Adipose Tissue-Specialized Immunologic Features Might Be the Potential Therapeutic Target of Prospective Medicines for Obesity.

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type 2 diabetes mellitus 2 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs
diabetes mellitus 2 endocrinologydiseases
obesity 17 endocrinologydiseases

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Insulin 18191 (Figure 2).4. Prospective Compounds for Local Adipose Tissue Chronic Inflammation and Obesity-Induced Insulin ResistanceBased on the above signaling pathways, prospective compounds have been studied for ameliorating
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diabetes mellitus 1582 and novel therapies for studying chronic inflammatory diseases, such as insulin resistance and type 2 diabetes mellitus .1. IntroductionThe World Health Organization (WHO) reported that more than 1.4 billion adults and older
diabetes mellitus 2170 other complications, such as atherosclerosis, cardiovascular problems, insulin resistance, and type 2 diabetes mellitus [[1]–[5]]. Adipose tissue also plays a crucial role in the generation of low-grade inflammation and
obesity 491 /2017Publication date (epub): 3/2017AbstractExcessive lipid accumulation in adipose tissue is either the source of obesity or the cause and result of chronic local inflammation, and recent studies indicate that the accumulation
obesity 1971 children under the age of 5 were classified as being obese in 2012. As a worldwide and dangerous epidemic, obesity increases the risk of some chronic diseases and induces low-grade inflammation with many other complications,
obesity 4658 of anti-inflammation to maintain homeostasis. In contrast, when the homeostasis is broken up, as in obesity , the number of macrophages will increase significantly, contributing up to 50% of the cells in adipose
obesity 5120 adipose tissue for disease treatments.2.1. Macrophage Recruitment and InfiltrationUnder diet-induced obesity conditions, the activation of macrophages results in chronic low-grade inflammation in local adipose
obesity 8331 Moreover, in a diet-induced obese mouse model, macrophage polarization can be regulated for influencing obesity -induced adipose tissue inflammation or insulin resistance. This might occur in interferon tau therapy,
obesity 12519 in type 2 diabetes that is related to insulin sensitivity. This may also be mainly associated with obesity -induced inflammation and insulin sensitivity. Additionally, in adipocytes, the accumulation of lipids,
obesity 16374 resistance. Therefore, the JNK pathway could also be a useful signaling pathway in the treatment of obesity -induced syndromes and diseases (Figure 1).3.3. Notch Signaling PathwayThe Notch signaling pathway could
obesity 16927 of Notch signaling in obese mice augmented Ucp1 expression, reduced blood glucose, and ameliorated obesity [[61]].In addition to the function of glucose reduction and obesity alleviation, the Notch signal modulated
obesity 16995 blood glucose, and ameliorated obesity [[61]].In addition to the function of glucose reduction and obesity alleviation, the Notch signal modulated macrophage polarization. The activation of A disinterring and
obesity 18352 prospective compounds have been studied for ameliorating local adipose tissue chronic inflammation with obesity -induced insulin resistance, also known as metaflammation [[64]]. Bitter melon has been found to ameliorate
obesity 21273 protein expression in the inflammation pathway, which might be a prospective drug for ameliorating obesity -associated chronic inflammation and improving insulin sensitivity. Both the structural analysis and
obesity 21697 or relevant diseases.5. ConclusionGenerally, as the number of obese people increases, a variety of obesity -related diseases and low-grade chronic inflammation cause injury in people's lives and health to different
obesity 21918 extents. These relative complications might obviously influence the health and quality of daily life. For obesity -induced inflammation, the possibility of macrophage accumulation has been concluded to have three aspects:
obesity 22263 shed light on the functional plasticity of macrophages and provide potential therapies to regulate of obesity -induced chronic inflammation. Moreover, AMPK, JNK, and Notch signaling should be the critical pathways
obesity 22549 pathways are associated with PPARγ or NF-κB to some extent. Therefore, the aim of the research on the obesity -induced local chronic inflammation mechanism might be focused on the mediators PPARγ or NF-κB, potentially
obesity 23451 might explain the pathogenesis of local insulin resistance and systemic insulin resistance induced by obesity in a local inflammatory method or low-grade inflammation. These discoveries could provide novel therapies
obesity 23593 low-grade inflammation. These discoveries could provide novel therapies or detection strategies for obesity -related inflammation and complications.Figure 1The AMPK and JNK signaling pathways are shown above.
type 2 diabetes mellitus 1575 thoughts and novel therapies for studying chronic inflammatory diseases, such as insulin resistance and type 2 diabetes mellitus .1. IntroductionThe World Health Organization (WHO) reported that more than 1.4 billion adults and older
type 2 diabetes mellitus 2163 many other complications, such as atherosclerosis, cardiovascular problems, insulin resistance, and type 2 diabetes mellitus [[1]–[5]]. Adipose tissue also plays a crucial role in the generation of low-grade inflammation and

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