Obesity, Inflammation, Toll-Like Receptor 4 and Fatty Acids.

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Term Occurence Count Dictionary
diabetes mellitus 1 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 28 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 2 endocrinologydiseasesdrugs
alpha-linolenic acid 2 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 30977 and the differentiation of myeloid cells, including the TLR2, TLR4, and TLR9 receptors [[92],[93]]. Insulin has a suppressive effect on the expression of TLR4 and on the activity of the PU.1 transcription factor;
Insulin 48413 GPR120, G-protein coupled receptor 120; EPA, eicosapentaenoic acid; DHA, Docosahexaenoic acid; IRS-1, Insulin receptor substrate 1; Ser-P, phosphorylated serine residues; PPARγ, Peroxisome proliferator-activated
alpha-linolenic acid 41551 which are involved in the resolution of inflammation and healing [[21],[25],[131]]. The ingestion of alpha-linolenic acid can also modulate the inflammatory response in humans. For example, Caughey et al. [[132]] observed
alpha-linolenic acid 41862 mononuclear cell cultures that were obtained from healthy subjects who consumed approximately 14 g/day alpha-linolenic acid for four weeks as compared to baseline and to a control group. The effect of α-linolenic acid may have
Select Disease Character Offset Disease Term Instance
diabetes mellitus 962 inflammatory condition that is directly involved in the etiology of cardiovascular diseases, type 2 diabetes mellitus , and certain types of cancer. The classic inflammatory response is an acute reaction to infections or
glucose intolerance 19602 intestinal lumen to the blood circulation. This metabolic endotoxemia is associated with increased body fat, glucose intolerance , and increased expression of proinflammatory mediators and macrophage infiltration in white adipose
hyperglycemia 10451 these animals to insulin action, establishing a link between inflammation, insulin resistance, and hyperglycemia . Macrophages from the stromal vascular fraction of adipose tissue appear to be the main cell type that
metabolic syndrome 1250 homeostasis. However, the inflammatory process that was observed in individuals affected by obesity and metabolic syndrome differs from the classical inflammatory response in certain respects. This inflammatory process manifests
obesity 1238 resolution and homeostasis. However, the inflammatory process that was observed in individuals affected by obesity and metabolic syndrome differs from the classical inflammatory response in certain respects. This inflammatory
obesity 1557 The toll-like receptor 4 (TLR4) signaling pathway is acknowledged as one of the main triggers of the obesity -induced inflammatory response. The aim of the present review is to describe the role that is played
obesity 2806 increased to 27.5% of adults and 47.1% of children in the past three decades [[5]]. The prevalence of obesity is currently higher in developed countries; nevertheless, approximately two-thirds of the obese population
obesity 3390 these age groups) in the United States. It is estimated that approximately 300,000 people die due to obesity in the United States (U.S.) every year, which is the second highest cause of preventable death [[8]].
