
Protein Kinase C Epsilon Deletion in Adipose Tissue, but Not in Liver, Improves Glucose Tolerance
A new study by Australian researchers, out today, is challenging what we know about the causes of diabetes. The new research points to fat tissue as a source of disease, and widens our understanding beyond the traditional focus on liver and pancreas as the main culprits. The findings, uncovered in mice, are published in the high-impact journal Cell Metabolism.
The new research is centred around the surprising finding that protein kinase C epsilon (PKCε), known to be involved in diabetes, isn’t acting in the liver or the pancreas as was once assumed. Researchers have long known that PKCε is important for the development of diabetes...
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![Temporally regulated TH signaling specifies cone subtypes. (A) Embryonic stem cell–derived human retinal organoids [wild type (WT)] generate S and L/M cones. Blue, S-opsin; green, L/M-opsin. (B) Organoids that lack thyroid hormone receptor β (Thrβ KO) generate all S cones. (C) Early activation of TH signaling (WT + T3) specifies nearly all L/M cones. (D) TH-degrading enzymes (such as DIO3) expressed early in development lower TH and promote S fate, whereas TH-activating regulators (such as DIO2) expressed later promote L/M fate.](https://infowebbie.com/scienceupdate/wp-content/uploads/2018/10/THeye-300x173.jpg)



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