Inflammation, obesity and comorbidities: the role of diet (original) (raw)
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Obesity, inflammation and diet
Pediatric gastroenterology, hepatology & nutrition, 2013
Obesity is a state in which there is an over-accumulation of subcutaneous and/or abdominal adipose tissue. This adipose tissue is no longer considered inert and mainly devoted to storing energy; it is emerging as an active tissue in the regulation of physiological and pathological processes, including immunity and inflammation. Adipose tissue produces and releases a variety of adipokines (leptin, adiponectin, resistin, and visfatin), as well as pro- and anti-inflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-4, IL-6, and others). Adipose tissue is also implicated in the development of chronic metabolic diseases such as type 2 diabetes mellitus or cardiovascular disease. Obesity is thus an underlying condition for inflammatory and metabolic diseases. Diet or dietary patterns play critical roles in obesity and other pathophysiological conditions. A healthy diet and some nutrients are generally considered beneficial; however, some dietary nutrients are still considered c...
Obesity, inflammation, and insulin resistance
Gastroenterology, 2007
White adipose tissue (WAT) is considered an endocrine organ. When present in excess, WAT can influence metabolism via biologically active molecules. Following unregulated production of such molecules, adipose tissue dysfunction results, contributing to complications associated with obesity. Previous studies have implicated pro-and anti-inflammatory substances in the regulation of inflammatory response and in the development of insulin resistance. In obese individuals, pro-inflammatory molecules produced by adipose tissue contribute to the development of insulin resistance and increased risk of cardiovascular disease. On the other hand, the molecules with anti-inflammatory action, that have been associated with the improvement of insulin sensitivity, have your decreased production. Imbalance of these substances contributes significantly to metabolic disorders found in obese individuals. The current review aims to provide updated information regarding the activity of biomolecules produced by WAT. Uniterms: Obesity. Inflammation. Adipose tissue. Adipokines. Insulin resistance. O tecido adiposo branco (WAT) é considerado um órgão endócrino, que, em excesso, é capaz de controlar o metabolismo, pela ação de moléculas biologicamente ativas. A produção desregulada destas substâncias pela disfunção do tecido adiposo pode contribuir para as complicações presentes na obesidade. As pesquisas atuais têm esclarecido fatores e mecanismos envolvidos na atuação de substâncias pró e anti-inflamatórias na modulação da inflamação e da resistência à insulina. Em indivíduos obesos, as moléculas pró-inflamatórias produzidas pelo tecido adiposo têm sido implicadas como fator contribuinte para o desenvolvimento da resistência à insulina e aumento do risco de doença cardiovascular. Por outro lado, as moléculas com ação anti-inflamatória, que atuam na melhora da sensibilidade à insulina, têm sua produção reduzida. O desequilíbrio entre essas substâncias contribui de forma significativa para as desordens metabólicas presente em indivíduos obesos. Assim, esta revisão visa a trazer informações atualizadas sobre a atuação de moléculas secretadas pelo tecido adiposo.
Obesity and inflammation: the linking mechanism and the complications
Archives of Medical Science, 2016
Obesity is the accumulation of abnormal or excessive fat that may interfere with the maintenance of an optimal state of health. The excess of macronutrients in the adipose tissues stimulates them to release inflammatory mediators such as tumor necrosis factor α and interleukin 6, and reduces production of adiponectin, predisposing to a pro-inflammatory state and oxidative stress. The increased level of interleukin 6 stimulates the liver to synthesize and secrete C-reactive protein. As a risk factor, inflammation is an imbedded mechanism of developed cardiovascular diseases including coagulation, atherosclerosis, metabolic syndrome, insulin resistance, and diabetes mellitus. It is also associated with development of non-cardiovascular diseases such as psoriasis, depression, cancer, and renal diseases. On the other hand, a reduced level of adiponectin, a significant predictor of cardiovascular mortality, is associated with impaired fasting glucose, leading to type-2 diabetes development, metabolic abnormalities, coronary artery calcification, and stroke. Finally, managing obesity can help reduce the risks of cardiovascular diseases and poor outcome via inhibiting inflammatory mechanisms.
Obesity and inflammation: A new look at an old problem
Current Atherosclerosis Reports, 2007
Obesity is a highly prevalent disease with multiple implications for cardiovascular morbidity and mortality. The traditional view of obesity is that excessive adipose tissue represents a passive storage depot of excess energy. However, obesity has been demonstrated to be a highly active endocrine organ with multiple metabolic pathways that interact with classic cardiac risk factors. The role of inflammation in atherosclerosis has been clarified by the ready availability of a variety of markers, including C-reactive protein, adiponectin, tumor necrosis factor-α, hemostatic markers, resistin, and a variety of emerging markers such as interleukins and adhesion molecules. Adipose tissue has been demonstrated to be the site of synthesis of a variety of proteins that are intimately involved in the regulation of inflammation. The concept that obesity represents an inflammatory state has gained credence over the past decade and has provided insights into the mechanisms of atherosclerosis and risk factor interaction.
