We are working to understand human metabolism and what happens when this biological system breaks down. The problem is more important than ever, given the increasing burden that diabetes and other metabolic dysfunctions have on human health and society.



How obesity can rewire the immune system and the response to immunotherapy—and how to change that

When mice with atopic dermatitis—a common type of allergic skin inflammation—are treated with drugs that target the immune system, their thickened, itchy skin generally heals quickly. Yet the same treatment in obese mice only worsens their skin, according to a study by Professor Ronald Evans, Associate Professor Ye Zheng and collaborators from Gladstone Institutes and UC San Francisco. Obesity changes the molecular underpinnings of allergic inflammation, both in mice and humans, the team found. Their study demonstrates how obesity can change the immune system and how available drugs might be able to improve health outcomes for people with obesity.

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The protein that keeps the pancreas from digesting itself

Every day, your pancreas produces about one cup of digestive juices, a mixture of molecules that can break down the food you eat. But if these powerful molecules become activated before they make their way to the gut, they can damage the pancreas itself—digesting the very cells that created them, leading to the painful inflammation known as pancreatitis and predisposing a person to pancreatic cancer. Now, Professor Ronald Evans, co-first author Tae Gyu Oh and colleagues have discovered that a protein called ERR gamma plays a crucial role in preventing pancreatic autodigestion in mice. What’s more, they discovered that people with pancreatitis have lower levels of this protein in cells affected by inflammation.

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PLOS Genetics

Why hungry worms take risks

Whether it’s making rash decisions or feeling grumpy, hunger can make us think and act differently—“hangry,” even. But little is known about how hunger signals in the gut communicate with the brain to change behavior. Associate Professor Sreekanth Chalasani, co-first author Molly Matty and colleagues are using worms as a model to examine the molecular underpinnings that help explain how hunger makes an organism sacrifice comfort and make risky decisions to get a meal. Their latest findings reveal that proteins in intestinal cells move dynamically to transmit signals about hunger, ultimately driving worms to cross toxic barriers to reach food. Similar mechanisms may also occur in humans and could explain how we prioritize basic needs over comfort.

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