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1 of events that maintains or prolongs the pro-catabolic state.
2 ays, shifting cartilage homeostasis toward a catabolic state.
3 econdary energy failure leading to a chronic catabolic state.
4 etabolism, all of which push the body into a catabolic state.
5 ganization of the cell from an anabolic to a catabolic state.
6 urgery depends on the patient's preoperative catabolic state.
7 that mediates muscle atrophy in a variety of catabolic states.
8 duced or suppressed in muscles in these four catabolic states.
9 ent muscle proteolysis in diabetes and other catabolic states.
10 he use of supraphysiologic GH doses to treat catabolic states.
11 ate to support key metabolic pathways during catabolic states.
12 egulators of skeletal muscle mass in various catabolic states.
13 ogramme that alternates between anabolic and catabolic states.
14 erone deficiency contributes to the profound catabolic state and loss of lean body mass associated wi
15 energy metabolism contributing to a chronic catabolic state and those who were studied further also
16 fragment in muscle biopsies is increased in catabolic states and could be used in conjunction with o
18 hus, 1) the atrophy associated with systemic catabolic states and following disuse involves similar t
19 ytokines or insulin resistance are common in catabolic states and will activate caspases, we examined
20 in metabolic rates, initially related to the catabolic state, are high; later, these rates are high r
22 uffer acute brain injury in the context of a catabolic state associated with nonspecific illness.
23 eptors for extracellular molecules creates a catabolic state characterized by atrophy and a decline i
24 inflammation, cancer or infections provoke a catabolic state characterized by enhanced muscle proteol
25 megestrol acetate) in malnutrition and other catabolic states has been the subject of considerable re
30 on in CF, we hypothesized that their protein catabolic state is related to reduced insulin secretion
31 , might play a cardio-protective role during catabolic states known to increase Arg plasma levels sev
33 tput to accompany the ever-changing anabolic/catabolic state of the liver cell, but the wiring of thi
35 readily revealed and play a crucial part in catabolic states or in hormone deficiencies that mimic s
37 levations in plasma aldosterone (ALDO) and a catabolic state that includes bone wasting are expected.
38 c changes consistent with the induction of a catabolic state that was not rescued by inositol supplem
39 combined with low-dose insulin reverses the catabolic state through suppression of hyperglucagonemia
40 net result was a change from an essentially catabolic state to a highly positive protein balance, bo
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