| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Anil K Agarwal, Katie Tunison, Jay D Horton, Abhimanyu Gar. Regulated regeneration of adipose tissue in lipodystrophic iScience. vol 27. issue 4. 2024-04-16. PMID:38623324. |
regulated regeneration of adipose tissue in lipodystrophic both humans and mice with congenital generalized lipodystrophy due to agpat2 deficiency develop diabetes mellitus, insulin resistance, and hepatic steatosis, which have been attributed to the near total loss of adipose tissue (at). |
2024-04-16 |
2024-04-18 |
mouse |
| Hoa Thanh Nguyen, Lingyun Li, Akifumi Eguchi, Tetsuro Agusa, Kimika Yamamoto, Kurunthachalam Kannan, Eun-Young Kim, Hisato Iwat. Effects of gestational exposure to bisphenol A on the hepatic transcriptome and lipidome of rat dams: Intergenerational comparison of effects in the offspring. The Science of the total environment. 2022-02-22. PMID:35192832. |
palmitic acid and genes related to circadian rhythm, insulin responses, and lipid metabolism (e.g., 1-acylglycerol-3-phosphate o-acyltransferase 2 (agpat2), b-cell cll/lymphoma 10 (bcl10), cry1, harvey rat sarcoma virus oncogene (hras), and nlr family member x1 (nlrx1)) were identified through diablo models as novel biomarkers of effects of bpa across two generations. |
2022-02-22 |
2023-08-13 |
rat |
| Marta Fernández-Galilea, Pablo Tapia, Kelly Cautivo, Eugenia Morselli, Víctor A Corté. AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism. Biochemical and biophysical research communications. vol 467. issue 1. 2016-04-08. PMID:26417690. |
mutations in 1-acylglycerol-3-phosphate o-acyltransferase 2 (agpat2) result in lipodystrophy, insulin resistance and diabetes. |
2016-04-08 |
2023-08-13 |
mouse |
| Jiang Wei Wu, Hao Yang, Shu Pei Wang, Krishnakant G Soni, Catherine Brunel-Guitton, Grant A Mitchel. Inborn errors of cytoplasmic triglyceride metabolism. Journal of inherited metabolic disease. vol 38. issue 1. 2015-10-08. PMID:25300978. |
we discuss known inborn errors of ctgm, including deficiencies of: agpat2 (a form of generalized lipodystrophy), lpin1 (childhood rhabdomyolysis), lpin2 (an inflammatory condition, majeed syndrome, described elsewhere in this issue), dgat1 (protein loosing enteropathy), perilipin 1 (partial lipodystrophy), cgi-58 (gene abhd5, neutral lipid storage disease (nlsd) with ichthyosis and "jordan's anomaly" of vacuolated polymorphonuclear leukocytes), adipose triglyceride lipase (atgl, gene pnpla2, nlsd with myopathy, cardiomyopathy and jordan's anomaly), hormone-sensitive lipase (hsl, gene lipe, hypertriglyceridemia, and insulin resistance). |
2015-10-08 |
2023-08-13 |
mouse |
| Víctor A Cortés, Kelly M Cautivo, Shunxing Rong, Abhimanyu Garg, Jay D Horton, Anil K Agarwa. Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors. Journal of lipid research. vol 55. issue 2. 2014-09-28. PMID:24293639. |
patients with congenital generalized lipodystrophy (cgl) due to mutations in 1-acylglycerol-3-phosphate-o-acyltransferase 2 (agpat2) and the cgl murine model (agpat2(-/-) mice) both have severe insulin resistance, diabetes mellitus, hepatic steatosis, and low plasma leptin levels. |
2014-09-28 |
2023-08-12 |
mouse |
| Víctor A Cortés, Kelly M Cautivo, Shunxing Rong, Abhimanyu Garg, Jay D Horton, Anil K Agarwa. Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors. Journal of lipid research. vol 55. issue 2. 2014-09-28. PMID:24293639. |
