Role of Cannabinoids in Obesity

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Liraglutide 1 endocrinologydiseasesdrugs
obesity 32 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Liraglutide 3006 [[7],[8],[9],[10],[11],[12]], Naltrexone/Bupropion [[13],[14],[15],[16],[17]], Lorcaserin [[7],[18],[19],[20]] and Liraglutide [[7],[21],[22],[23],[24]]. These medications share common pharmacodynamical mechanisms, except for Orlistat
Select Disease Character Offset Disease Term Instance
obesity 1044 that in response to various stimuli can turn from white to brown and could be protective against the obesity , enhancing energy expenditure. The conversion of white in beige adipose tissue is a potential new therapeutic
obesity 1173 expenditure. The conversion of white in beige adipose tissue is a potential new therapeutic target for obesity . Cannabinoid receptors (CB) regulate thermogenesis, food intake and inflammation. CB1 ablation or inhibition
obesity 1391 helps reducing body weight and food intake. Stimulation of CB2 limits inflammation and promotes anti- obesity effects by reducing food intake and weight gain. Its genetic ablation results in adiposity development.
obesity 1670 tissue towards beige or brown adipocytes, therefore their modulation can be considered potential anti- obesity target. CB1 principal localization in central nervous system represents an important limit. Stimulation
obesity 1868 limit. Stimulation of CB2, principally localized on peripheral cells instead, should facilitate the anti- obesity effects without exerting remarkable psychotropic activity.1. ObesityObesity is a public health problem.
obesity 2522 still obese at 35 years of age [[2]]. To date, lifestyle intervention constitutes the first line of obesity treatment. However, it is limited by low efficacy and high drop-out rates. Currently, only one medication,
obesity 2817 for weight loss in children and adolescents. In adults, the FDA have approved six different drugs for obesity treatment: Orlistat [[3],[4],[5],[6],[7]], Phentermine/Topiramate [[7],[8],[9],[10],[11],[12]], Naltrexone/Bupropion
obesity 4860 and their induction or recruitment, together with the activation of BAT, could be protective against obesity [[28]] enhancing body energy expenditure. Several activators have been associated with WAT browning,
obesity 5129 capsaicin etc. The conversion of WAT in beige adipose tissue is a potential new therapeutic target for obesity . It might increase the resting energy expenditure improving the energy balance. The ECS is known to
obesity 5383 thermogenesis, and inflammation [[25],[29]]. Through a revision of the literature on this system in obesity , we evaluate its role and potential as therapeutic target in this pathology.2. The “Browning” Process
obesity 7434 expressed in the nervous system and its expression levels are very low in peripheral cells, it increases in obesity . Genetic ablation of CB1 results in a reduction of body weight as well as its selective blockade reduces
obesity 7913 on thermogenesis. It was observed that CB1-lacking mice have less fat and are more protected against obesity than the correspondent wild-type mice [[33]]. These data suggest that the blockade of CB1 receptor could
obesity 10864 [[44]]. These findings emphasize the potential role of browning in addressing the global epidemiology of obesity and its related comorbidities. The recent evidence of beige fat in humans supports this hypothesis.In
obesity 12696 with energy expenditure, so they could be a potential suitable target.The effects of CB2 receptor on obesity are poorly characterized, because only recently was its localization observed in other sites than immune
obesity 15005 [[26]]. Antagonists at CB1 have been demonstrated to restore hypothalamic leptin sensitivity reducing obesity in diet-induced obese (DIO) mice [[33]]. Conversely, leptin reduces endocannabinoid synthesis by lowering
obesity 17421 impaired leptin signaling is associated with over activation of the central EC system, contributing to obesity development [[63],[64]]. Low levels of leptin are correlated with a higher risk of obesity in humans
obesity 17512 contributing to obesity development [[63],[64]]. Low levels of leptin are correlated with a higher risk of obesity in humans too [[65]]. CB1 regulates cell proliferation, differentiation, and survival of neuron progenitors
obesity 18219 independently of insulin. Therefore, the focal point is the possibility to use antagonists at CB1 in anti- obesity treatments. Rimonabant, antagonist at CB1, has long been used as an anti-obesity drug able to induce
obesity 18300 antagonists at CB1 in anti-obesity treatments. Rimonabant, antagonist at CB1, has long been used as an anti- obesity drug able to induce weight loss, improve blood lipid parameters and increase the adiponectin level in
obesity 19114 on immune cells and it is involved in inflammatory responses. CB2 receptor stimulation promotes anti- obesity effects by reducing food intake and weight gain without an adverse impact on mood and inhibiting activated
obesity 19656 short-term activation has little effect on synaptic activity [[60],[68]]. A therapeutic use of CB2 as anti- obesity target might presume a related chronic neuronal activation, that, in turn, increasing excitatory synaptic
obesity 19822 activation, that, in turn, increasing excitatory synaptic transmission, should facilitate the peripheral anti- obesity effects without exerting remarkable psychotropic activity. Nevertheless, selective CB2 agonists that
obesity 20213 remodeling and altered secretion of adipokines are presented together with increased inflammation in obesity . The association between obesity and chronic inflammation is suggested by several observations, such
obesity 20246 of adipokines are presented together with increased inflammation in obesity. The association between obesity and chronic inflammation is suggested by several observations, such as the production of TNF-α and
obesity 20592 of pro-inflammatory cytokines from adipose tissue is associated with the risk of adverse outcomes in obesity (type 2 diabetes, cardiovascular diseases, nonalcoholic fatty liver disease and cancer) [[69]]. It was
obesity 20832 inhibit the expression of adiponectin [[70]], which is an adipokine, inversely correlated with the obesity [[71]], its increase plays an important anti-inflammatory role.In the literature the role of EC system
obesity 21596 inflammatory adipokine release together with fat storage, while the stimulation of CB2 reverses all the obesity -related effects. These observations suggest the possibility of using CB2 as a novel anti-obesity pharmacological
obesity 21693 the obesity-related effects. These observations suggest the possibility of using CB2 as a novel anti- obesity pharmacological target.Lipid endocannabinoid signaling, through CB2 receptor, is a part of a protective
obesity 22947 the lack of CB2 has protective effects, which implies that it could be a potential target to contrast obesity and insulin resistance. Also, Deveaux et al. [[75]] observed that the induction of CB2 receptor in the
obesity 23245 cases, data suggest that CB2 receptor antagonists could represent a novel therapeutic approach for obesity -associated metabolic disorders. However, in the literature the data suggesting anti-inflammatory properties
obesity 23887 [[1],[77],[78],[79],[80],[81]]. Since an obese child will likely be an obese adult, planning childhood intervention on obesity would be the most advisable solution. Diet intervention and correct lifestyle are surely the best solution,
obesity 24728 findings in the field of browning in humans have pointed out the potential role of this phenomenon in obesity treatment. In addition, BAT activity has been associated with an improving of metabolic profile in adults

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