Hormonal
Cideb deficiency improves insulin sensitivity in the liver by increasing tyrosine phosphorylation of IRS-1 and phosphorylation of AKT, independent of changes in adiposity.
This study suggests that targeting liver-specific pathways like Cideb can improve insulin sensitivity without requiring immediate weight loss. This highlights the importance of metabolic health markers (like insulin sensitivity) beyond just body weight. Future therapies might target these specific liver mechanisms to treat type 2 diabetes and metabolic syndrome.
Cideb-null mice showed drastically reduced levels of blood glucose when injected with excessive amounts of insulin compared with those of wild-type mice (ITT; Fig. 5D; P < 0.001)... Levels of IRS-1 tyrosine phosphorylation were significantly increased in the liver of Cideb mutant mice after insulin stimulation... The improved liver insulin sensitivity in Cideb-null mice is not dependent on adiposity, as Cideb-null mice with 1-month high-fat diet feeding already show improved insulin sensitivity but no difference in adiposity.
Why this rating
Strong mechanistic evidence with clear molecular markers (IRS-1, AKT) and functional tests (ITT, GTT).
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
- 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.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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