p53 Functions in Adipose Tissue Metabolism and Homeostasis

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Term Occurence Count Dictionary
metabolic syndrome 4 endocrinologydiseases
obesity 24 endocrinologydiseases
rosiglitazone 1 endocrinologydiseasesdrugs
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 3 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
glucose intolerance 2 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 15491 is involved in adipocyte maintenance and nutrient homeostasis.3. p53 in Obesity and Adipose Tissue Insulin ResistanceObesity develops due to an imbalance between calorie intake and expenditure, which can be
Insulin 15959 to insulin resistance and type 2 diabetes mellitus, cardiovascular disease, and cancer [[25],[61]]. Insulin maintains glucose homeostasis by inhibiting glucose production (gluconeogenesis) in the liver and stimulating
Insulin 26666 stage, lipogenesis was slightly induced while inflammation was increased only after 18 weeks of HFD. Insulin resistance was also observed after 18 weeks and not present in mice after 2 weeks on HFD. Short-term
rosiglitazone 20764 vitro experiments showed that the anti-inflammatory effects of endogenously produced adiponectin or of rosiglitazone treatment reduced p53 expression in differentiated adipocytes. In line, addition of LPS-treated macrophage-conditioned
Select Disease Character Offset Disease Term Instance
diabetes mellitus 15892 major determinant for the metabolic syndrome and predisposes patients to insulin resistance and type 2 diabetes mellitus , cardiovascular disease, and cancer [[25],[61]]. Insulin maintains glucose homeostasis by inhibiting
glucose intolerance 21269 patients [[71]]. Opposing this finding, Ortega et al. found that p53 mRNA was inversely associated with glucose intolerance in human non-obese or obese subjects [[72]]. These seemingly contradictory results may be due to p53’s
glucose intolerance 24890 protein levels was noted in liver, kidney, or skeletal muscle. A similar degree of insulin resistance and glucose intolerance was observed in both mouse models, effects which were reversed after p53 inhibition by pifithrin or
hypoglycemia 36885 [[96]]. Additionally, liver-specific p53 knockout mice showed defects in amino acid metabolism and hypoglycemia under starvation [[97]]. In support of the progluconeogenic role of p53 are findings showing that p53
metabolic syndrome 6620 manipulation has become a promising strategy in the fight against obesity and its associated diseases (i.e., metabolic syndrome ). In this context, BAT activation and heat dissipation of energy or WAT features such as expandability,
metabolic syndrome 6894 targeted for therapeutic intervention [[23]]. In addition to its contribution to the development of the metabolic syndrome , obesity shows a strong association with cancer [[24],[25]]. Hence, tumor suppressors that contribute
metabolic syndrome 15815 most cases, systemic low grade chronic inflammation [[61]]. Obesity is a major determinant for the metabolic syndrome and predisposes patients to insulin resistance and type 2 diabetes mellitus, cardiovascular disease,
metabolic syndrome 55051 is a paucity of clinical data that evaluate p53 in adipose tissue in cohorts with varying degrees of metabolic syndrome or in clinical trials with acute and chronic nutrient challenges. Secondly, most data are available
obesity 2332 regulator of in vitro adipogenesis; (2) p53 levels in white AT are increased in diet-induced and genetic obesity mouse models and in obese humans; (3) functionally, elevated p53 in white AT increases senescence and
obesity 6577 whole body energy homeostasis, its manipulation has become a promising strategy in the fight against obesity and its associated diseases (i.e., metabolic syndrome). In this context, BAT activation and heat dissipation
obesity 6914 intervention [[23]]. In addition to its contribution to the development of the metabolic syndrome, obesity shows a strong association with cancer [[24],[25]]. Hence, tumor suppressors that contribute to regulation
obesity 7098 that contribute to regulation of cellular metabolism could present an important connection linking obesity and cancer. Paradoxically, despite p53 being frequently mutated in liposarcoma [[26],[27]] and its involvement
obesity 7908 tissue depots and the impact on systemic energy metabolism in the context of insulin resistance and obesity .2. p53 Signaling during In Vitro Adipogenic DifferentiationThe potential of WAT to store excess lipids
