Mixed
Genetic deficiency of the liver-expressed protein Cideb confers resistance to high-fat diet-induced obesity and liver steatosis by enhancing fatty acid oxidation and suppressing lipogenesis.
This research identifies Cideb as a critical regulator in the liver. While you cannot directly 'take' Cideb, the findings suggest that therapies targeting this protein or its downstream effects (increasing fatty acid oxidation and decreasing lipogenesis) could treat obesity and fatty liver. For now, the key takeaway is that enhancing fatty acid oxidation and reducing de novo lipogenesis are effective strategies for managing diet-induced obesity.
Cideb-null mice had lower levels of plasma triglycerides and free fatty acids and were resistant to high-fat diet–induced obesity and live steatosis. In addition, Cideb mutant mice displayed significantly increased insulin sensitivity and enhanced rate of whole-body metabolism and hepatic fatty acid oxidation.
Why this rating
High-quality mechanistic evidence using knockout mice with multiple metabolic endpoints, though not a human clinical trial.
Source
Cideb Regulates Diet-Induced Obesity, Liver Steatosis, and Insulin Sensitivity by Controlling Lipogenesis and Fatty Acid Oxidation
John Li et al. · Diabetes · 2007
DOI 10.2337/db07-0040
More from this paper
- Cideb deficiency improves insulin sensitivity in the liver by increasing tyrosine phosphorylation of IRS-1 and phosphorylation of AKT, independent of changes in adiposity.Good
- Cideb deficiency reduces hepatic lipogenesis by downregulating SREBP1c and its downstream targets (ACC, FAS, SCD1), while simultaneously increasing fatty acid oxidation.Good
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