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. 2021 May 10;12:670719. doi: 10.3389/fendo.2021.670719

Figure 6.

Figure 6

Metabolic effects of snoRNAs. (A) Exposure of Chinese hamster ovarian cells and C2C12 Murine Myoblasts to saturated fatty acids including palmitate, results in an increase in the 4 snoRNAs encoded by the introns of Rlp13a gene. These four snoRNAs are known to induce 2’-O-Methylations of target RNAs and mediate palmitate-induced lipotoxic effects on mitochondrial dysfunction and oxidative stress. (B) Mice invalidated for the 4 snoRNAs U32a (SNORD32a), U33 (SNORD33), U34 (SNORD34), and U35a (SNORD 35a) named Rpl13a-snoless mice, display reduced Reactive Oxygen Species (ROS) production, increased insulin secretion and improved glucose tolerance. (C) Rpl13a-snoless mice treated with the β-cell death inducer Streptozotocin (STZ) or bred with Ins2C96Y Akita mice or non-obese diabetic (NOD) mice are protected against the development of chronic hyperglycemia, show less oxidative stress and improved glucose tolerance. (D) Patients with Prader-Willi syndrome (PWS) who develop severe obesity and metabolic disorders carry a loss of paternally expressed genes on chromosome 15 which encodes for SNORD116. To reproduce the genetic background of PWS patients, a paternal Snord116 mouse knockout (Snord116p–/m+) has been generated. Genetic deletion of SNORD116 leads to defects in pancreatic endocrine development along with metabolic disturbances.