Researchers from the Ling Qi Laboratory at UVA have identified the SEL1L-HRD1 protein complex as crucial for regulating leptin receptor turnover, shedding light on the molecular mechanisms behind metabolic disorders. Their study in Nature Communications highlights the role of endoplasmic reticulum-associated protein degradation (ERAD) in the hypothalamus, with significant implications for diet-induced obesity (DIO) and type 2 diabetes.
The team found that SEL1L is vital in POMC-expressing neurons, essential for energy balance and appetite regulation. The absence of SEL1L impairs leptin signaling, increasing susceptibility to high-fat diet-induced issues like fatty liver disease, glucose intolerance, and insulin and leptin resistance.
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