Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue.

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rosiglitazone 2 endocrinologydiseasesdrugs
Liraglutide 1 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperglycemia 3 endocrinologydiseases
obesity 40 endocrinologydiseases

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Liraglutide 30713 modulate several serological markers including cholesterol, triglyceride, and insulin [[72]] (Figure 3). Liraglutide , another drug prescribed for weight loss, is known to improve type 2 diabetes in humans and works through
rosiglitazone 29989 of WAT toward brown fat. One study examined peptide-functionalized nanoparticles containing the TZD rosiglitazone or a prostaglandin E2 analog (16,16-dimethyl PGE2). When injected into adipose tissue vasculature of
rosiglitazone 30110 prostaglandin E2 analog (16,16-dimethyl PGE2). When injected into adipose tissue vasculature of mice, rosiglitazone promoted both transformation of WAT into brown-like adipose tissue and angiogenesis. Intravenous administration
Select Disease Character Offset Disease Term Instance
diabetes mellitus 47413 of lipid metabolism in humans [[103]].The reported susceptibility of children exposed to gestational diabetes mellitus to metabolic dysfunction might involve epigenetic programming of impaired BAT function. Fetal exposure
hyperglycemia 43377 improved glucose metabolism or prevent the development of obesity-associated insulin resistance and hyperglycemia [[98]].Other environmental changes, such as increased exercise or injury, are known to modulate the
hyperglycemia 47546 dysfunction might involve epigenetic programming of impaired BAT function. Fetal exposure to maternal hyperglycemia is associated with DNA methylation variations in genes involved in BAT genesis and activation. Maternal
hyperglycemia 48051 methylation levels are also correlated with cord blood leptin levels. These results suggest that maternal hyperglycemia during pregnancy is associated with altered placental DNA methylation patterns in BAT-related genes
obesity 1034 ongoing exploration of BAT has emphasized its therapeutic potential in addressing the global epidemics of obesity and diabetes. The recent appreciation that adult humans possess functional BAT strengthens this prospect.
obesity 1745 pharmacologic targets of BAT/Beige cells that have been reported to have therapeutic potential to combat obesity will be discussed.1. IntroductionThermogenesis is the process of biological heat generation that plays
obesity 2696 has been the subject of great interest for its therapeutic potential in the treatment of diabetes and obesity .BAT has been canonically associated with small mammals such as rodents and in newborns and infants of
obesity 4757 whole-body metabolism, insulin resistance, and the systemic low-grade inflammation associated with obesity [[9], [10]]. Additionally, WAT plays a role as a thermal insulator and also acts as a shock absorber
obesity 8359 circumstances [[17]–[19]].The activity of these cells has been negatively associated with diet-induced obesity in animal models, while ablation or loss of function has resulted in increased susceptibility to diet-induced
obesity 8477 models, while ablation or loss of function has resulted in increased susceptibility to diet-induced obesity . The last decade has witnessed numerous studies elucidating the physiology of BAT and beige cells, as
obesity 9470 Finally, we will provide perspective on the current therapeutic potential of BAT/Beige cells to combat obesity .2. Origins of Brown and Beige CellsBAT is one of the earliest fat depots to form during embryonic development
obesity 14043 apolipoprotein-2 (Ap2) driven adipose tissue specific overexpression of Ucp1 made mice resistant to obesity induced by a HFD, presumably due to ectopic synthesis of Ucp1 in WAT. These animals exhibited atrophy
obesity 15496 brown adipocytes recruitment, increased systemic energy expenditure, and protected against HFD-induced obesity . Cox2 is a downstream effector of β-adrenergic signaling in WAT and is required for the induction of
obesity 16369 and Ucp1 activity [[46]]. In addition, transgenic Alox5ap mice were protected against diet-induced obesity , insulin resistance, and inflammation, with browning of WAT being the prominent mechanistic finding
obesity 17888 via an adiponectin- driven cre led to increased energy expenditure and protection from HFD-induced obesity . Mitochondrial Ucp1 and other markers of brown fat are upregulated in both white and brown FLCN-null
obesity 20434 relative of the BMP family. TGF-β/Smad3 signaling downregulation confers protection against diet-induced obesity and associated comorbidities. Smad3-deficient mice gain significantly less weight when fed a HFD and
obesity 21045 hydrolase and is believed to play a role in endocannabinoid signaling as well as in the pathogenesis of obesity and liver steatosis [[57]]. Loss of ABHD6 in HFD-fed mice resulted in modestly reduced food intake,
obesity 26544 transgenic rodent models of browning has considerably advanced our understanding of the role of browning in obesity .4. Pharmacological/Chemical Agents and Additional Pathways Involved in Browning Advances in the area
obesity 27616 leanness but also retards the development of WAT hyperplasia during the early stages of diet-induced obesity [[66]]. Further studies by Guerra et al. demonstrated that treatment with CL 316243 increased levels
obesity 33614 browning of WAT. However, administration of dietary capsaicin did not protect TRPV1−/− mice from obesity [[77]] (Table 1). Importantly, in humans, a single oral dose of capsinoids, less-pungent capsaicin-like
