Microglia activation due to obesity programs metabolic failure leading to type two diabetes.

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Term Occurence Count Dictionary
diabetes mellitus 2 endocrinologydiseases
glucose intolerance 2 endocrinologydiseases
hyperglycemia 1 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases
hypertriglyceridemia 1 endocrinologydiseases
hyperlipidemia 2 endocrinologydiseases
metabolic syndrome 12 endocrinologydiseases
obesity 51 endocrinologydiseases
type 2 diabetes mellitus 2 endocrinologydiseases

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diabetes mellitus 1682 an important risk factor for the morbidity and mortality associated with metabolic syndrome, type 2 diabetes mellitus , hypertension, dyslipidemia, cancer, neurodegenerative diseases and other non-communicable chronic diseases.[1]
diabetes mellitus 35323 favorable drug target since inhibition of the molecular binomial TBK1/IKK-ɛ prevents generation of type 2 diabetes mellitus in obese mice.[96] In this context, our research group has demonstrated that stimulation with saturated
glucose intolerance 28178 macrophages and B cells to the SNC, which promotes the generation of inflammation.[63] The link between glucose intolerance and central inflammation was reported by Kumar M (2014), showing that in the genetic diabetic model
glucose intolerance 31496 diet exposed, leading to bone marrow-derived monocytic cells accumulates and promoting obesity and glucose intolerance .[79] These evidences indicate that hypothalamus seems to be an early target of inflammation during positive
hyperglycemia 16282 inducing apoptosis through the activation of NF-κB. Moreover, blockage of IL-1β production reduces hyperglycemia and tissue inflammation.[36], [37] In a recent study, it was demonstrated that a high content of fatty
hyperinsulinemia 11029 obese humans.[23] Subsequently, was showed a positive correlation between the degree of obesity and hyperinsulinemia , and TNF-α levels and mRNA in adipose tissue.[24] Additionally, molecular markers of inflammation have
hyperinsulinemia 28822 modulates body glucose homeostasis, supporting that hypothalamic TNFα administration to rats leads to hyperinsulinemia and insulin resistance in liver and skeletal muscle,[65]and also generates pancreas dysfunction.[66],
hyperlipidemia 1100 metabolic-related comorbidities like metabolic syndrome (insulin resistance, glucose tolerance, hypertension and hyperlipidemia ). Recent evidence suggests that microglia activation in the central nervous system (CNS) is a priority
hyperlipidemia 38424 activation of NF-κB during obesity, will be deciphered.[105]Figure 1Microglia cytokine secretion during hyperlipidemia . Excess of saturated fatty acids (SFA) induce heterodimerization of toll-like receptor 1 (TLR1) with
hypertriglyceridemia 14294 of IL-6 by adipose tissue could directly affect liver metabolism by inducing secretion of VLDL and hypertriglyceridemia , through the portal venous system.[32] Similarly, the action of this cytokine inhibits phosphorylation
metabolic syndrome 1024 in obesity. Chronic inflammation modulates the development of metabolic-related comorbidities like metabolic syndrome (insulin resistance, glucose tolerance, hypertension and hyperlipidemia). Recent evidence suggests that
metabolic syndrome 1518 inflammatory stage in the brain in the context of obesity, and its influence on the development of metabolic syndrome and type two diabetes.IntroductionObesity is an important risk factor for the morbidity and mortality
metabolic syndrome 1655 diabetes.IntroductionObesity is an important risk factor for the morbidity and mortality associated with metabolic syndrome , type 2 diabetes mellitus, hypertension, dyslipidemia, cancer, neurodegenerative diseases and other
metabolic syndrome 5311 with genetic or nutritionally induced obesity.Lipotoxicity is a pathogenic mechanism in key organs for metabolic syndrome The epidemiological data confirm a strong relationship between the increase in the degree of obesity
metabolic syndrome 7057 immune system, triggering a process of chronic inflammation, which has been observed in obesity and metabolic syndrome .[16], [17] The first evidence demonstrating the presence of an inflammatory mechanism in diabetes was
metabolic syndrome 9352 liver disease, impaired function of the myocardium and β-cell insufficiency, respectively.Obesity and metabolic syndrome , a chronic inflammatory process induced by an imbalance in adipose tissue homeostasis and infiltrating
