Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experiment was conducted using a total of 336 one-day-old, Arbor Acres commercial male broilers to investigate the effect of dietary Mn supplementation on carcass traits, meat quality, lipid oxidation, relative enzyme activities in abdominal fat and meat, and Mn-containing superoxide dismutase (MnSOD) mRNA level in meat. Broilers were randomly allotted by BW to 1 of 8 replicate cages (6 chicks per cage) for each of 7 treatments in a completely randomized design involving a 2 x 3 factorial + 1 arrangement of treatments. Dietary treatments included the corn-soybean meal-based diet (control) and the basal diet supplemented with 100 or 200 mg of Mn/kg as MnSO(4) x H(2)O, Mn AA A with a chelation strength of 26.3 formation quotient (8.34% Mn), or Mn AA B with a chelation strength of 45.3 formation quotient (6.48% Mn). Birds fed supplemental Mn had lower (P < 0.10) percentages of abdominal fat, lipoprotein lipase (LPL), and malate dehydrogenase activities and greater (P < 0.07) hormone-sensitive lipase activities in abdominal fat than birds fed a control diet. Birds fed supplemental Mn from Mn AA A or Mn AA B had lower (P < 0.05) LPL activities in abdominal fat than those fed supplemental MnSO(4) x H(2)O. Birds fed supplemental Mn had lower (P < 0.03) malondialdehyde content in leg muscle and greater (P < 0.02) MnSOD activities and MnSOD mRNA level in breast or leg muscle than those fed the control diet. Birds fed supplemental Mn from Mn AA A had a greater (P < 0.02) MnSOD mRNA level in leg muscle than those fed supplemental MnSO(4) x H(2)O. Results from this study indicated that organic Mn was more available than inorganic Mn for decreasing LPL activity in abdominal fat of broilers, and dietary Mn might reduce abdominal adipose deposition by decreasing LPL and malate dehydrogenase activities or increasing hormone-sensitive lipase activity in abdominal adipose tissue. The results also indicated that dietary Mn upregulated muscle MnSOD gene expression pretranslationally in association with increased MnSOD activity, which might explain the decrease of malondialdehyde content in leg muscle.
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PMID:Effect of manganese supplementation and source on carcass traits, meat quality, and lipid oxidation in broilers. 1704 Sep 39

According to the concept of lipotoxicity, ectopic accumulation of lipids in non-adipose tissue induces pathological changes. The most prominent effects are seen in fatty liver disease, lipid cardiomyopathy, non-insulin-dependent diabetes mellitus, insulin resistance and skeletal muscle myopathy. We used the MCK(m)-hLPL mouse distinguished by skeletal and cardiac muscle-specific human lipoprotein lipase (hLPL) overexpression to investigate effects of lipid overload in skeletal muscle. We were intrigued to find that ectopic lipid accumulation induced proteasomal activity, apoptosis and skeletal muscle damage. In line with these findings we observed reduced Musculus gastrocnemius and Musculus quadriceps mass in transgenic animals, accompanied by severely impaired physical endurance. We suggest that muscle loss was aggravated by impaired muscle regeneration as evidenced by reduced cross-sectional area of regenerating myofibers after cardiotoxin-induced injury in MCK(m)-hLPL mice. Similarly, an almost complete loss of myogenic potential was observed in C2C12 murine myoblasts upon overexpression of LPL. Our findings directly link lipid overload to muscle damage, impaired regeneration and loss of performance. These findings support the concept of lipotoxicity and are a further step to explain pathological effects seen in muscle of obese patients, patients with the metabolic syndrome and patients with cancer-associated cachexia.
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PMID:Skeletal muscle damage and impaired regeneration due to LPL-mediated lipotoxicity. 2282 72