Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0235394 (
wasting
)
8,040
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A sample of 107 boys aged 7-10 in a rural area of Southern Italy was studied for riboflavin deficiency and its association with milk consumption. The boys represented 74 per cent of the total male population of that age group in the study area. The nutritional status was assessed by means of anthropometric indicators, dietary intakes by a 24-h recall method and the riboflavin status was evaluated by the assay of erythrocyte
glutathione reductase
activity. The nutritional status was found to be generally satisfactory with about one tenth of the children presenting stunting,
wasting
, or obesity. This picture is comparable to that recorded at the national level. The overall incidence of biochemical riboflavin deficiency was 13 per cent. No clinical sign of riboflavin deficiency was observed. None of the anthropometric indicators of malnutrition appeared to be related to biochemical evidence of riboflavin malnutrition. Dietary data showed that the children consumed a relatively small amount of milk and dairy products (mean 224 +/- 109 g/d). Thirteen out of 14 children with biochemical evidence of riboflavin deficiency belonged to the group who consumed less than 300 g/d of milk. However, only 15 per cent of the children consuming less than 300 g/d of milk and dairy products had biochemical evidence of riboflavin deficiency. It appears that the dietary pattern in rural areas with traditionally low milk consumption is compatible with a relatively satisfactory riboflavin nutriture. This finding suggests that milk and dairy products may occupy, under different dietary practices, a role less critical than usually attributed.
...
PMID:Riboflavin status among rural children in Southern Italy. 689 99
Skeletal muscle atrophy/
wasting
is associated with impaired protein metabolism in diverse physiological and pathophysiological conditions. Elevated levels of reactive oxygen species (ROS), disturbed redox status, and weakened antioxidant defense system are the major contributing factors toward atrophy. Regulation of protein metabolism by controlling ROS levels and its associated catabolic pathways may help in treating atrophy and related clinical conditions. Although cinnamaldehyde (CNA) enjoys the established status of antioxidant and its role in ROS management is reported, impact of CNA on skeletal muscle atrophy and related pathways is still unexplored. In the current study, the impact of CNA on C2C12 myotubes and the possible protection of cultured cells from H
2
O
2
-induced atrophy is examined. Myotubes were treated with H
2
O
2
in the presence and absence of CNA and the changes in the antioxidative, proteolytic systems, and mitochondrial functions were scored. Morphological analysis showed significant protective effects of CNA on length, diameter, and nuclei fusion index of myotubes. The evaluation of biochemical markers of atrophy; creatine kinase, lactate dehydrogenase, succinate dehydrogenase along with the study of muscle-specific structural protein (i.e., myosin heavy chain-fast [MHCf] type) showed significant protection of proteins by CNA. CNA pretreatment not only checked the activation of proteolytic systems (ubiquitin-proteasome E3-ligases [MuRF1/Atrogin1]), autophagy [Beclin1/LC3B], cathepsin L, calpain, caspase), but also prevented any alteration in the activities of antioxidative defense enzymes (catalase, glutathione- S-transferase, glutathione-peroxidase, superoxide dismutase,
glutathione reductase
). The results suggest that CNA protects myotubes from H
2
O
2
-induced atrophy by inhibiting/resisting the amendments in proteolytic systems and maintains cellular redox-balance.
...
PMID:Cinnamaldehyde regulates H
2
O
2
-induced skeletal muscle atrophy by ameliorating the proteolytic and antioxidant defense systems. 3031 70
