Research

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.

GoodSupportsHIGH confidence
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.
John Li et al. · Diabetes · 2007

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

mechanism_onlyCited 185×
Read the paper
DOI resolved against Crossref · corpus check 2026-06-10

This is one finding among thousands. Every one is graded and traced to its source, so you can see what the evidence actually supports. Browse the research →