obesity 16752 regulator of insulin resistance together with muscle and liver.First evidence about p53’s involvement in obesity came from a study done in genetically obese (ob/ob) mice and showed p53 mRNA and protein induction in
obesity 17392 mice [[66],[67],[68],[69]], rats [[70]], and humans [[71],[72]] was observed. While its induction in obesity was reproduced in many studies, the mechanisms of p53 activation and its role on adipocyte function
obesity 17706 senescence is linked to impaired immune responses, leading to a chronic inflammatory state observed in both obesity and aging [[73]]. Obesity can be perceived as an accelerated form of adipose tissue senescence, linked
obesity 18962 resistant phenotype and p53 induction similar to that of Ay mice was also observed in mice with dietary obesity fed a high-fat, high-sucrose (HFHS) diet [[71]]. Adipose tissue-specific p53 knockout (via Fabp4-Cre
obesity 19958 (Sema3e)-plexin D1 axis mediates inflammation orchestrated by p53 induction in visceral WAT during dietary obesity [[67]]. Using several elegant in vivo approaches, it was demonstrated that p53 induces upregulation
obesity 22232 MDM2 was observed in human omental WAT [[72]], implying a disturbed MDM2-mediated p53 regulation in obesity . Mice harboring a mutation in Mdm2 (Mdm2C305F), which results in higher availability of Mdm2 due to
obesity 22504 consequently higher ubiquitination and reduced activity of p53, are resistant to high-fat diet (HFD)-induced obesity [[66]]. Reduction of p53 activity in Mdm2C305F mice resulted in lower adiposity, improved glucose tolerance,
obesity 24503 palmitic acid [[68]].In addition to mediating insulin resistance in the background of diet-induced obesity , p53 was also shown to mediate insulin resistance caused by excess growth hormone (Gh) [[76]]. Upregulation
obesity 26120 observed for pifithrin [[77],[78]].Perhaps the most comprehensive study of p53’s role in the etiology of obesity and insulin resistance considered the temporal and causative component of the events occurring in obesity
obesity 26226 obesity and insulin resistance considered the temporal and causative component of the events occurring in obesity development [[69]]. By using diet-induced obese mice, primary adipocytes, and the 3T3L1 cell line, Vergoni
obesity 29853 function of p53 in adipose tissue-resident macrophages, as they are the most abundant immune cell type in obesity -related inflammation. The strong influence of endothelial p53 on the development of obesity and related
obesity 29945 type in obesity-related inflammation. The strong influence of endothelial p53 on the development of obesity and related metabolic abnormalities has been demonstrated in research conducted in mice in which p53
obesity 30998 as a stress response protein. The experimental conditions during investigations of p53’s role in obesity or insulin resistance development can be interpreted as different stress circumstances that elicit a
obesity 34782 the previous chapter. The effects of HFD on p53 induction are usually monitored after the onset of obesity (6–20 weeks on HFD), except in one study which showed p53 induction in visceral WAT after 2 weeks
obesity 35902 sirtuin 1 (Sirt1)), resulting in reduced NAD+ levels and energy expenditure, ultimately leading to obesity . Disruption of Rpl11 binding by mutated Mdm2 blocked HFD-induced p53 activation and led to increased
obesity 36076 p53 activation and led to increased energy expenditure and improved resistance to the development of obesity [[66]]. The authors hypothesize that the p53 response to nutrient availability represents a conserved
obesity 36267 represents a conserved stress response needed for survival, which is causing unfavorable effects (e.g., obesity ) in modern societies where nutrients are chronically abundant [[66],[93]].Our own data confirmed the
obesity 40265 other hand, chronic nutrient abundance may result in chronic elevation of p53 signaling contributing to obesity and insulin resistance development [[69],[93]]. Although the experimental settings for prolonged starvation
obesity 41597 potential of activating energy dissipation in BAT to curb diseases arising from energy surplus amounting to obesity and its associated metabolic pathologies. Together, this research has established a crucial role for
type 2 diabetes mellitus 15885 is a major determinant for the metabolic syndrome and predisposes patients to insulin resistance and type 2 diabetes mellitus , cardiovascular disease, and cancer [[25],[61]]. Insulin maintains glucose homeostasis by inhibiting

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