Regulation of Adipose Tissue Metabolism by the Endocannabinoid System

Eenige, Robin van; Stelt, Mario van der; Rensen, Patrick C.N.; Kooijman, Sander

doi:10.1016/j.tem.2018.03.001

Cited by 45 publications

(38 citation statements)

References 100 publications

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“…Obesity is associated with a higher rate for noncommunicable diseases, including type 2 diabetes, cardiovascular diseases, musculoskeletal disorders, and some cancers [2, 9, 10]. White adipose tissue (WAT) is an endocrine organ and its importance for whole-body metabolism has been well-recognized [11]. Adipokines are a wide variety of cytokines secreted by adipose tissues [12], which participate in many pathophysiological processes including the regulation of appetite and satiety, immunity, inflammation adipogenesis, insulin sensitivity, and others [12–14].…”

Section: Introductionmentioning

confidence: 99%

Polydatin Inhibits Adipose Tissue Inflammation and Ameliorates Lipid Metabolism in High-Fat-Fed Mice

Zheng

et al. 2019

BioMed Research International

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Polydatin (PD), an active component of Chinese herbs, is reported to have many biological functions, such as cardioprotective actions, anti-inflammatory activities, and antitumor effects. In this study, we investigated the effects of PD on body weight control, glucose and lipid metabolic regulation, and anti-inflammation in a high-fat-diet- (HFD-) induced obese mice model. After treatment of PD (100 mg/kg/d for 4 weeks), HFD mice reduced body weight, retroperitoneal fat mass, and adipose cell sizes; significantly lowered serum total cholesterol triglyceride (TG) and low-density lipoprotein (LDL) levels; and increased high-density lipoprotein (HDL) levels compared with the HFD control mice. Further studies showed that PD downregulated the mRNA and protein expressions of peroxisome proliferator-activated receptor gamma (PPARγ), a transcription factor involving in the regulation of adipocyte differentiation, in the retroperitoneal fat of HFD mice. Additionally, PD significantly upregulated the mRNA and protein expressions of leptin, an adipocyte-derived anorexic hormone that regulates food intake and energy expenditure, in the adipose tissues of HFD mice. Moreover, PD reduced the expression levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α) in the retroperitoneal and epididymal tissues of HFD mice, suggesting that PD prevented adipose tissue inflammation. In conclusion, PD may serve as a pharmaceutic candidate for obesity-related lipid metabolism, anti-inflammation, and body weight loss.

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Section: Introductionmentioning

confidence: 99%

Polydatin Inhibits Adipose Tissue Inflammation and Ameliorates Lipid Metabolism in High-Fat-Fed Mice

Zheng

et al. 2019

BioMed Research International

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“…Currently, CB1R antagonists and inverse agonists can favor weight loss through peripheral actions on the CB1R of adipose cells, increasing metabolism (i.e., inducing browning) [91][92][93]. Browning represents the modification of white adipocytes (that store energy) into brown adipocytes (that are related to non-shivering thermogenesis).…”

Section: Pep19 Therapeutics Pharmacology Characterizationmentioning

confidence: 99%

“…EDMP are not confined to the CNS and data obtained using pharmacological and genetic tools inactivating CB1 receptors point to the inhibition of sympathetic inputs upon brown adipose tissue (BAT). Also, decreased thermogenesis is one of the most important mechanisms through which CB1R activation reduces energy expenditure by BAT [91] and causes white adipose tissue accumulation in diet-induced obesity (DIO) mice [113,114].…”

Section: Molecular Physiology Of Energy Expenditurementioning

confidence: 99%

Peptides from Natural or Rationally Designed Sources Can Be Used in Overweight, Obesity, and Type 2 Diabetes Therapies

et al. 2020

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Overweight and obesity are among the most prominent health problems in the modern world, mostly because they are either associated with or increase the risk of other diseases such as type 2 diabetes, hypertension, and/or cancer. Most professional organizations define overweight and obesity according to individual body–mass index (BMI, weight in kilograms divided by height squared in meters). Overweight is defined as individuals with BMI from 25 to 29, and obesity as individuals with BMI ≥30. Obesity is the result of genetic, behavioral, environmental, physiological, social, and cultural factors that result in energy imbalance and promote excessive fat deposition. Despite all the knowledge concerning the pathophysiology of obesity, which is considered a disease, none of the existing treatments alone or in combination can normalize blood glucose concentration and prevent debilitating complications from obesity. This review discusses some new perspectives for overweight and obesity treatments, including the use of the new orally active cannabinoid peptide Pep19, the advantage of which is the absence of undesired central nervous system effects usually experienced with other cannabinoids.

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“…The role of the central endocannabinoid system in the regulation of metabolic homeostasis and pathophysiological conditions has been extensively reviewed by others. 8,9,12,13 Here, we will focus on recent findings on peripheral endocannabinoid signalling, which might be relevant for therapeutic approaches targeting vascular, immune cell, liver as well as adipocyte cannabinoid receptors in atherosclerosis and related metabolic dysfunctions.…”

Section: Introductionmentioning

confidence: 99%

Endocannabinoid Signalling in Atherosclerosis and Related Metabolic Complications

Guillamat-Prats¹,

Rami²,

Herzig

et al. 2019

Thromb Haemost

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Endocannabinoids are a group of arachidonic acid-derived lipid mediators binding to cannabinoid receptors CB1 and CB2. An overactivity of the endocannabinoid system plays a pathophysiological role in the development of visceral obesity and insulin resistance. Moreover, elevated circulating endocannabinoid levels are also prevalent in atherosclerosis. The pathophysiological increase of endocannabinoid levels is due to an altered expression of endocannabinoid synthesizing and degrading enzymes induced by inflammatory mediators such as cytokines or lipids. Emerging experimental evidence suggests that enhanced endocannabinoid signalling affects atherosclerosis via multiple effects, including a modulation of vascular inflammation, leukocyte recruitment, macrophage cholesterol metabolism and consequently atherosclerotic plaque stability. In addition, recent findings in various metabolic disease models highlight the relevance of peripheral CB1 cannabinoid receptors in adipose tissue, liver and pancreas, which crucially regulate lipid and glucose metabolism as well as macrophage properties in these organs. This suggests that targeting the endocannabinoid system in the vasculature and peripheral organs might have a therapeutic potential for atherosclerosis by inhibiting vascular inflammation and improving metabolic risk factors. This review will provide a brief update on the effects of endocannabinoid signalling in atherosclerosis and related metabolic complications.

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Regulation of Adipose Tissue Metabolism by the Endocannabinoid System

Cited by 45 publications

References 100 publications

Polydatin Inhibits Adipose Tissue Inflammation and Ameliorates Lipid Metabolism in High-Fat-Fed Mice

Polydatin Inhibits Adipose Tissue Inflammation and Ameliorates Lipid Metabolism in High-Fat-Fed Mice

Peptides from Natural or Rationally Designed Sources Can Be Used in Overweight, Obesity, and Type 2 Diabetes Therapies

Endocannabinoid Signalling in Atherosclerosis and Related Metabolic Complications

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