Regulation of Immune Cell Function by PPARs and the Connection with Metabolic and Neurodegenerative Diseases.

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obesity 19 endocrinologydiseases
metabolic syndrome 3 endocrinologydiseases

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metabolic syndrome 1811 processes. Several of these pathologies, in which inflammation is a common denominator, are grouped under metabolic syndrome , including obesity, type 2 diabetes, cardiovascular disease, and fatty liver disease [[1]].Over the
metabolic syndrome 29835 informative.5. ConclusionsIn summary, inflammation has been shown to be a common denominator in both metabolic syndrome and NDDs, and targeting this inflammation from a therapeutic standpoint could potentially have beneficial
metabolic syndrome 30681 addressed. While many studies strongly suggest that beneficial effects of PPAR activation in the context of metabolic syndrome and NDDs can be explained by anti-inflammatory effects, direct proof of an important role for PPAR-induced
obesity 944 immune cell function, with a focus on macrophages and T cells, and how this was shown to contribute to obesity -associated inflammation and insulin resistance, atherosclerosis, and neurodegenerative disorders. We
obesity 1841 pathologies, in which inflammation is a common denominator, are grouped under metabolic syndrome, including obesity , type 2 diabetes, cardiovascular disease, and fatty liver disease [[1]].Over the past two decades, a
obesity 1990 and fatty liver disease [[1]].Over the past two decades, a clear link has been established between obesity -associated inflammation and the development of insulin resistance, which eventually leads to type 2
obesity 2545 the body’s increased need for insulin.Initially, studies showed that adipose tissue expansion in obesity is accompanied by an increase in cytokine and chemokine expression, such as tumor necrosis factor (TNF)-α,
obesity 2926 normally insulin-sensitive tissues, leading to insulin resistance. Later, it was demonstrated that this obesity -induced adipose tissue inflammation was largely the result of a shift in the balance of anti-inflammatory
obesity 3458 anti-inflammatory cytokines promote anti-inflammatory M2 polarized macrophages in adipose tissue. By contrast, obesity -associated adipose tissue expansion is accompanied by an increase in elastase-secreting neutrophils,
obesity 5553 goes both ways, since hypothalamic inflammation has been linked to the development and progression of obesity and its sequelae [[11],[12]]. Hypothalamic inflammation induced by obesogenic diets occurs before significant
obesity 5883 intake and energy expenditure, not only leading to overeating and weight gain, but also contributes to obesity -associated insulin resistance via altered neurocircuit functions. For example, hypothalamic inflammation
obesity 6246 counterpart of macrophages, play a major role in the neuroinflammation observed in both NDDs and the obesity -associated hypothalamic inflammation [[10],[11]]. The aggregates of amyloid β-peptide (Aβ) and α-synuclein,
obesity 24490 Metabolic DiseasesWe focus here on the role of PPARs in immune cells in the context of atherosclerosis and obesity -associated inflammation and insulin resistance. Again, for reasons mentioned above (Section 3.2), studies
obesity 25730 showed that macrophage-specific deletion of PPARγ predisposes mice to development of diet-induced obesity and insulin resistance [[50],[99]]. Similar results were obtained when the effect of PPARβ-deficient
obesity 25904 when the effect of PPARβ-deficient bone marrow or macrophage-specific PPARβ−/− on HFD-induced obesity and insulin resistance was studied [[65],[66]]. However, one study found preserved glucose tolerance
obesity 26369 them as macrophage specific. T cell-specific actions of PPARs, in the context of atherosclerosis or obesity -associated inflammation and insulin resistance, have largely been unexplored, with the exception of
obesity 26942 agonist treatment, is the specific role of PPARα in immune cells in the context of atherosclerosis and obesity -associated inflammation and insulin resistance.4.2. Neurodegenerative DiseasesEven though neuroinflammation
obesity 31551 imbalance between caloric intake and energy expenditure has been linked to both metabolic disease ( obesity and atherosclerosis) and neurodegenerative disorders. These pathologies all have a state of unresolved
obesity 31733 all have a state of unresolved chronic inflammation in common. The link between neuroinflammation and obesity and associated sequelae is bidirectional, since hypothalamic inflammation leads to uncoupling of caloric
obesity 31888 hypothalamic inflammation leads to uncoupling of caloric intake and energy expenditure, leading to obesity , but also contributes to obesity-induced insulin resistance (and subsequent type 2 diabetes) via altered
obesity 31921 to uncoupling of caloric intake and energy expenditure, leading to obesity, but also contributes to obesity -induced insulin resistance (and subsequent type 2 diabetes) via altered neurocircuit functions.Figure
obesity 32914 immune cells might contribute to the severity of the disease state both in metabolic diseases (e.g., obesity -induced insulin resistance) and neurodegenerative disorders NDDs

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