in this study, we show that continuous leptin treatment of agpat2(-/-) mice for 28 days reduced plasma insulin and glucose levels and normalized hepatic steatosis and hypertriglyceridemia. |
2014-09-28 |
2023-08-12 |
mouse |
| Shireesha Sankella, Abhimanyu Garg, Jay D Horton, Anil K Agarwa. Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice. The Journal of biological chemistry. vol 289. issue 8. 2014-04-22. PMID:24425876. |
this activation was suppressed by insulin in the wt primary hepatocytes but not in the agpat2(-/-) primary hepatocytes. |
2014-04-22 |
2023-08-12 |
mouse |
| Shireesha Sankella, Abhimanyu Garg, Jay D Horton, Anil K Agarwa. Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice. The Journal of biological chemistry. vol 289. issue 8. 2014-04-22. PMID:24425876. |
thus, the lack of normal insulin signaling in agpat2(-/-) livers allows unrestricted pa-induced gluconeogenesis significantly contributing to the development of hyperglycemia in these mice. |
2014-04-22 |
2023-08-12 |
mouse |
| Shireesha Sankella, Abhimanyu Garg, Jay D Horton, Anil K Agarwa. Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice. The Journal of biological chemistry. vol 289. issue 8. 2014-04-22. PMID:24425876. |
in this study we examined the role of phosphatidic acid (pa) in hepatic glucose production (hgp) and development of hepatic insulin resistance in mice that lack 1-acylglycerol-3-phosphate o-acyltransferase 2 (agpat2). |
2014-04-22 |
2023-08-12 |
mouse |
| Parastoo Rostami, Maryam Nakhaeimoghadam, Faezeh-Moghimpour Bijani, Arya Sotoudeh, Ali Rabbani, Pascale Hilbert, Nima Rezae. AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome. Annales d'endocrinologie. vol 74. issue 1. 2013-09-04. PMID:23337016. |
berardinelli-seip congenital lipodystrophy (bscl) syndrome is an autosomal recessive disorder, caused by mutation in the agpat2 gene, which could lead to insulin resistance and variety of complications. |
2013-09-04 |
2023-08-12 |
Not clear |
| Angela R Subauste, Arun K Das, Xiangquan Li, Brandon G Elliott, Brandon Elliot, Charles Evans, Mahmoud El Azzouny, Mary Treutelaar, Elif Oral, Todd Leff, Charles F Buran. Alterations in lipid signaling underlie lipodystrophy secondary to AGPAT2 mutations. Diabetes. vol 61. issue 11. 2013-01-14. PMID:22872237. |
congenital generalized lipodystrophy (cgl), secondary to agpat2 mutation is characterized by the absence of adipocytes and development of severe insulin resistance. |
2013-01-14 |
2023-08-12 |
human |
| Marie-Christine Vantyghem, Anne-Sophie Balavoine, Claire Douillard, Frédérique Defrance, Lucile Dieudonne, Fanny Mouton, Christine Lemaire, Nicole Bertrand-Escouflaire, Marie-Françoise Bourdelle-Hego, Fabrice Devemy, Anne Evrard, Dominique Gheerbrand, Caroline Girardot, Sophie Gumuche, Christine Hober, Hélène Topolinski, Blandine Lamblin, Bénédicte Mycinski, Amélie Ryndak, Wassila Karrouz, Etienne Duvivier, Emilie Merlen, Christine Cortet, Jacques Weill, Dominique Lacroix, Jean-Louis Wémea. How to diagnose a lipodystrophy syndrome. Annales d'endocrinologie. vol 73. issue 3. 2012-11-13. PMID:22748602. |
the genetically determined generalized forms are also very rare and are linked to mutations of seipin agpat2, fbn1, which is accompanied by marfan syndrome, or of banf1, which is characterized by a progeroid syndrome without insulin resistance and with early bone complications. |
2012-11-13 |
2023-08-12 |
Not clear |