Diet Induction of Monocyte Chemoattractant Protein1 and its Impact on Obesity
Obesity, 2005
Objective: To examine the effect of a high-fat diet on gene expression in adipose tissues and to determine induction kinetics of adipose monocyte chemoattractant protein-1 and −3 (MCP-1 and MCP-3) in diet-induced obesity (DIO) and the effect of a lack of MCP-1 signaling on DIO susceptibility and macrophage recruitment into adipose tissue.Research Methods and Procedures: Obese and lean adipose tissues were profiled for expression changes. The time-course of MCP-1 and MCP-3 expression was examined by reverse transcriptase-polymerase chain reaction. Plasma MCP-1 levels were determined by enzyme-linked immunosorbent assay (ELISA). Chemokine receptor-2 (CCR2) knockout mice were placed on the high-fat diet to determine DIO susceptibility. Macrophage infiltration in adipose tissue was examined by immunohistochemistry with F4/80 antibody.Results: DIO elevated adipose expression of many inflammatory genes, including MCP-1 and MCP-3. Adipose MCP-1 and MCP-3 mRNA levels increased within 7 days of starting a high-fat diet, with elevation of plasma MCP-1 detected after 4 weeks on the diet. The induction of MCP-1 and MCP-3 expression preceded that of tumor necrosis factor-α. The elevated plasma MCP-1 concentration in obese mice was partially reversed by treatment with AM251. No change in DIO susceptibility and macrophage accumulation in adipose tissue were observed in CCR2 knockout mice, which lack the MCP-1 receptor CCR2.Discussion: A high-fat diet elevated adipose expression of inflammatory genes, including early induction of MCP-1 and MCP-3, supporting the view that obese adipose tissues contribute to systemic inflammation. However, despite increased MCP-1 in obesity, disruption of MCP-1 signaling did not confer resistance to DIO in mice or reduce adipose tissue macrophage infiltration.
Nutrition, 2008
Circulating levels of adiponectin are low in obesity and metabolic disorders associated with increasing fat mass including insulin resistance and dyslipidemia. Body fat stores may be positively related to intake of dietary fat, but little is known of mechanisms by which serum adiponectin may be regulated through diet. We investigated acute effects of a high-fat load and changes in fatty acid saturation on circulating adiponectin and associated mediators of inflammation including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP). A high-fat test meal (59 +/- 4 g fat; 71% of energy as fat) containing a high ( approximately 71:29) or low ( approximately 55:45) ratio of saturated:unsaturated fatty acids was given at breakfast on two occasions. Blood samples were collected at 0 (baseline), 1, 3, and 6 h for measurement of adiponectin, IL-6, TNF-alpha, and high-sensitivity CRP. A fat-exclusion lunch, snack, and dinner were also given and blood samples collected at 10 and 24 h. Eighteen healthy, lean men completed the trial. There was no evidence of acute change in circulating adiponectin in response to the lipid bolus or a differential effect of fatty acid saturation on adiponectin, high-sensitivity CRP, or IL-6 (P > 0.05). IL-6 increased over 6 h on both treatments (time, P < 0.05). TNF-alpha decreased on the high saturated:unsaturated fatty acid treatment (treatment by time, P < 0.05). There were no significant correlations between circulating adiponectin and insulin on either dietary treatment in these normoglycemic subjects. Acute changes in the content of saturated and unsaturated fatty acids had no adverse effect on postprandial circulation of the adipose-related factors adiponectin, IL-6, TNF-alpha, or high-sensitivity CRP.
Journal of physiology and pharmacology: an official journal of the Polish Physiological Society
Obesity and obesity related diseases are a major public health problem. Recent studies have shown that fat tissue is not a simple energy storage organ, but exerts important endocrine and immune functions. These are achieved predominantly through release of adipocytokines, which include several novel and highly active molecules released abundantly by adipocytes like leptin, resistin, adiponectin or visfatin, as well as some more classical cytokines released possibly by inflammatory cells infiltrating fat, like TNF-α, IL-6, MCP-1 (CCL-2), IL-1. All of those molecules may act on immune cells leading to local and generalized inflammation and may also affect vascular (endothelial) function by modulating vascular nitric oxide and superoxide release and mediating obesity related vascular disorders (including hypertension, diabetes, atherosclerosis, and insulin resistance) but also cancer or non-alcoholic fatty liver diseases. Present review, in a concise form, focuses on the effects of major adipocytokines, characteristic for adipose tissue like leptin, adiponectin, resistin and visfatin on the immune system, particularly innate and adaptive immunity as well as on blood vessels. Macrophages and T cells are populating adipose tissue which develops into almost an organized immune organ. Activated T cells further migrate to blood vessels, kidney, brain and other organs surrounded by infiltrated fat leading to their damage, thus providing a link between metabolic syndrome, inflammation and cardiovascular and other associated disorders. Ceretain treatments may lead to significant changes in adipocytokine levels. For example include beta-2 adrenoreceptor agonists, thiazolidinediones as well as androgens lead to decrease of plasma leptin levels. Moreover future treatments of metabolic system associated disorders should focus on the regulation of adipocytokines and their modes of action.
Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj Napoca Veterinary Medicine, 2008
BACKGROUND Obesity, with all its comorbidities, is increasingly recognized as a major health problem (1). Recent literature indicates a link between the process of fat formation and inflammation (2,3). Obesity, alone or as a part of the metabolic syndrome, is characterized by a state of chronic low-level inflammation as revealed by raised plasma levels of inflammatory cytokines and acute-phase proteins. When adipocytes increase in size during weight-gain, they secrete tumor necrosis factor (TNF-α), which, in turn, stimulates monocyte chemoattractant protein MCP-1 release. MCP-1 recruits monocytes from the circulation, which infiltrate adipose tissue and stimulate adipocytes to produce the inflammatory cytokines (1). The altered production of pro inflammatory molecules (so-called "adipokines") by adipose tissue has been implicated in the metabolic complications of obesity. Compared with adipose tissue of lean individuals, adipose tissue of the obese expresses increased amounts of pro inflammatory proteins such as TNF-α, IL-6, iNOS (also known as NOS2), TGF-β1, C-reactive protein, soluble ICAM, and monocyte chemotactic protein-1 (MCP-1) and procoagulant proteins such as plasminogen activator inhibitor type-1 (PAI-1), tissue factor, and factor VII. That adipocytes express receptors for several pro inflammatory molecules (e.g., TNF-α, IL-6) supports models in which adipocytes were both the source and target of pro inflammatory signals (4). Obesity induces adipose tissue macrophage infiltration in both humans and mice (5). Macrophage numbers and/or macrophage inflammatory gene expression in white adipose tissue are positively correlated with adipocyte size and body mass index (BMI) in mice and negatively correlated with weight loss in obese humans (4). Macrophages are the predominant source of tumor necrosis factor-(TNF-) and a significant source of interleukin-6 and nitric oxide in white adipose tissue of obese (ob/ob, db/db) mice and humans (4,6). A "spike" in macrophage inflammatory gene expression in white adipose tissue immediately precedes or is coincident with the onset of hyperinsulinemia in murine dietinduced obesity. These observations implicate macrophage activation in the development of obesity associated white adipose tissue inflammation and insulin resistance (7). Chronic inflammation and angiogenesis are two processes that assemble together. These two phenomena have long been coupled together in many chronic inflammatory disorders with distinct etiopathogenic origin, including psoriasis, rheumatoid arthritis, Crohn's disease, diabetes, and cancer. Lately, this concept has further been substantiated by the
Inflammatory state of periaortic adipose tissue in mice under obesogenic dietary regimens
Journal of Nutrition & Intermediary Metabolism, 2016
High-fat diet or high-sugar diet causes obesity and a chronic low-grade inflammation that leads to the development of diabetes and cardiovascular diseases. Inflammation of the surrounding fat of thoracic aorta namely periaortic adipose tissue (PAAT) has been associated with increased prevalence of vascular diseases in obesity. C57Bl/6 male mice (12 weeks of age) fed a whole grain-based commercial diet (WGD), refined carbohydrate diet (RCD), refined carbohydrate diet plus sweetened condensed milk ad libitum (RCD þ CM) or high-fat diet (HFD) for eight weeks were studied. Serum fatty acid (FA) composition was evaluated by gas chromatography. The cellularity (as indicated by DNA and protein contents) and the inflammatory state (as indicated by the contents of TNF-a, IL-6, IL-1b, IL-10, VCAM-1, ICAM-1, leptin and adiponectin measured by ELISA) of the PAAT and thoracic aorta (TA) were evaluated. Both obesogenic regimens (RCD þ CM and HFD) increased the content of total fatty acids (FA) in serum and the cellularity of the PAAT compared to WGD. RCD þ CM increased serum monounsaturated fatty acid (MUFA) levels and HFD increased serum saturated fatty acid (SFA) levels compared to WGD. RCD (one of the diets used as control) and RCD þ CM increased the levels of TNF-a, IL-1b, IL-10 and VCAM-1 in the PAAT compared to WGD. Mice fed with HFD showed decreased contents of TNF-a, VCAM-1 and IL-10 in the PAAT compared to animals fed RCD. The RCD raised the levels of SFA in serum, cellularity and inflammatory state in the PAAT compared to WGD. In conclusion, the effects of obesogenic dietary regimens on PAAT can be interpreted differently when the results are compared with WGD or RCD. We found marked changes in the PAAT and no significant modifications in TA indicating this adipose tissue as the major starting point of vascular diseases.