دورية أكاديمية
Butyrylcholinesterase gene transfer in obese mice prevents postdieting body weight rebound by suppressing ghrelin signaling.
| العنوان: | Butyrylcholinesterase gene transfer in obese mice prevents postdieting body weight rebound by suppressing ghrelin signaling. |
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| المؤلفون: | Chen VP; Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905 chen.vicky@mayo.edu brimijoin@mayo.edu., Gao Y; Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905., Geng L; Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905., Brimijoin S; Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905 chen.vicky@mayo.edu brimijoin@mayo.edu. |
| المصدر: | Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2017 Oct 10; Vol. 114 (41), pp. 10960-10965. Date of Electronic Publication: 2017 Sep 25. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Washington, DC : National Academy of Sciences |
| مواضيع طبية MeSH: | Caloric Restriction*, Butyrylcholinesterase/*metabolism , Ghrelin/*antagonists & inhibitors , Hyperphagia/*prevention & control , Obesity/*prevention & control, Animals ; Appetite ; Body Weight ; Eating ; Ghrelin/metabolism ; Hyperphagia/metabolism ; Hyperphagia/pathology ; Male ; Mice ; Mice, Obese ; Obesity/metabolism ; Obesity/pathology ; Signal Transduction ; Weight Gain ; Weight Loss |
| مستخلص: | The worldwide prevalence of obesity is increasing at an alarming rate but treatment options remain limited. Despite initial success, weight loss by calorie restriction (CR) often fails because of rebound weight gain. Postdieting hyperphagia along with altered hypothalamic neuro-architecture appears to be one direct cause of this undesirable outcome. In response to calorie deficiency the circulating levels of the appetite-promoting hormone, acyl-ghrelin, rise sharply. We hypothesize that proper modulation of acyl-ghrelin and its receptor's sensitivity will favorably impact energy intake and reprogram the body weight set point. Here we applied viral gene transfer of the acyl-ghrelin hydrolyzing enzyme, butyrylcholinesterase (BChE), in a mouse model of diet-induced obesity. Our results confirmed that BChE overexpression decreased circulating acyl-ghrelin levels, suppressed CR-provoked ghrelin signaling, and restored central ghrelin sensitivity. In addition to maintaining healthy body weights, BChE treated mice had modest postdieting food intake and showed normal glucose homeostasis. Spontaneous activity and energy expenditure did not differ significantly between treated and untreated mice after body weight rebound, suggesting that BChE gene transfer did not alter energy expenditure in the long term. These findings indicate that combining BChE treatment with CR could be an effective approach in treating human obesity and aiding lifelong weight management. Competing Interests: The authors declare no conflict of interest. |
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| معلومات مُعتمدة: | DP1 DA031340 United States DA NIDA NIH HHS; UG3 DA042492 United States DA NIDA NIH HHS; UH3 DA042492 United States DA NIDA NIH HHS |
| فهرسة مساهمة: | Keywords: body weight rebound; butyrylcholinesterase; diet-induced obesity; food intake; ghrelin |
| المشرفين على المادة: | 0 (Ghrelin) EC 3.1.1.8 (Butyrylcholinesterase) |
| تواريخ الأحداث: | Date Created: 20171005 Date Completed: 20180626 Latest Revision: 20240604 |
| رمز التحديث: | 20240604 |
| مُعرف محوري في PubMed: | PMC5642694 |
| DOI: | 10.1073/pnas.1706517114 |
| PMID: | 28973869 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1091-6490 |
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| DOI: | 10.1073/pnas.1706517114 |