obesity 34025 [[79]].Exercise, while not a pharmaceutical, is another commonly used intervention in the treatment of obesity and obesity-associated cardiometabolic complications. In 2012, Boström's group showed that the exercise-induced,
obesity 34037 [[79]].Exercise, while not a pharmaceutical, is another commonly used intervention in the treatment of obesity and obesity -associated cardiometabolic complications. In 2012, Boström's group showed that the exercise-induced,
obesity 36879 of symbiotic equilibrium between the host and gut microbiota contributes to the pathophysiology of obesity [[87]]. Since the microbiome plays a critical role in energy homeostasis and is a probable source of
obesity 37982 [[89]] showed that depletion of the gut microbiome helps to increase browning of WAT and ameliorate obesity and associated defects in leptin deficient and diet-induced obese mice. In this study, microbiome depletion
obesity 38844 mice exhibit lower body fat mass than their conventional counterparts and are resistant to HFD-induced obesity [[92]]. On the other hand, C57Bl/6J conventional male mice (with an intact microbiome) gain weight faster
obesity 39320 regulating BAT physiology [[93]], since gender-dependent differences in the development of diet-induced obesity were associated with changes in gut microbiome and BAT fat oxidation activity. Moreover, microbiome
obesity 39964 gut function, are known to modulate host energy metabolism, and contribute to the pathophysiology of obesity and diabetes [[95]]. While the role of SCFAs in regulation of host metabolism and their underlying mechanism(s)
obesity 40512 thereby increasing thermogenesis and fatty acid oxidation and providing protection against HFD-induced obesity in mice. In another study consistent with findings reported above, SCFAs produced in response to butyrate-producing
obesity 40689 SCFAs produced in response to butyrate-producing probiotics (VSL#3) significantly reduced HFD-induced obesity in mice. Moreover, preliminary findings from our groups have found that BAT histomorphology in mice
obesity 41175 two organ systems are linked may allow for the development of novel therapeutics for the treatment of obesity and diabetes.6. Browning in HumansUntil recently, it was widely believed that BAT was present in significant
obesity 41944 interest in understanding BAT function in adults and its possible use as a therapeutic agent to counter obesity .The BAT activity induced by cold exposure, diet, or pharmacological agents is correlated with increased
obesity 42680 support the notion that BAT serves an important role in modulating the risk of complications derived from obesity . Cold exposure is one of the more established environmental factors impacting variability in BAT activity.
obesity 43335 prolonged exposure to mild cold may lead to improved glucose metabolism or prevent the development of obesity -associated insulin resistance and hyperglycemia [[98]].Other environmental changes, such as increased
obesity 48831 induce brown and beige adipocyte activity but the side effects of these compounds limit their use in obesity treatment. Furthermore, species variations in pharmacological responses may result in practical obstacles.
obesity 50532 consequences inherent in some browning regimes will be important.8. Summary and ConclusionThe epidemic of obesity and diabetes presents significant global health concerns and supports further investigation into the
obesity 52310 plant-based products) that induce browning/browning in adipose tissue and provide protection from HFD-induced obesity .Browning agentsEffect on browning and metabolic outcomeReferenceGain of function/overexpressionUcp1Less
obesity 52482 outcomeReferenceGain of function/overexpressionUcp1Less lipid accumulation in adipocytes, resistance to HFD-induced obesity , beige cell phenotype in WAT, atrophy of BAT, and reduced Ucp1 and mitochondrial DNA content in BAT[[38],
obesity 52932 increased thermogenesis, attenuated weight loss and energy expenditure, and protection against HFD-induced obesity [[44], [45]]LXA4Higher LXA4 levels were related to browning of WAT, leaner body type, increased energy
obesity 53225 signaling was associated with reduced fat mass and browning of WAT and protection against HFD-induced obesity [[48]]PtenBAT in Pten-overexpressing mice had high levels of Ucp1 and increased energy expenditure[[49]]AM2Overexpression
obesity 53548 Pgc1α, Prdm16, and Ucp1 in adipocytes, induction of browning in WAT, and protection against HFD-induced obesity [[52]]Loss of function/knockdownBMP7Absence of BMP7 led to reduced interscapular BAT at birth[[53], [54]]Smad3/TgfbImproved
obesity 53770 [54]]Smad3/TgfbImproved glucose homeostasis with induction of beige cells in WAT which provided protection against obesity and increased mitochondrial bioenergetic profile of WAT[[56]]ABHD6Increased energy expenditure, cold-induced
obesity 53996 thermogenesis, Ucp1 expression in WAT, fatty acid oxidation, browning of WAT, protection against HFD-induced obesity , and associated complications[[58]]GaActivation of Gα signaling abrogates brown adipogenesis, whereas
obesity 55802 expenditure[[61]]ButyrateIncreased expression of Ucp-1 and Pgc1α and protected high fat diet-induced obesity in mice[[73]]RapamycinβAR-dependent increase in Ucp1 expression and expansion of beige adipocyte in
obesity 56541 Pgc1α and Prdm16 and induced browning in adipose tissue, and provided protection from HFD-induced obesity [[77]

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