Central Modulation of Neuroinflammation by Neuropeptides and Energy-Sensing Hormones during Obesity.

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type 2 diabetes mellitus 1 endocrinologydiseases
cortisol 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
metabolic syndrome 1 endocrinologydiseases
obesity 24 endocrinologydiseases

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cortisol 25569 [[64]]. Ghrelin seems to induce acute peripheral insulin resistance independent of growth hormone (GH), cortisol , and basal serum free fatty acids [[65]] and both insulin and ghrelin exert regulatory effects on each
Select Disease Character Offset Disease Term Instance
diabetes mellitus 13159 these molecular pathways have been widely identified in the generation of insulin resistance and type 2 diabetes mellitus in obese subjects. In fact, it has been proposed that the activation of T lymphocytes in adipose tissue
hyperinsulinemia 34625 mice [[99]]. Also, GRP120 stimulation by a selective agonist improved glucose tolerance, decreased hyperinsulinemia , increased insulin sensitivity and decreased hepatic steatosis in a DIO mice model [[100]]. Of note,
metabolic syndrome 4905 regulates body metabolism and plays an important role in the development of metabolic disorders such as metabolic syndrome and obesity. Obesity has been characterized as an atypical form of inflammation induced primarily by
obesity 1203 possessing resident immunological cells, called microglia. In this way, positive energy balance during obesity promotes an inflammatory state in the CNS. Saturated fatty acids from the diet have been pointed out
obesity 1915 this review, we will discuss the role of lipotoxicity associated with positive energy balance during obesity in proinflammatory response in microglia, B and T lymphocytes, and its modulation by neuropeptides.1.
obesity 3659 such as cancer, hypertension, cardiovascular disorders, and metabolic disorders including diabetes and obesity .The link between the immune system and the regulation of body energy metabolism has started to be understood
obesity 4928 and plays an important role in the development of metabolic disorders such as metabolic syndrome and obesity . Obesity has been characterized as an atypical form of inflammation induced primarily by the accumulation
obesity 5304 “metainflammation” or “metabolic inflammation” [[5]].Positive energy balance during maternal overnutrition or obesity lead to changes in plasma and tissue specific lipidomic profile that might promote inflammation. In
obesity 7043 Inflammation in the CNSEpidemiological data confirms a strong link between the increase in the level of obesity and the development of type 2 diabetes, indicating that for every kilogram of gained weight, at the
obesity 7287 increase in the diabetes rate [[11]]. Experimental evidence, in obese humans and animal models with obesity , suggests that the leakage of lipids from adipose tissue and ectopic accumulation of ceramides (a type
obesity 8232 processes in many cellular types of the body [[14]]. In this regard, it has been suggested that, during obesity , new lipid species, which are potentially toxic for the body's organs, are produced, including ceramides,
obesity 9169 peripheral immune system cells including B cells and T lymphocytes in genetic and nutritional models of obesity has proposed that the metabolic inflammation observed during obesity is able to colonize the CNS and
obesity 9238 genetic and nutritional models of obesity has proposed that the metabolic inflammation observed during obesity is able to colonize the CNS and promote central inflammation such as microglia activation [[1]]. Each
obesity 9629 that have been implicated in the process of neuroinflammation activation in a lipotoxic context during obesity .2.1. MicrogliaMicroglia represent a selective cell type with characteristics of CNS resident macrophages,
obesity 10194 acting as major APCs in the CNS [[20]].The relationship between lipotoxic damage in the context of obesity and the activation of central inflammation is based on evidence showing that the exposure of high fat
obesity 14998 inflammation.Activation and recruitment of lymphocytes to adipose tissue during positive energy balance in obesity also cause them to migrate to more distant borders and interact with CNS cells, including microglia,
obesity 18033 [42]].Unlike the role of macrophages and Th1 lymphocytes in the modulation of metabolic inflammation during obesity , the impact of B lymphocytes in this context has not yet been fully understood [[43]]. However, there
obesity 19399 partially true, since the elimination of B lymphocytes using a CD20-specific antibody in a murine model of obesity induced by high fat diet improved glucose tolerance, reduced insulin levels, and reduced the inflammatory
obesity 26703 (435 pg/mL) than nonobese patients (167 pg/mL) [[70]]. Although it has been stated that during obesity ghrelin plasma levels are decreased in obese individuals as a compensatory mechanism to reduce appetite
obesity 27059 hormone may be potentially related to a decrease in DAG concentration [[70]]. In fact, diet induced obesity (DIO) in mice by high fat diet exposure leads to 15% increase in preproghrelin mRNA-producing cells
obesity 27609 unacetylated form of ghrelin, but it has been reported that knocking down the GOAT gene protects mice from obesity induced diet, improves insulin sensitivity, and reduces adiposity when fed HFD and high glucose diet
obesity 28107 related to GOAT activity is potentially important to contribute to metabolic alterations observed during obesity and diabetes. This proposal is tested in recent reports showing that decreasing AG plasma levels associates
obesity 33708 polyunsaturated fatty acids (PUFAs) had beneficial effects on several metabolic related-diseases, such as obesity . For instance, omega-3 fatty acids (ω-3 PUFAs) inhibit mammary tumor progression in obese mice [[92]],
obesity 35313 recently that TBK1 may have a significant role in the microglia-mediated neuroinflammation observe during obesity [[28]]. In fact, it has been demonstrated that the administration of an specific TBK1-IKKε inhibitor
obesity 36237 a synthetic triterpenoids has been proposed as a potential therapeutic agent to treat diabetes and obesity ., due to its ability to inhibit ghrelin acylation by the human isoform of GOAT (hGOAT), these compounds
obesity 36583 inhibitor such as TBK1, and reducing AG plasma levels, might be potential pharmacologic treatments to obesity and metabolic disorders.5. ConclusionsWe contemplate that the activation inflammation associated central
obesity 39177 into the CNS via the BBB and may represent a molecular node during positive energy balance as is the obesity and maternal overnutrition.Figure 1Immunomodulatory mechanism exerted by neuropeptides in microglia
type 2 diabetes mellitus 13152 of these molecular pathways have been widely identified in the generation of insulin resistance and type 2 diabetes mellitus in obese subjects. In fact, it has been proposed that the activation of T lymphocytes in adipose tissue

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