المؤلفون: Herman, R.J., Hayes, M.R., Audrain-McGovern, J., Ashare, R.L., Schmidt, H.D.

المصدر: Psychopharmacology; Jun2023, Vol. 240 Issue 6, p1373-1386, 14p, 5 Graphs

مصطلحات موضوعية: WEIGHT gain, NICOTINE, GLUCAGON-like peptide-1 receptor, HYPERPHAGIA, LIRAGLUTIDE, HIGH-fat diet

الشركة/الكيان: UNITED States. Food & Drug Administration

مستخلص: Rationale: Nicotine cessation is associated with increased consumption of highly palatable foods and body weight gain in most smokers. Concerns about body weight gain are a major barrier to maintaining long-term smoking abstinence, and current treatments for nicotine use disorder (NUD) delay, but do not prevent, body weight gain during abstinence. Glucagon-like peptide-1 receptor (GLP-1R) agonists reduce food intake and are FDA-approved for treating obesity. However, the effects of GLP-1R agonist monotherapy on nicotine seeking and withdrawal-induced hyperphagia are unknown. Objectives: We screened the efficacy of the long-lasting GLP-1R agonist liraglutide to reduce nicotine-mediated behaviors including voluntary nicotine taking, as well as nicotine seeking and hyperphagia during withdrawal. Methods: Male and female rats self-administered intravenous nicotine (0.03 mg/kg/inf) for ~21 days. Daily liraglutide administration (25 μg/kg, i.p.) started on the last self-administration day and continued throughout the extinction and reinstatement phases of the experiment. Once nicotine taking was extinguished, the reinstatement of nicotine-seeking behavior was assessed after an acute priming injection of nicotine (0.2 mg/kg, s.c.) and re-exposure to conditioned light cues. Using a novel model of nicotine withdrawal-induced hyperphagia, intake of a high fat diet (HFD) was measured during home cage abstinence in male and female rats with a history of nicotine self-administration. Results: Liraglutide attenuated nicotine self-administration and reinstatement in male and female rats. Repeated liraglutide attenuated withdrawal-induced hyperphagia and body weight gain in male and female rats at a dose that was not associated with malaise-like effects. Conclusions: These findings support further studies investigating the translational potential of GLP-1R agonists to treat NUD. [ABSTRACT FROM AUTHOR]

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المؤلفون: Liu, Shengnan, Zheng, Menglin, Li, Yixuan, He, Ling, Chen, Tong

المصدر: Psychopharmacology; Feb2020, Vol. 237 Issue 2, p465-477, 13p, 1 Diagram, 10 Graphs

مصطلحات موضوعية: MYELOID differentiation factor 88, COGNITION disorders, CREB protein, BRAIN-derived neurotrophic factor, GLUCAGON-like peptide-1 receptor, HIGH-fat diet

مستخلص: The purpose of the present study was to elucidate the pharmacological effects of Geniposide (GEN) on high diet fed and streptozotocin (STZ)-caused diabetic cognitive impairment. The mice were fed with high fat diet (HFD) for 4 weeks and intraperitoneally injected with 60 mg/kg STZ for three times within 72 h. The mice with glucose level over 15 mmol/l were regarded as diabetic and selected for further studies. The animals were intragastrically treated with metformin or GEN once daily for 4 weeks. Afterwards, the animals were applied for Y maze, novel object recognition (NOR) test, step-through passive avoidance test, and Morris water maze (MWM) test. The blood glucose and body weight were examined. The SH-SY5Y cells were treated with GEN in the presence or absence of ibrutinib and stimulated with high-glucose culture medium. The tumor necrosis factor-a (TNF-α) and interleukin (IL)-6 in serum, hippocampus, and supernatant were measured using ELISA method. The protein expressions of Bruton's tyrosine kinase (BTK), Toll-like receptor 4 (TLR4), myeloid differentiating factor 88 (MyD88), nuclear factor kappa-B (NF-κB), p-NF-κB, brain-derived neurotrophic factor (BDNF), cAMP-response element binding protein (CREB), p-CREB, and glucagon-like peptide-1 receptor (GLP-1R) were detected by western blot analyses. As a result, the GEN treatment notably attenuated the body weight, blood glucose, and cognitive decline. GEN also inhibited the generations of inflammatory cytokines. Furthermore, the administrations of GEN ameliorated the alterations of BTK, TLR4, MyD88, NF-κB, and BDNF in HFD + STZ–induced mice. With the application of ibrutinib, the selective inhibitor of BTK, it was also found that BTK/TLR4/NF-κB pathway was associated with the GEN treatment in high glucose–induced SH-SY5Y cells. In summary, the results suggested that GEN exerted the protective effect on STZ-induced cognitive impairment possibly through the modulation of BTK/TLR4/NF-κB signaling. [ABSTRACT FROM AUTHOR]

: Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: Thomsen, Morgane, Holst, Jens Juul, Molander, Anna, Linnet, Kristian, Ptito, Maurice, Fink-Jensen, Anders

المصدر: Psychopharmacology; Jan2020, Vol. 237 Issue 1, p287-287, 1p, 1 Graph

مصطلحات موضوعية: GLUCAGON-like peptide 1, CERCOPITHECUS aethiops, GLUCAGON-like peptide-1 receptor, ALCOHOL

مستخلص: After publication of this paper, the authors determined an error in Fig. 4. Below is the correct Fig. 4. [ABSTRACT FROM AUTHOR]

: Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)