| First Author | Kennaway DJ | Year | 2012 |
| Journal | Obesity (Silver Spring) | Volume | 20 |
| Issue | 2 | Pages | 295-305 |
| PubMed ID | 21918578 | Mgi Jnum | J:322727 |
| Mgi Id | MGI:7259921 | Doi | 10.1038/oby.2011.276 |
| Citation | Kennaway DJ, et al. (2012) Adipokines and adipocyte function in Clock mutant mice that retain melatonin rhythmicity. Obesity (Silver Spring) 20(2):295-305 |
| abstractText | Clock(delta19)+MEL mutant mice, which retain melatonin rhythmicity, but lack peripheral tissue rhythmicity have impaired glucose tolerance, but reduced plasma free fatty acids, increased plasma adiponectin, and improved insulin sensitivity. Here, we report their response to a high-fat diet and adipocyte rhythmicity and function. The diet increased epigonadal fat weight similarly (twofold) in both wild-type and Clock(delta19)+MEL mice. The Clock(delta19) mutation abolished rhythmicity of Per2, Rev erbalpha and peroxisome proliferator-activated receptor-gamma (Ppargamma ) mRNA in epigonadal fat, but not Bmal1 mRNA, and reduced Rev erbalpha mRNA by 59 and 70% compared to the wild-type mice on the control and high-fat diets, respectively. The mutants had increased Adipoq mRNA expression in epigonadal fat (22%; P < 0.05) on a control diet, but showed no further change on a high-fat diet, and no change in Lep, Nampt or Retn mRNA on either diet. The Clock(delta19) mutation abolished rhythmicity of genes in epigonadal fat that contribute to plasma free fatty acids for mice on both diets, and increased Lipe mRNA expression in those on the high-fat diet. The persistent melatonin rhythm and reduced plasma free fatty acids in Clock(delta19)+MEL mutants may contribute to their enhanced insulin sensitivity, ameliorate the extent of impaired glucose homeostasis, and protect against the adverse effects of a high-fat diet. |
