catabolic


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cat·a·bol·ic

(kat'ă-bol'ik),
Relating to or promoting catabolism.

cat·a·bol·ic

(kat'ă-bol'ik)
Relating to or promoting catabolism.

Catabolic

A metabolic process in which energy is released through the conversion of complex molecules into simpler ones.
Mentioned in: Anabolic Steroid Use
References in periodicals archive ?
Figure 1: On the left is Western blot analysis on non-tumour (NT) and tumour (T) tissues from HCC patients enrolled at NCCS, showing a sharp decrease in expression of three important BCAA catabolic enzymes (The GAPDH enzyme was used as loading control).
Heightened catabolic responses in the 4-5 year old trees may be a result of intercropping, in which cover canopies do not exist, and sunlight may penetrate through the foliage.
This indicates the high contents of catabolic substances in the blood of these rats (Figure 1).
NF-[kappa]B signaling pathway is intimately involved in the impaired anabolism and enhanced catabolism by upregulating catabolic cytokines, MMP-1 and MMP-13 in intervertebral disc cells [41].
Effect of training on plasma anabolic and catabolic steroid hormones and their response during physical exercise.
Catabolic effects of continuous human PTH (1-38) in vivo is associated with sustained stimulation of RANKL and inhibition of osteoprotegerin and gene-associated bone formation.
In this case, the child was symptomatic immediately after birth and deteriorated further when feeding was established and catabolic stress increased.
Notably, 50% Lr-PRG supernatant exhibited a trend to counteract the COL2A1 downregulation (catabolic) effect of LPS in this in vitro system of synovitis, which could indicate that PRP (particularly Lr-PRP) preparations could be useful to induce chondrogenic differentiation of stem cells from synovial membrane in patients with OA [24, 25].
These findings provide a morphological evidence of imbalance within the so-called inflammatory factor network between catabolic proinflammatory and anabolic anti-inflammatory mediators among JT, OA, and RA patients.
Senescent cells are viable and manifest a proinflammatory and catabolic phenotype defined as senescence-associated secretory phenotype (SASP).
Recent reports show that enhancement of autophagy significantly reduces cartilage degradation by reducing the death of chondrocytes and catabolic factors such as MMP-13 expression [12, 13].
Repletion of deficient amino acids, zinc, micro nutrients, and intravenous glucose infusion may attenuate the catabolic state.