metabolic syndrome 10486 systemic inflammation. The importance of adipose tissue in promoting inflammation in obesity and the metabolic syndrome is evidenced by the presence of an inflammatory profile that correlates with macrophage infiltration
metabolic syndrome 10757 insulin resistance.[21], [22] The first evidence that linked the inflammatory process with obesity and metabolic syndrome was the overexpression of tumor necrosis factor alpha (TNF-α) in adipose tissue in obesity models in
metabolic syndrome 11572 tissue, which together contribute to the metabolic dysregulation and inflammation observed in obesity and metabolic syndrome . The role that each of these markers has in the development of inflammation and metabolic damage are
metabolic syndrome 13515 adipose tissue, production of IL-6, like TNF-α, is higher in visceral adipose tissue in obesity and metabolic syndrome .[31] One of the main actions of IL-6, is control of the liver's production of inflammatory molecules
metabolic syndrome 27620 of neuronal deficits in humans and if it is exacerbated during lipotoxic insult such as obesity or metabolic syndrome . We will address this question below.Inflammation of the nervous system during obesity is key in the
metabolic syndrome 37895 central and peripheral inflammation as a common pathogenic mechanism of the various manifestations of the metabolic syndrome . Inflammation in the CNS seems to be earlier than peripheral derangements. The TBK1/IKKɛ -NF-κB is
obesity 55 Title: Nutrition & DiabetesMicroglia activation due to obesity programs metabolic failure leading to type two diabetesAlternative Title: Microglia activation due to
obesity 165 programs metabolic failure leading to type two diabetesAlternative Title: Microglia activation due to obesity programs metabolic failureR Maldonado-RuizL Montalvo-MartínezL Fuentes-MeraA CamachoPublication date
obesity 928 inhibitor-1 (PAI-1), among others, has been associated with the development of chronic inflammation in obesity . Chronic inflammation modulates the development of metabolic-related comorbidities like metabolic syndrome
obesity 1469 molecular signals during microglia activation and inflammatory stage in the brain in the context of obesity , and its influence on the development of metabolic syndrome and type two diabetes.IntroductionObesity
obesity 2110 In children under age 5, 42 million worldwide were obese.[2] It has been proposed that increase in obesity is related to global trade liberalization, economic growth and rapid urbanization, changing diets and
obesity 2289 urbanization, changing diets and population lifestyles. Developing countries are the most affected by obesity and are predicted to continue to be so in the next years.[2] Statistical analysis predicts that by 2025,
obesity 2409 predicted to continue to be so in the next years.[2] Statistical analysis predicts that by 2025, global obesity will reach a prevalence of 18% in men and 21% in women.[2] Therefore, the study of molecular mechanisms
obesity 2533 prevalence of 18% in men and 21% in women.[2] Therefore, the study of molecular mechanisms involved in obesity is fundamental to tackle this major public health problem.Development of obesity requires a positive
obesity 2614 mechanisms involved in obesity is fundamental to tackle this major public health problem.Development of obesity requires a positive energy balance. However, to date, it is not entirely clear why the expansion of
obesity 3058 proportion of adipokines, promoting insulin resistance.[3], [4] The second hypothesis suggests that obesity promotes a failure of adipose tissue expansion and function, resulting in the release of fatty acids,
obesity 4443 The alterations in the lipid profile in obese humans can be reproduced in animal models with genetic obesity (ob/ob) or in obesity induced by a high-fat diet.[9] In a second study, genetic obesity increased triacylglycerols
obesity 4465 lipid profile in obese humans can be reproduced in animal models with genetic obesity (ob/ob) or in obesity induced by a high-fat diet.[9] In a second study, genetic obesity increased triacylglycerols levels
obesity 4531 with genetic obesity (ob/ob) or in obesity induced by a high-fat diet.[9] In a second study, genetic obesity increased triacylglycerols levels by 40% (values of 18 mm) and long-chain fatty acids by 25% (values
obesity 5076 (values of 5 μm), ceramides (values 140 μM), and diacylglycerol (600 μm) in muscle.[10] Overall, obesity in humans promotes increased triacylglycerol, ceramide and diacylglycerol levels that can be reproduced
