| First Author | Watson RA | Year | 2017 |
| Journal | Dis Model Mech | Volume | 10 |
| Issue | 12 | Pages | 1481-1488 |
| PubMed ID | 29084768 | Mgi Jnum | J:255303 |
| Mgi Id | MGI:6114501 | Doi | 10.1242/dmm.031864 |
| Citation | Watson RA, et al. (2017) Lyplal1 is dispensable for normal fat deposition in mice. Dis Model Mech 10(12):1481-1488 |
| abstractText | Genome-wide association studies (GWAS) have detected association between variants in or near the Lysophospholipase-like 1 (LYPLAL1) locus and metabolic traits, including central obesity, fatty liver and waist-to-hip ratio. LYPLAL1 is also known to be upregulated in the adipose tissue of obese patients. However, the physiological role of LYPLAL1 is not understood. To investigate the function of Lyplal1 in vivo we investigated the phenotype of the Lyplal1(tm1a(KOMP)Wtsi) homozygous mouse. Body composition was unaltered in Lyplal1 knockout mice as assessed by dual-energy X-ray absorptiometry (DEXA) scanning, both on normal chow and on a high-fat diet. Adipose tissue distribution between visceral and subcutaneous fat depots was unaltered, with no change in adipocyte cell size. The response to both insulin and glucose dosing was normal in Lyplal1(tm1a(KOMP)Wtsi) homozygous mice, with normal fasting blood glucose concentrations. RNAseq analysis of liver, muscle and adipose tissue confirmed that Lyplal1 expression was ablated with minimal additional changes in gene expression. These results suggest that Lyplal1 is dispensable for normal mouse metabolic physiology and that despite having been maintained through evolution Lyplal1 is not an essential gene, suggesting possible functional redundancy. Further studies will be required to clarify its physiological role. |