| Anil K Agarwal, Suja Sukumaran, Víctor A Cortés, Katie Tunison, Dario Mizrachi, Shireesha Sankella, Robert D Gerard, Jay D Horton, Abhimanyu Gar. Human 1-acylglycerol-3-phosphate O-acyltransferase isoforms 1 and 2: biochemical characterization and inability to rescue hepatic steatosis in Agpat2(-/-) gene lipodystrophic mice. The Journal of biological chemistry. vol 286. issue 43. 2011-12-15. PMID:21873652. |
from these studies, we suggest that the role of agpat1 or agpat2 in liver lipogenesis is minimal and that accumulation of liver fat is primarily a consequence of insulin resistance and loss of adipose tissue in agpat2(-/-) mice. |
2011-12-15 |
2023-08-12 |
mouse |
| H Ben Turkia, N Tebib, H Azzouz, M Slim Abdelmoula, A Ben Chehida, P Hubert, W Douira, M F Ben Drid. [Congenital generalized lipodystrophy: a case report with neurological involvement]. Archives de pediatrie : organe officiel de la Societe francaise de pediatrie. vol 16. issue 1. 2009-04-24. PMID:19026526. |
at least 2 genes located in 9q34 (agpat2) and 11q13 (seipin) are implicated in type 1 and 2, respectively, and result in insulin resistance. |
2009-04-24 |
2023-08-12 |
Not clear |
| Víctor A Cortés, David E Curtis, Suja Sukumaran, Xinli Shao, Vinay Parameswara, Shirya Rashid, Amy R Smith, Jimin Ren, Victoria Esser, Robert E Hammer, Anil K Agarwal, Jay D Horton, Abhimanyu Gar. Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy. Cell metabolism. vol 9. issue 2. 2009-03-18. PMID:19187773. |
agpat2(-/-) mice develop severe lipodystrophy affecting both white and brown adipose tissue, extreme insulin resistance, diabetes, and hepatic steatosis. |
2009-03-18 |
2023-08-12 |
mouse |
| Anil K Agarwal, Abhimanyu Gar. Genetic disorders of adipose tissue development, differentiation, and death. Annual review of genomics and human genetics. vol 7. 2008-04-17. PMID:16722806. |
the loss of body fat in inherited lipodystrophies can be caused by defects in the development and/or differentiation of adipose tissue as a consequence of mutations in a number of genes, including pparg (encoding a nuclear hormone receptor), agpat2 (encoding an enzyme involved in the biosynthesis of triglyceride and phospholipids), akt2 (encoding a protein involved in insulin signal transduction), and bscl2 (encoding seipin, whose role in the adipocyte biology remains unclear). |
2008-04-17 |
2023-08-12 |
Not clear |
| J Capeau, J Magré, O Lascols, M Caron, V Béréziat, C Vigouroux, J P Bastar. Diseases of adipose tissue: genetic and acquired lipodystrophies. Biochemical Society transactions. vol 33. issue Pt 5. 2006-05-02. PMID:16246048. |
congenital generalized lipodystrophy or berardinelli-seip syndrome, autosomal recessive, is characterized by a complete early lipoatrophy and severe insulin resistance and results, in most cases, from mutations either in the seipin gene of unknown function or agpat2 encoding an enzyme involved in triacylglycerol synthesis. |
2006-05-02 |
2023-08-12 |
human |
| Robert A Hegel. Monogenic forms of insulin resistance: apertures that expose the common metabolic syndrome. Trends in endocrinology and metabolism: TEM. vol 14. issue 8. 2004-07-09. PMID:14516935. |
monogenic forms of insulin resistance, such as familial partial lipodystrophy, which results from mutations in either lmna (encoding lamin a/c) or pparg (encoding peroxisome proliferator-activated receptor gamma), and congenital generalized lipodystrophy, which results from mutations in either agpat2 (encoding 1-acylglycerol-3-phosphate o-acyltransferase) or bscl2 (encoding seipin), can display features seen in the common metabolic syndrome. |
2004-07-09 |
2023-08-12 |
Not clear |