obesity 5246 diacylglycerol levels that can be reproduced using animal models with genetic or nutritionally induced obesity .Lipotoxicity is a pathogenic mechanism in key organs for metabolic syndromeThe epidemiological data
obesity 5422 syndromeThe epidemiological data confirm a strong relationship between the increase in the degree of obesity and the development of diabetes, indicating that for every kilogram of weight gained, at the population
obesity 5711 experimental evidence in humans and animal models that lipotoxicity, associated with increased lipids in obesity , may cause alterations in pancreatic beta cell function, and in skeletal and cardiac muscle, and can
obesity 7045 overactivation of the immune system, triggering a process of chronic inflammation, which has been observed in obesity and metabolic syndrome.[16], [17] The first evidence demonstrating the presence of an inflammatory mechanism
obesity 7401 development of insulin resistance induced by fatty acids. This finding led to the discoveries of the obesity gene (ob) and a number of hormones derived from adipocytes such as leptin, adiponectin, and resistin,
obesity 8566 indicating active lipogenesis in macrophages.[20] With this, it is proposed that during the development of obesity there is adipocyte hypertrophy as a result of an increase in lipid-fat content and the presence of activation
obesity 10470 development of systemic inflammation. The importance of adipose tissue in promoting inflammation in obesity and the metabolic syndrome is evidenced by the presence of an inflammatory profile that correlates with
obesity 10745 humans with insulin resistance.[21], [22] The first evidence that linked the inflammatory process with obesity and metabolic syndrome was the overexpression of tumor necrosis factor alpha (TNF-α) in adipose tissue
obesity 10860 metabolic syndrome was the overexpression of tumor necrosis factor alpha (TNF-α) in adipose tissue in obesity models in mice and rats, and in adipose tissue and muscle in obese humans.[23] Subsequently, was showed
obesity 11017 and muscle in obese humans.[23] Subsequently, was showed a positive correlation between the degree of obesity and hyperinsulinemia, and TNF-α levels and mRNA in adipose tissue.[24] Additionally, molecular markers
obesity 11560 adipose tissue, which together contribute to the metabolic dysregulation and inflammation observed in obesity and metabolic syndrome. The role that each of these markers has in the development of inflammation and
obesity 12388 transcription of the TNF-α gene, promoting positive feedback to the inflammatory cascade.In conditions of obesity , the increase in plasma levels of TNF-α activates the PKC, IKKβ and JNK kinases, which consequently
obesity 13503 adipocytes. In adipose tissue, production of IL-6, like TNF-α, is higher in visceral adipose tissue in obesity and metabolic syndrome.[31] One of the main actions of IL-6, is control of the liver's production of
obesity 13925 and circulating levels of CRP.[32] In addition, IL-6 plays a central role in the relationship between obesity , inflammation, and coronary heart disease; in fact, intra- abnominal visceral adipose tissue can produce
obesity 14121 tissue can produce greater amounts of IL-6 than subcutaneous adipose tissue,[32] proving that central obesity increases cardiovascular risk in humans. Moreover, the production of IL-6 by adipose tissue could directly
obesity 15391 been found that this cytokine is increased in adipose tissue, where its release has been greater in obesity .[36] Normally, insulin action requires activation of the substrate of insulin receptor 1 (IRS1), a component
obesity 16547 IL-1β, IL-6 and IL-8 via activation of the inflammasomes NLRP3,[38] and induces the development of obesity and insulin resistance. This amplification of cell damage is associated with the production of IL-1β,
obesity 16882 IP-10, MIP-1α and MCP-4.[39] In conclusion, the diverse action of IL-1β promotes the development of obesity and insulin resistance.Interleukin-8 (IL-8)Serum levels of IL-8 correlate with liver inflammation and
obesity 17121 liver disease resulting from the accumulation of free fatty acids in that organ as a consequence of obesity .[40]Inflammasome NLPR3Inflammasomes are cytoplasmic multiprotein complexes that are part of the components
obesity 17788 biologically active forms, IL-1β and IL-18, and more recently, IL-6 and IL -8.[40], [41]Its relationship with obesity emerges from a recent study, which demostrated that obesity induces the assembly of inflammasome NLRP3
