Nutritional status‐dependent endocannabinoid signalling regulates the integration of rat visceral information

Khlaifia, Abdessattar; Matías, Isabelle; Cota, Daniela; Tell, Fabien

doi:10.1113/jp273484

Cited by 3 publications

(2 citation statements)

References 75 publications

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“…For instance, Xia et al showed that miR-384-3p inhibited retinal neovascularization during diabetic retinopathy [48]. KEEG analysis also revealed that the miRNAs of interest control activity-dependent synaptic plasticity, such as long-term potentiation (LTP) and LTD. Interestingly, several studies highlighted that energy state may control the LTP as well as LTD [49,50]. Particularly, a tetanic stimulation protocol induced LTD at POMC neurons in fed mice but weak LTP in food-deprived mice [50].…”

Section: Discussionmentioning

confidence: 99%

Leptin Modulates the Expression of miRNAs-Targeting POMC mRNA by the JAK2-STAT3 and PI3K-Akt Pathways

Derghal

Astier

Sicard

et al. 2019

JCM

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The central control of energy balance involves a strongly regulated neuronal network within the hypothalamus and the brainstem. In these structures, pro-opiomelanocortin (POMC) neurons are known to decrease food intake and to increase energy expenditure. Thus, leptin, a peripheral signal that relays information regarding body fat content, modulates the activity of POMC neurons. MicroRNAs (miRNAs) are short non-coding RNAs of 22–26 nucleotides that post-transcriptionally interfere with target gene expression by binding to their mRNAs. It has been demonstrated that leptin is able to modulate the expression of miRNAs (miR-383, miR-384-3p, and miR-488) that potentially target POMC mRNA. However, no study has identified the transduction pathways involved in this effect of leptin on miRNA expression. In addition, miRNAs targeting POMC mRNAs are not clearly identified. In this work, using in vitro models, we have identified and confirmed that miR-383, miR-384-3p, and miR-488 physically binds to the 3′ untranslated (3′UTR) regions of POMC mRNA. Importantly, we show that leptin inhibits these miRNAs expression by different transduction pathways. Taken together, these results allowed us to highlight the miRNA involvement in the regulation of POMC expression downstream of the leptin signaling and satiety signal integration.

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Section: Discussionmentioning

confidence: 99%

Leptin Modulates the Expression of miRNAs-Targeting POMC mRNA by the JAK2-STAT3 and PI3K-Akt Pathways

Derghal

Astier

Sicard

et al. 2019

JCM

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“…Following fasting, elevated ghrelin levels impair eCB-mediated LTD, which can be restored by the elevation of CCK. This mechanism can be thought of as an integrator between visceroafferents and blood-borne signals: the humoral satiety signal CCK attenuates neuronal transmission while the “hunger hormone” ghrelin leads to a more reliable conveyance of afferent signals [ 117 ]. Both humoral and neuronal pathways are linked by eCBs, underlining their importance as local modulators, especially in feeding circuits.…”

Section: Endocannabinoids In Central Control Of Body Weightmentioning

confidence: 99%

Endocannabinoids in Body Weight Control

et al. 2018

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Maintenance of body weight is fundamental to maintain one’s health and to promote longevity. Nevertheless, it appears that the global obesity epidemic is still constantly increasing. Endocannabinoids (eCBs) are lipid messengers that are involved in overall body weight control by interfering with manifold central and peripheral regulatory circuits that orchestrate energy homeostasis. Initially, blocking of eCB signaling by first generation cannabinoid type 1 receptor (CB1) inverse agonists such as rimonabant revealed body weight-reducing effects in laboratory animals and men. Unfortunately, rimonabant also induced severe psychiatric side effects. At this point, it became clear that future cannabinoid research has to decipher more precisely the underlying central and peripheral mechanisms behind eCB-driven control of feeding behavior and whole body energy metabolism. Here, we will summarize the most recent advances in understanding how central eCBs interfere with circuits in the brain that control food intake and energy expenditure. Next, we will focus on how peripheral eCBs affect food digestion, nutrient transformation and energy expenditure by interfering with signaling cascades in the gastrointestinal tract, liver, pancreas, fat depots and endocrine glands. To finally outline the safe future potential of cannabinoids as medicines, our overall goal is to address the molecular, cellular and pharmacological logic behind central and peripheral eCB-mediated body weight control, and to figure out how these precise mechanistic insights are currently transferred into the development of next generation cannabinoid medicines displaying clearly improved safety profiles, such as significantly reduced side effects.

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