Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperproliferation and delayed expression of enzyme activity occur in small intestinal enterocytes of aging rats, and starvation and refeeding result in impaired control of these processes. Since altered polyamine metabolism may accompany changes in enterocyte proliferation, we studied the effects of nutrient manipulation upon cell numbers, ornithine decarboxylase (ODC) activity and polyamine content in jejunum and ileum of 4- to 5- and 26- to 27-month Fischer rats. In both groups, cell numbers fell during starvation and and increased during refeeding. Crypt cell hyperplasia was found in aging animals. Jejunal putrescine, spermine and spermidine content were greater in older rats, fell during starvation, and rose during refeeding. Ileal ODC activity was 66% greater in the aging rats, but jejunal ODC activity was modestly increased in young animals. Intestinal polyamine content correlates with proliferative changes and polyamine metabolism responds appropriately to nutrient manipulation during aging. Dissociation of ODC activity and polyamine content in aging jejunum probably occurred because enterocyte differentiation was delayed. Investigation of intestinal polyamine metabolism may be useful in elucidating deranged proliferative activities found in the intestine of aging rodents.
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PMID:Aging and intestinal polyamine metabolism in the rat. 236 31

Ceramide is a sphingolipid bioactive molecule that induces apoptosis and other forms of cell death, and triggers macroautophagy (referred to below as autophagy). Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner. Dissociation of the Beclin 1:Bcl-2 complex, and the subsequent stimulation of autophagy have been observed in various contexts in which the cellular level of long-chain ceramides was increased. It is notable that the conversion of short-chain ceramides (C(2)-ceramide and C(6)-ceramide) into long-chain ceramide via the activity of ceramide synthase is required to trigger autophagy. The dissociation of the Beclin 1:Bcl-2 complex has also been observed in response to tamoxifen and PDMP (an inhibitor of the enzyme that converts ceramide to glucosylceramide), drugs that increase the intracellular level of long-chain ceramides. However, and in contrast to starvation, overexpression of Bcl-2 does not blunt ceramide-induced autophagy. Whether this autophagy that is unchecked by forced dissociation of the Beclin 1:Bcl-2 complex is related to the ability of ceramide to trigger cell death remains an open question. More generally, the question of whether ceramide-induced autophagy is a dedicated cell death mechanism deserves closer scrutiny.
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PMID:Ceramide-induced autophagy: to junk or to protect cells? 1933 26

Physico-chemical and biological parameters were monitored both throughout different oxygen cut off and starvation (OCS) times (6 h-72 h) and after the restoration of normal operational conditions. Sludge apparent viscosity and soluble extracellular polymeric substances (EPS) characteristics were measured to determine the activated sludge (AS) properties. Oxygen transfer, biological activity with specific oxygen uptake rate (SOUR) measurements during endogenous/exogenous conditions (without any external substrate/with external substrate consumption) and chemical oxygen demand (COD) removal were measured to assess the AS performances. During the different stress times, AS deflocculated as a decrease of apparent viscosity was observed and microorganisms biodegraded the released EPS to survive. After aeration return, and under endogenous conditions, size exclusion chromatographic fingerprints of soluble EPS were modified and macromolecules probably of type humic-like substances appeared in significant quantities. These new macromolecules presumably acted as biosurfactants. Consequently, the liquid surface tension, as well as the oxygen transfer rate (OTR), decreased. Under exogenous conditions, high biological activity (SOUR = 11.8 +/- 2.1 mg(O2 x g(MLVSS)(-1) x h(-1)) compensated the decrease of oxygen transfer. Finally, AS biomass maintained a constant COD degradation rate (15.7 +/- 1.9 mg(O2) x g(MLVSS)(-1) x h(-1)) before and after the disturbances for all times tested. This work demonstrates that AS microorganisms can counteract concomitant oxygen and nutrients shortage when the duration of such a condition does not exceed 72 h. Dissociation of endogenous/exogenous conditions appears to offer an ideal laboratory model to study EPS and biomass activity effects on oxygen transfer.
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PMID:Impact of oxygen cut off and starvation conditions on biological activity and physico-chemical properties of activated sludge. 2383 41

Mitophagy is a critical process that safeguards mitochondrial quality control in order to maintain proper cellular homeostasis. Although the mitochondrial-anchored receptor Atg32-mediated cargo-recognition system has been well characterized to be essential for this process, the signaling pathway modulating its expression as a contribution of governing the mitophagy process remains largely unknown. Here, bioinformatics analyses of epigenetic or transcriptional regulators modulating gene expression allow us to identify the Paf1 complex (the polymerase-associated factor 1 complex, Paf1C) as a transcriptional repressor of ATG genes. We show that Paf1C suppresses glucose starvation-induced autophagy, but does not affect nitrogen starvation- or rapamycin-induced autophagy. Moreover, we show that Paf1C specifically regulates mitophagy through modulating ATG32 expression. Deletion of the genes encoding two core subunits of Paf1C, Paf1 and Ctr9, increases ATG32 and ATG11 expression and facilitates mitophagy activity. Although Paf1C is required for many histone modifications and gene activation, we show that Paf1C regulates mitophagy independent of its positive regulatory role in other processes. More importantly, we also demonstrate the mitophagic role of PAF1C in mammals. Overall, we conclude that Paf1C maintains mitophagy at a low level through binding the promoter of the ATG32 gene in glucose-rich conditions. Dissociation of Paf1C from ATG32 leads to the increased expression of this gene, and mitophagy induction upon glucose starvation. Thus, we uncover a new role of Paf1C in modulating the mitophagy process at the transcriptional level.
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PMID:The Paf1 complex transcriptionally regulates the mitochondrial-anchored protein Atg32 leading to activation of mitophagy. 3152 19