Essential role of SBP‐1 activation in oxygen deprivation induced lipid accumulation and increase in body width/length ratio in <i>Caenorhabditis elegans</i>

Taghibiglou, Changiz; Martin, Henry G. S.; Rose, Jacqueline K.; Ivanova, Nadia; Lin, Conny H.; Lau, H. Lee; Rai, Susan; Wang, Yu Tian; Rankin, Catharine H.

doi:10.1016/j.febslet.2009.01.045

Cited by 18 publications

(10 citation statements)

References 42 publications

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“…However, whether oxygen controls SREBP activity in other systems is unclear. One report in C. elegans indicates that low oxygen up-regulates SBP-1, but the mechanism by which this occurs is not known (Taghibiglou et al 2009). The ability of fission yeast cells to sense ergosterol synthesis as a measure of environmental oxygen is coupled to the fact that this yeast does not import exogenous sterols.…”

Section: Oxygen Regulation Of Metazoan Srebpsmentioning

confidence: 99%

Evolutionary conservation and adaptation in the mechanism that regulates SREBP action: what a long, strange tRIP it's been

Osborne

Espenshade²

2009

Genes Dev.

229

249

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Sterol regulatory element-binding proteins (SREBPs) are a subfamily of basic helix–loop–helix leucine zipper (bHLH-LZ) transcription factors that are conserved from fungi to humans and are defined by two key features: a signature tyrosine residue in the DNA-binding domain, and a membrane-tethering domain that is a target for regulated proteolysis. Recent studies including genome-wide and model organism approaches indicate SREBPs coordinate cellular lipid metabolism with other cellular physiologic processes. These functions are broadly related as cellular adaptation to environmental changes ranging from nutrient fluctuations to toxin exposure. This review integrates classic features of the SREBP pathway with newer information regarding the regulation and sensing mechanisms that serve to assimilate different cellular physiologic processes for optimal function and growth.

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Section: Oxygen Regulation Of Metazoan Srebpsmentioning

confidence: 99%

Evolutionary conservation and adaptation in the mechanism that regulates SREBP action: what a long, strange tRIP it's been

Osborne

Espenshade²

2009

Genes Dev.

229

249

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“…61 C. elegans adapts to hypoxia through activation of the hypoxia-inducible factor, which leads to the transcription of a number of genes, including sbp-1, which cause accumulation of body fat. 62 Obesity therapeutics C. elegans exposed to compounds that can potentially increase or decrease body weight can identify active obesity interventions. 63 Atypical antipsychotic medications are well known to result in weight gain when used clinically in humans.…”

Section: Elegans In Obesity Research J Zheng and Fl Greenwaymentioning

confidence: 99%

Caenorhabditis elegans as a model for obesity research

Zheng

Greenway

2011

Int J Obes

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Caenorhabditis elegans (C. elegans) is a small nematode that conserves 65% of the genes associated with human disease, has a 21-day lifespan, reproductive cycles of 3 days, large brood sizes, lives in an agar dish and does not require committee approvals for experimentation. Research using C. elegans is encouraged and a Caenorhabditis Genetics Center (CGC, Minnesota) is funded by the National Institutes of Health-National Center for Research Resources. Many genetically manipulated strains of C. elegans are available at nominal cost from the CGC. Studies using the C. elegans model have explored insulin signaling, response to dietary glucose, the influence of serotonin on obesity, satiety, feeding and hypoxia-associated illnesses. C. elegans has also been used as a model to evaluate potential obesity therapeutics, explore the mechanisms behind single gene mutations related to obesity and to define the mechanistic details of fat metabolism. Obesity now affects a third of the US population and is becoming a progressively more expensive public health problem. Faster and less expensive methods to reach more effective treatments are clearly needed. We present this review hoping to stimulate interest in using the C. elegans model as a vehicle to advance the understanding and future treatment of obesity.

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“…Instead, increased fatty acid synthesis may be important for anabolic activity and to regenerate reducing equivalents for continued glycolytic activity. Fatty acid synthesis is a hallmark of hypoxic tumor cells (Romero-Garcia et al, 2011), and in C. elegans the SREBP homolog sbp-1 is required for fatty acid accumulation after anoxia (Taghibiglou et al, 2009). This result suggests that changes in lipid metabolism are essential parts of the response to hypoxia.…”

Section: Adaptations To Anoxiamentioning

confidence: 99%

Interactions between oxygen homeostasis, food availability, and hydrogen sulfide signaling

Iranon¹,

Miller²

2012

Front. Gene.

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The ability to sense and respond to stressful conditions is essential to maintain organismal homeostasis. It has long been recognized that stress response factors that improve survival in changing conditions can also influence longevity. In this review, we discuss different strategies used by animals in response to decreased O2 (hypoxia) to maintain O2 homeostasis, and consider interactions between hypoxia responses, nutritional status, and H2S signaling. O2 is an essential environmental nutrient for almost all metazoans as it plays a fundamental role in development and cellular metabolism. However, the physiological response(s) to hypoxia depend greatly on the amount of O2 available. Animals must sense declining O2 availability to coordinate fundamental metabolic and signaling pathways. It is not surprising that factors involved in the response to hypoxia are also involved in responding to other key environmental signals, particularly food availability. Recent studies in mammals have also shown that the small gaseous signaling molecule hydrogen sulfide (H2S) protects against cellular damage and death in hypoxia. These results suggest that H2S signaling also integrates with hypoxia response(s). Many of the signaling pathways that mediate the effects of hypoxia, food deprivation, and H2S signaling have also been implicated in the control of lifespan. Understanding how these pathways are coordinated therefore has the potential to reveal new cellular and organismal homeostatic mechanisms that contribute to longevity assurance in animals.

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Essential role of SBP‐1 activation in oxygen deprivation induced lipid accumulation and increase in body width/length ratio in Caenorhabditis elegans

Cited by 18 publications

References 42 publications

Evolutionary conservation and adaptation in the mechanism that regulates SREBP action: what a long, strange tRIP it's been

Evolutionary conservation and adaptation in the mechanism that regulates SREBP action: what a long, strange tRIP it's been

Caenorhabditis elegans as a model for obesity research

Interactions between oxygen homeostasis, food availability, and hydrogen sulfide signaling

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