Ncb5or Deficiency Increases Fatty Acid Catabolism and Oxidative Stress

Xu, Ming; Wang, Wenfang; Frontera, Jennifer R.; Neely, Melanie C.; Lu, Jane; Aires, Daniel; Hsu, Fong‐Fu; Turk, John; Swerdlow, Russell H.; Carlson, Susan E.; Zhu, Hao

doi:10.1074/jbc.m110.196543

Cited by 31 publications

(44 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The previous studies provided evidence showing that the mRNA level of SCD2 in the liver of mice or rat is extremely low or not detectable, 7,13) and, recently, transcript level of SCD2 has been shown to be 84 to 462 times lower than that of SCD1 in the liver of mice. 14) Accordingly, transcript level of SCD2 relative to that of SCD1 in the liver of rats are significantly lower than that of mice. It is noted that SCD2 is predominantly expressed in the brain, 7) the peripheral nervous system, 15) the testis, 16) the ovary, 13) brown adipose tissue, 7) the skin (embryo and neonates) 17) and the liver (embryo and neonates).…”

Section: Discussionmentioning

confidence: 97%

Differential Induction of Stearoyl-CoA Desaturase 1 and 2 Genes by Fibrates in the Liver of Rats

Yamazaki

Okada

Sakamoto

et al. 2012

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

The administration of fibrates (fenofibrate, bezafibrate and clofibric acid) to rats induced stearoyl-CoA desaturase (SCD) in the liver, and increased relative expression of mRNAs encoding SCD1 and SCD2 in dose-and time-dependent manners. The magnitudes of the increases in SCD2 mRNA level caused by fenofibrate and clofibric acid were much higher than those of SCD1 at relatively higher doses of the fibrates, and a relatively long time (7 or 14 d) was required for significant induction of SCD2 mRNA expression compared with that of SCD1. Although the absolute number of transcripts for SCD2 was 1,800 times lower than that of SCD1 in the control liver, it was strikingly increased by fibrates. These results suggest that differential regulations operate for the gene expression between SCD1 and SCD2, and that the physiological significance of SCD2 is distinct from that of SCD1 in the liver.

show abstract

Section: Discussionmentioning

confidence: 97%

Differential Induction of Stearoyl-CoA Desaturase 1 and 2 Genes by Fibrates in the Liver of Rats

Yamazaki

Okada

Sakamoto

et al. 2012

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…Ncb5or is an endoplasmic reticulum-bound protein that has been implicated in lipid metabolism and diabetes (11,12). Ncb5or contains two redox domains; the amino-terminal portion is highly homologous to classical microsomal cytochrome b 5 , and the carboxyl-terminal portion of the protein is highly similar to cytochrome b 5 reductase domain (10).…”

Section: Fatty Acid Desaturases (Fads)mentioning

confidence: 99%

“…Furthermore, ␤-cells of 12-week-old (diabetic) Ncb5or knock-out mice have mitochondrial hypertrophy and hyperplasticity (31). Recently Xu et al (11) suggest that increased free FA accumulation and catabolism and oxidative stress are the major consequences of Ncb5or deficiency in liver.…”

Section: Fatty Acid Desaturases (Fads)mentioning

confidence: 99%

NAD(P)H Cytochrome b5 Oxidoreductase Deficiency in Leishmania major Results in Impaired Linoleate Synthesis Followed by Increased Oxidative Stress and Cell Death

Mukherjee

Santara

Das

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: NAD(P)H cytochrome b 5 oxidoreductase (Ncb5or) participates in a variety of metabolic conversions. Results: A new Ncb5or acts as a redox partner of ⌬12 fatty acid desaturase. Conclusion: Ncb5or null mutant suffers from impaired linoleate synthesis leading to oxidative stress and cell death. Significance: Our results have exposed a novel fatty acid synthesis pathway in L. major that differs from the mammalian system.

show abstract

“…Although the molecular and cellular mechanisms underlying FFA-induced ␤-cell apoptosis are not fully understood, participating processes include generation of reactive oxygen species (ROS) and mitochondrial dysfunction (8 -11), production of ceramide and nitric oxide (NO) (4,12), and induction of endoplasmic reticulum stress (13)(14)(15)(16)(17)(18).…”

mentioning

confidence: 99%

Group VIA Phospholipase A2 Mitigates Palmitate-induced β-Cell Mitochondrial Injury and Apoptosis

Song

Wohltmann

Tan

et al. 2014

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background: Lipid-induced ␤-cell loss contributes to type 2 diabetes mellitus (T2DM). Results: Palmitate-induced ␤-cell lipid oxidation, mitochondrial dysfunction, and apoptosis correlate inversely with expression of iPLA 2 ␤, which associates with mitochondria, generates monolysocardiolipin, and lowers oxidized phospholipid content. Conclusion: iPLA 2 ␤ mitigates palmitate-induced ␤-cell mitochondrial injury and apoptosis and may facilitate repair of oxidized lipids. Significance: Understanding lipid-induced ␤-cell loss could lead to T2DM therapies.

show abstract

Ncb5or Deficiency Increases Fatty Acid Catabolism and Oxidative Stress

Abstract: liver has a greater increase in Scd1 mRNA and protein levels. Together, these findings suggest that increased FFA accumulation and catabolism and oxidative stress are major consequences of Ncb5or deficiency in liver.

Cited by 31 publications

References 74 publications

Differential Induction of Stearoyl-CoA Desaturase 1 and 2 Genes by Fibrates in the Liver of Rats

Differential Induction of Stearoyl-CoA Desaturase 1 and 2 Genes by Fibrates in the Liver of Rats

NAD(P)H Cytochrome b5 Oxidoreductase Deficiency in Leishmania major Results in Impaired Linoleate Synthesis Followed by Increased Oxidative Stress and Cell Death

Group VIA Phospholipase A2 Mitigates Palmitate-induced β-Cell Mitochondrial Injury and Apoptosis

Contact Info

Product

Resources

About