obesity 3683 and cancer stand out among the main health issues that are responsible for morbidity related to the obesity [[9]]. Obesity treatment and the treatment of its associated complications in developing countries has
obesity 4651 including genetic, metabolic, behavioral, and environmental ones. Accordingly, the dramatic increase in obesity prevalence rates suggests that behavioral and environmental components are the main factors that are
obesity 4776 suggests that behavioral and environmental components are the main factors that are responsible for obesity , with an emphasis on eating habits and exercise. With regard to eating, modern societies converge to
obesity 5154 and carbohydrate, especially sugars, that are found in these food types, a fact that contributes to obesity development [[13],[14]].The profile of fatty acids that are present in a diet may also be relevant to
obesity 5264 development [[13],[14]].The profile of fatty acids that are present in a diet may also be relevant to obesity . It is worth highlighting that, according to anthropological and epidemiological studies, humans from
obesity 6096 response, which is linked to the physiopathology of different non-transmissible chronic diseases, such as obesity , DM2, cardiovascular diseases, hypertension, and cancer [[15],[16],[17]]. 2. Inflammation, Adipose Tissue
obesity 9888 present at lower intensities than has been seen in the classic inflammatory diseases. Evidence that obesity results in inflammation started emerging in the 1990s. This inflammation is directly involved in the
obesity 11499 expressed on monocytes present in peripheral blood and on adipose tissue macrophages. This implies that obesity favors the process of migration of blood monocytes into the visceral adipose tissue of obese individuals,
obesity 12647 activity [[40]]. In this context, individuals with low amounts of BAT would be prone to the development of obesity . Studies in animals lacking BAT or uncoupling protein 1 (UCP1) have clearly demonstrated the involvement
obesity 12820 have clearly demonstrated the involvement of BAT thermogenesis in the protection against diet-induced obesity (DIO) [[41]]. Decreasing BAT activity or the removal of BAT in mice provokes increased glycemia and
obesity 14655 to insulin resistance in obese patients [[48]].Among the inflammatory biomarkers that are related to obesity , IL-6 favors insulin-action resistance in obese individuals due to the induction of the cytokine signaling
obesity 15322 allowing a better understanding of the IL-6 effect on the insulin-action resistance that is induced by obesity [[49]]. Understanding that the immune system and different metabolic pathways are closely related to
obesity 15537 other, as well as that they are functionally dependent, is essential for studies that are focused on obesity and on its possible metabolic repercussions. Thus, signaling pathways that are responsive to nutrient
obesity 15768 presence of pathogens are evolutionarily conserved and greatly integrated [[50]]. The excessive intake of obesity -associated nutrients can be detected by innate recognition receptors, and this results in the activation
obesity 17570 [[58]]. It seems likely that the chronic low-grade inflammation that develops in adipose tissue with obesity is “transferred” to these other tissues through the appearance of active inflammatory mediators
obesity 17733 appearance of active inflammatory mediators in the bloodstream. In the context of inflammation and obesity , the role of gut microbiota in the development of metabolic disease should be noted. Studies have shown
obesity 18855 intestinal microbiota plays in energy homeostasis and its potential involvement in the etiology of obesity . Germ-free mice are resistant to diet -induced adiposity, which is associated with increased activity
obesity 23582 hyaluronic acid, polysaccharide fragments of heparan sulfate, and fibrinogen [[78]]. In the context of obesity , the increase in the plasma fibrinogen levels, which represents a positive acute phase protein, acts
obesity 29677 fact that points towards the causal role played by TLR4 in metabolic changes driven by over-eating and obesity [[87],[88]].Humans with type I diabetes exhibit a greater expression of TLR2 and TLR4 in the cellular
obesity 31217 effect of the hormone would be expected to be reduced due to the insulin-action resistance related to obesity . Such a reduction would increase the expression of TLR4 in peripheral blood monocytes [[94]]. In view
obesity 32985 blood mononuclear cells. This reinforces the potential importance of postprandial inflammation for obesity , DM2, and cardiovascular disease physiopathology [[98],[99]]. A high-fat meal also leads to increased
obesity 46381 context, the TLR4 signaling pathway has been recognized as one of the main triggers in increasing the obesity -induced inflammatory response. This pathway responds to the increased exposure to saturated fatty acids
obesity 46550 increased exposure to saturated fatty acids and to LPS. Both of these are relevant in the context of obesity , with saturated fatty acids arising from within the adipose tissue triglyceride stores and the LPS arising
obesity 46883 increases insulin resistance, both locally and systemically, so contributing to the co-morbidities of obesity , like DM2. Studies indicate that omega-3 fatty acids, namely EPA and DHA, have an anti-inflammatory
type 2 diabetes mellitus 955 to an inflammatory condition that is directly involved in the etiology of cardiovascular diseases, type 2 diabetes mellitus , and certain types of cancer. The classic inflammatory response is an acute reaction to infections or

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