Hyperglycemic Stress and Carbon Stress in Diabetic Glucotoxicity

Xiaoting Luo; Jinzi Wu; Siqun Jing; Liang-Jun Yan

doi:10.14336/ad.2015.0702

A chromium alloy containing zirconium, niobium and carbon: Stress-rupture properties and the control of ductility by modification of microstructure

Journal of the Less Common Metals ◽

10.1016/0022-5088(72)90015-x ◽

1972 ◽

Vol 26 (1) ◽

pp. 127-138 ◽

Cited By ~ 1

Author(s):

D.E. Miles ◽

J.A. Rogers

Keyword(s):

Stress Rupture ◽

Chromium Alloy ◽

Stress Rupture Properties ◽

Rupture Properties ◽

Carbon Stress

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PHB accumulation in Nostoc muscorum under different carbon stress situations

Journal of Applied Phycology ◽

10.1007/s10811-011-9663-6 ◽

2011 ◽

Vol 24 (2) ◽

pp. 157-162 ◽

Cited By ~ 32

Author(s):

Sandra Mareike Haase ◽

Bernhard Huchzermeyer ◽

Thomas Rath

Keyword(s):

Nostoc Muscorum ◽

Carbon Stress

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Reactive Acyl-CoA Species Modify Proteins and Induce Carbon Stress

Trends in Biochemical Sciences ◽

10.1016/j.tibs.2018.02.002 ◽

2018 ◽

Vol 43 (5) ◽

pp. 369-379 ◽

Cited By ~ 23

Author(s):

Alec G. Trub ◽

Matthew D. Hirschey

Keyword(s):

Carbon Stress

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Protein Modifications as Manifestations of Hyperglycemic Glucotoxicity in Diabetes and Its Complications

Biochemistry Insights ◽

10.4137/bci.s36141 ◽

2016 ◽

Vol 9 ◽

pp. BCI.S36141 ◽

Cited By ~ 25

Author(s):

Hong Zheng ◽

Jinzi Wu ◽

Zhen Jin ◽

Liang-Jun Yan

Keyword(s):

Oxidative Stress ◽

Posttranslational Modifications ◽

Metabolic Pathways ◽

Polyol Pathway ◽

Protein Modifications ◽

Redox Imbalance ◽

Adp Ribosylation ◽

Carbon Stress

Diabetes and its complications are hyperglycemic toxicity diseases. Many metabolic pathways in this array of diseases become aberrant, which is accompanied with a variety of posttranslational protein modifications that in turn reflect diabetic glucotoxicity. In this review, we summarize some of the most widely studied protein modifications in diabetes and its complications. These modifications include glycation, carbonylation, nitration, cysteine S-nitrosylation, acetylation, sumoylation, ADP-ribosylation, O-GlcNAcylation, and succination. All these posttranslational modifications can be significantly attributed to oxidative stress and/or carbon stress induced by diabetic redox imbalance that is driven by activation of pathways, such as the polyol pathway and the ADP-ribosylation pathway. Exploring the nature of these modifications should facilitate our understanding of the pathological mechanisms of diabetes and its associated complications.

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Stress-Induced Cell Death Is Mediated by Ceramide Synthesis in Neurospora crassa

Eukaryotic Cell ◽

10.1128/ec.00147-08 ◽

2008 ◽

Vol 7 (12) ◽

pp. 2147-2159 ◽

Cited By ~ 19

Author(s):

Nora S. Plesofsky ◽

Steven B. Levery ◽

Sherry A. Castle ◽

Robert Brambl

Keyword(s):

Cell Death ◽

Heat Shock ◽

Neurospora Crassa ◽

Glucose Deprivation ◽

Acid Synthesis ◽

Mitogen Activated Protein Kinase ◽

Ceramide Synthase ◽

Wild Type ◽

Combined Stresses ◽

Carbon Stress

ABSTRACT The combined stresses of moderate heat shock (45°C) and analog-induced glucose deprivation constitute a lethal stress for Neurospora crassa. We found that this cell death requires fatty acid synthesis and the cofactor biotin. In the absence of the cofactor, the stressed cells are particularly sensitive to exogenous ceramide, which is lethal at low concentrations. When we extracted endogenous sphingolipids, we found that unique ceramides were induced (i) by the inhibitory glucose analog 2-deoxyglucose and (ii) by combined heat shock and 2-deoxyglucose. We determined that the former is a 2-deoxyglucose-modified ceramide. By structural analysis, we identified the latter, induced by dual stress, as C18(OH)-phytoceramide. We also identified C24(OH)-phytoceramide as a constitutive ceramide that continues to be produced during the combined stresses. The unusual C18(OH)-phytoceramide is not made by germinating asexual spores subjected to the same heat and carbon stress. Since these spores, unlike growing cells, do not die from the stresses, this suggests a possible connection between synthesis of the dual-stress-induced ceramide and cell death. This connection is supported by the finding that a (dihydro)ceramide synthase inhibitor, australifungin, renders cells resistant to death from these stresses. The OS-2 mitogen-activated protein kinase, homologous to mammalian p38, may be involved in the cell death signaling pathway. Strains lacking OS-2 survived the combined stresses better than the wild type, and phosphorylated OS-2 increased in wild-type cells in response to heat shock and combined heat and carbon stress.

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