Identification of a Novel Peroxisome Proliferator Responsive cDNA Isolated from Rat Hepatocytes as the Zinc-Finger Protein ZFP-37

1998 ◽  
Vol 152 (1) ◽  
pp. 107-118 ◽  
Author(s):  
John P. Vanden Heuvel ◽  
Peter Holden ◽  
Jonathan Tugwood ◽  
Christine Ingle ◽  
Weiyi Yen ◽  
...  
Keyword(s):  
Zinc Finger ◽  
Zinc Finger Protein ◽  
Rat Hepatocytes ◽  
Peroxisome Proliferator ◽  
Finger Protein

Connecting homocysteine and obesity through pyroptosis, gut microbiome, epigenetics, peroxisome proliferator-activated receptor γ, and zinc finger protein 407

2018 ◽  
Vol 96 (10) ◽  
pp. 971-976 ◽  
Author(s):  
Anwesha Laha ◽  
Avisek Majumder ◽  
Mahavir Singh ◽  
Suresh C. Tyagi
Keyword(s):  
Zinc Finger ◽  
Gut Microbiome ◽  
Metabolic Disorders ◽  
Zinc Finger Protein ◽  
Specific Gene ◽  
Peroxisome Proliferator ◽  
Gene Promoters ◽  
Divalent Metal Ions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Finger Protein

Although homocysteine (Hcy), a part of the epigenome, contributes to cell death by pyroptosis and decreases peroxisome proliferator-activated receptor γ (PPARγ) levels, the mechanisms are unclear. Hcy is found in high concentrations in the sera of obese individuals, which can elicit an immune response as well by hypermethylating CpG islands of specific gene promoters, a marker of epigenetics. Hcy has also been established to chelate divalent metal ions like Cu2+ and Zn2+, but this role of Hcy has not been established in relationship with obesity. It has been known for a while that PPARγ dysregulation results in various metabolic disorders including glucose and lipid metabolism. Recently, zinc finger protein 407 (Zfp407) is reported to regulate PPARγ target gene expression without affecting PPARγ transcript and protein levels by synergistically working with PPARγ. However, the mechanism(s) of this synergy, as well as other factors contributing to or inhibiting this synergism, have not been proven. This review suggests that Hcy contributes to pyroptosis, changes gut microbiome, and alters PPARγ-dependent mechanism(s) via Zfp407-mediated upregulated adipogenesis and misbalanced fatty acid metabolism, which can predispose to obesity and, consequently, obesity-related metabolic disorders.

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