obesity 17848 and IL -8.[40], [41]Its relationship with obesity emerges from a recent study, which demostrated that obesity induces the assembly of inflammasome NLRP3 by macrophages in adipose tissue, which mediates insulin
obesity 18573 NLRP3 and IL-1β expression in subcutaneous adipose tissue. Moreover, direct participation of NLRP3 in obesity has been confirmed in studies that have shown that in gene-deficient mice fed with a high-fat diet,
obesity 20190 visceral fat and circulating adiponectin levels. This suggest an obvious relationship that exists between obesity and low levels of adiponectin in plasma, other research has linked low levels of adiponectin with insulin
obesity 20517 fatty acid oxidation, which reduces triglyceride (TG) content in the muscle and liver. However, during obesity , increased lipid reserves in insulin target tissues, such as muscle and liver, are generated, leading
obesity 21636 been associated with macrophage infiltration in adipose tissue of obese mice models and in humans with obesity .[49] In addition to CCL2, it is known that there is overexpression of other chemokines and their receptors
obesity 22258 atherosclerosis,[48] indicating that MRP-2 could be associated with the pathological inflammatory process related to obesity . Moreover, it has been reported that the macrophage inflammatory protein-1 alpha (MIP-1α or CCL3) and
obesity 23044 subcultures of obese subjects, playing an important role in promoting inflammation of adipose tissue in obesity .Serum amyloid A (SAA)SAA is an inflammatory protein codified by the SAA1 and SAA2 genes that appear
obesity 23584 IL-8, and CXCL1).[52] SAA is expressed in adipose tissue, and its expression is increased greatly in obesity ; circulating levels of SAA show a positive correlation with insulin resistance in obesity and type 2
obesity 23674 greatly in obesity; circulating levels of SAA show a positive correlation with insulin resistance in obesity and type 2 diabetes.[53], [54] Furthermore, SAA induces the production of IL-8 through the formyl peptide
obesity 27609 consequence of neuronal deficits in humans and if it is exacerbated during lipotoxic insult such as obesity or metabolic syndrome. We will address this question below.Inflammation of the nervous system during
obesity 27718 or metabolic syndrome. We will address this question below.Inflammation of the nervous system during obesity is key in the generation of metabolic damage and diabetesSubstantial evidence has shown that chronic
obesity 27843 generation of metabolic damage and diabetesSubstantial evidence has shown that chronic inflammation in obesity is not limited to adipose tissue, but invades borders that are farther away, and can be detected in
obesity 29704 and liver might lead to inflammation; however, it is also possible that central inflammation during obesity compromises vagal innervation/stimulation, promoting organ dysfunction and plasma glucose increase.The
obesity 31484 by high-fat diet exposed, leading to bone marrow-derived monocytic cells accumulates and promoting obesity and glucose intolerance.[79] These evidences indicate that hypothalamus seems to be an early target
obesity 32902 regard, in an elegant study Li J et al. demonstrated that activation of the IKKβ-NF-κB pathway during obesity , decreases neurogenesis, increases cognitive deterioration and degeneration of hypothalamic stem cells.[86],
obesity 37646 and cognitive impairment in an obese rodent model.[104]ConclusionsThe lipotoxicity associated with obesity generates metabolic disorders related to impaired glucose homeostasis. The molecular pathways linked
obesity 38347 together with TBK1/IKKɛ-NF-κB, which contribute to the regulation of the activation of NF-κB during obesity , will be deciphered.[105]Figure 1Microglia cytokine secretion during hyperlipidemia. Excess of saturated
type 2 diabetes mellitus 1675 diabetes.IntroductionObesity is an important risk factor for the morbidity and mortality associated with metabolic syndrome, type 2 diabetes mellitus , hypertension, dyslipidemia, cancer, neurodegenerative diseases and other non-communicable chronic diseases.[1]
type 2 diabetes mellitus 35316 favorable drug target since inhibition of the molecular binomial TBK1/IKK-ɛ prevents generation of type 2 diabetes mellitus in obese mice.[96] In this context, our research group has demonstrated that stimulation with saturated

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