Search

A proteomic approach was used to identify proteins differentially expressed in the plasma of mice following alternate day fasting. Male mice (C57Bl6, 9 months old) were randomly assigned to ad libitum (AL, n = 10) and calorie-restricted (IF, n = 10, AL on alternate day basis) groups for 4 weeks. After staining, the gels were imaged and differential protein expression patterns were interrogated using image analysis software. Spots showing a different expression level were identified through a comparison with 2D maps found in databases officially recognized (ExPASy). Master gels of AL and IF mice exhibited slightly different 2-DE patterns as only 14 spots out of 500 appeared differentially expressed: 12 spots were downregulated and identified as apolipoprotein E (APO-E), haptoglobin (HPT), alpha-1-antitrypsin (A1AT), pro- thrombin, and serum amyloid P component (SPA), whereas two spots were unidentified. In conclusion 4 weeks of alternate feeding results in a slight perturbation of the host plasma proteome. Of particular interest is the reduced plasma content in APO-E and acute-phase proteins HPT, A1AT and SPA that confirms a powerful anti-inflammatory effect of this dietary regimen.

Introduction: Myopathy is the most common side effect of statins. Because nitric oxide (NO) has a key role in regulating skeletal muscle function, we studied whether the NO-donating atorvastatin NCX 6560 could show a better profile on skeletal muscle function and structure compared with ator- vastatin. Methods: C57BL/6 mice received atorvastatin 40 mg/ kg/day or an equivalent dose of NCX 6560 for 2 months. Mus- cle function assessed by treadmill test, serum creatine kinase (CK) activity, citrate synthase (CS) activity, and muscle histol- ogy were evaluated. Results: Atorvastatin significantly (P < 0.001) reduced muscle endurance, increased serum CK by 6- fold, and induced muscle fiber atrophy. Conversely, NCX 6560 preserved muscle function, prevented CK increase and did not modify muscle structure. Interestingly, atorvastatin reduced CS activity, a marker for mitochondrial function, in gastrocnemius, diaphragm, and heart, whereas NCX 6560 prevented such decrease. Conclusions: These findings suggest that NO may prevent statin-induced myopathy. Muscle Nerve 47: 72-80, 2013