adipokines and cytokines . Both stem cells (one every 5. These cells, when stimulated and activated, have the capacity to divide and give rise to new adipocytes. Once formed, the new white adipocytes will remain so until the death of the individual: they can then increase or decrease in volume but not in number . It is therefore important to prevent an excessive increase of adipose tissue and the number of adipocytes, especially in children, in which this phenomenon would condemn them, with high probability, to remain obese for the rest of life . How to Tone Your Blood Vessels and Reduce Your Risk of Heart Disease. Saturday, July 07, 2007 by: Jack Challem Tags: blood vessels, heart health, health news. Through words and images, the Journal has studiously reported the gradual transformation of innumerable aspects of respiratory medicine across the last hundred years. Find patient medical information for SPEARMINT on WebMD including its uses, effectiveness, side effects and safety, interactions, user ratings and products that have it. Table 1. Diagnostic criteria for obesity in according to WHO classification. Category. BMI value(kg/mq)Underweight. Adipocytes, to ascertaining which of lipids, vary their size (diameter 2. Adipocytes modulate a variety of physiological responses which include the metabolism of lipids and glucose, inflammation, blood pressure and ultimately angiogenesis and homeostasis . Body fat may increase in two ways (Figure 2): Hypertrophy: increase in the volume of adipocytes. Hyperplasia: increase in the number of adipocytes. The hyperplasia of adipose tissue occurs during certain periods of life (last half of pregnancy, the first year of life and the beginning of puberty) or in special situations, such as obesity. In all other cases remain the phenomena of hypertrophy . It is important to remember that the hyperplasia, unlike hypertrophy, is an irreversible process, so even in the event of slimming exasperated cells does not decrease in number but, only in their volume . When an obese person slimming, fat cells lose a certain amount of fat, reducing their volume, but the number of adipocytes cannot be reduced. That's the reason a person with obesity regained in the short term much of body fat lost when suspending the crash diet. An excessive accumulation of triglyceride inside white adipocytes causes a progressive increase of their volume. The adipocyte hypertrophy creates the risk of compromising the integrity of the adipocytes themselves who do not have unlimited power to increase the volume; therefore reached a certain limit an adipocyte excessively hypertrophic undergoes events of hypoxia and necrosis . These alterations are implicated in the mechanism of carcinogenesis, progression and tumor metastasis . Recent studies demonstrated that in obese animals is established a status of adipocyte hypoxia and in this hypoxic state interaction between adipocytes and stromal vascular cells contribute to tumor development and progression . In obesity, adipose tissue hypoxia may cause cellular mechanisms that lead to the development of insulin resistance, to a state of chronic inflammation with infiltration of macrophages, the reduction of adiponectin and increased of leptin, adipocyte death, ER stress and mitochondrial dysfunction . Therefore, adipose tissue hypoxia might contribute to cancer risk in the obese population . Hypoxia- inducible factor 1 alpha (HIF- 1a), is an important transcription factor that is regulated by hypoxia and in tumors leads to increased vascularization. HIF- 1a is involved in the regulation of transcription of genes implicated in the mechanisms of carcinogenesis. These include angiogenesis, cell survival, invasion and metabolism of glucose. Finally, HIF- 1a was associated with an increase occurrence of metastases. Furthermore HIF- 1a inhibition might improve sensitivity of tumors to radiation . Figure 2. Adipocyte hypertrophy and hyperplasia induces an inflammatory cascade and accumulation of immune cells, activation of leukocytes, endothelial cells coupled with angiogenesis, adipogenesis and death of adipocytes. Excessive adipose tissue is related to the changes of the lipids concentrations in the circulation, levels of species reactive oxygen as well as to secretion of adipokines and circulating hormones. The hypertrophy and hypoxia of adipose tissue cause chronic inflammation. Thus, cytokines secreted by inflamed adipose tissue, production of angiogenic factors, infiltration of macrophages M1 and insulin resistance associated with obesity may favor stimulation of a favorable microenvironment for tumorigenesis. The adipocytes have a robust protein synthesis capable of producing specific proteins in norm- volume condition, but in the presence of hypertrophy undergo a change in their protein synthesis, with production of inflammatory proteins (cytokines) . While the majority of adipokines, such as tumor necrosis factor- . Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro- inflammatory factors and reduced adiponectin . Figure 4. Dysfunctional adipose tissue in obesity is associated with disturbed profile of mediators released from this tissue establishing a state of chronic inflammation. An increase of pro- inflammatory cytokines and leptin causes a down regulation of adiponectin. This results in a reduction of anti- inflammatory and anti- tumor activity explicated by adiponectin. In obesity high levels of pro- inflammatory cytokines such as TNF- . Adipose tissue play an active role in controlling the physiological and pathological process through various adipokines. Dysfunctional adipose tissue in obesity releases a disturbed profile of adipokines with elevated levels of pro- inflammatory factors like leptin, IL- 6 and TNF- alfa and reduced adiponectin that is protective against tumourigenesis. These adipokines have been implicated in cancer development and progression through their effects on insulin resistance, lipolysis and various inflammatory pathways. In the context of obesity, the hypertrophic expansion of adipose tissue induces local hypoxia, inflammatory activation and reactive angiogenesis, changes which favour tumourigenesis. From the functional viewpoint adipokines are polyvalent molecules, involved in a large number of physiological and pathological processes in fact modulate the sensitivity of peripheral tissues to insulin, regulate appetite, energy expenditure, and glucose and lipids metabolism, homeostasis, angiogenesis, blood pressure and all the axis of endocrine and reproductive systems . In addition, many appear to be strongly related to immunity and inflammation . Within this wide range of signals and protein factors, it is evident how the white adipose tissue plays an active role in controlling the physiological and pathological processes, in particular the metabolism and energy homeostasis .
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