کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8323476 | 1539891 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Obestatin and Nt8U influence glycerolipid metabolism and PPAR gamma signaling in mice
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کلمات کلیدی
ADIPOQCD36ANGPTL4LPLPNPLA3PPARγrxrgDGAT2diacylglycerol O-acyltransferase 2PNPLA2mgllangiopoietin-like 4 - آنژیوپوئیتین مانند 4Obestatin - اوستاتینMonoglyceride lipase - لیپاز مونوگلیسیریدLipoprotein lipase - لیپو پروتئین لیپازpatatin-like phospholipase domain containing 2 - پاتین مانند فسفولیپاز حاوی 2patatin-like phospholipase domain containing 3 - پاتین مانند فسفولیپاز حاوی 3Peroxisome proliferator-activated receptor gamma - گاما گیرنده گیرنده فعال پرولیفیزوم فعال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Obestatin, its N-terminal fragment and the N-terminal fragment analog Nt8U were previously shown to reduce food intake, gain in body weight and triglyceride levels in albino mice. To establish their mode of action, mRNA profiling of the epididymal adipose tissue of mice treated with these peptides were performed. The differential expressions were markedly indicative of their involvement in lipid metabolism. Obestatin showed a significant upregulation of the genes patatin-like phospholipase domain containing 3, diacylglycerol O-acyltransferase 2, monoglyceride lipase, aldo-keto reductase family 1, member 7 which are involved in glycerolipid metabolism. It also upregulated peroxisome proliferator-activated receptor gamma, retinoid X receptor gamma, cluster of differentiation 36, adiponectin, C1Q and collagen domain containing, angiopoietin-like 4, lipoprotein lipase, stearoyl-coenzyme A and desaturase 3 involved in the peroxisome proliferator-activated receptor signaling pathway. Nt8U upregulated genes implicated in the same two pathways but with lesser significance and also upregulated APOL2. The N-terminal fragment though differentially regulated a small subset of the genes differentially regulated by obestatin and Nt8U, no conclusive evidence was obtained as to assign a specific pathway for its mode of action. We hypothesize that reduced food intake brought about by obestatin and Nt8U triggers lipid catabolism. The free fatty acids and lysophosphatidic acid thus produced in turn activates peroxisome proliferator-activated receptor gamma and the genes involved in peroxisome proliferator-activated receptor signaling. All of them together lead to reduction in gain in bodyweight, stored fat and circulating lipids. These results also correlate well with the observed efficacy of the peptides.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 53, August 2014, Pages 414-422
Journal: The International Journal of Biochemistry & Cell Biology - Volume 53, August 2014, Pages 414-422
نویسندگان
ShreeRanga Nagaraj, Angad V. Raghavan, Sudha N. Rao, Uma V. Manjappara,