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Cornell Researchers Unlock the Secret to Age-Defying Weight Management

by Universalwellnesssystems

New research from Cornell University’s Department of Nutritional Sciences reverses the effects of a slowing metabolism by stimulating the production of beige fat cells to prevent age-related weight gain, obesity and related health problems. Beige adipocytes, a subtype of white adipose tissue, share thermogenic properties with brown adipose tissue and may help lower blood sugar levels and fatty acids that contribute to heart disease. increase. As we age, we become less sensitive to cold temperatures, which stimulate the production of beige fat. In this study, a specific signaling pathway was discovered that suppresses beige adipogenesis in aged mice. By suppressing this pathway, scientists were able to encourage the production of beige-colored fat in older animals that would otherwise not be produced.

Researchers at Cornell University have found that stimulating the production of beige fat cells can prevent age-related weight gain and related health problems. may increase beige fat production in aged mice, providing a therapeutic approach in humans.

New research suggests strategies to prevent age-related weight gain. This helps prevent obesity and related health problems such as type 2 diabetes, heart disease and chronic inflammation.

The effects of slowing metabolism can be reversed by stimulating the production of specific types of fat cells, according to new research by researchers at Cornell University’s Department of Nutritional Sciences at the University of Human Ecology and the College of Agriculture. life science.

Mammals, including humans, have two main types of fat. White adipose tissue (WAT), which stores energy from excess calorie intake, and brown adipose tissue (BAT), which burns calories and produces heat to maintain body temperature.

A study published in the journal on March 31

When a person experiences sustained exposure to cold temperatures, stem cells known as adipose progenitor cells form thermogenic beige fat cells within white fat. As people age, the response to that stimulus weakens, tipping the balance toward white fat production.

“There are seasonal changes in beige fat in young humans,” said Dan Berry, assistant professor in the Division of Nutritional Sciences, “but an older person would have to stand outside in the snow in their underwear to get those same effects.”

In earlier work, Berry observed that the aging process impairs the formation of beige fat cells in response to cold temperatures. Identify the biochemistry behind the slowdown, he said, and the same process could be reversed to achieve therapeutic outcomes.

“This is the ultimate goal,” said Abigail Benvie, lead author of the new study and a doctoral student researcher in Berry’s lab. “Without having to subject people to cold exposure for prolonged periods of time, are there metabolic pathways we can stimulate that could produce the same effect?”

In the paper, they reveal the role of a specific signaling pathway that suppresses beige fat formation in older mice by antagonizing the immune system. By suppressing that pathway in aging mice, the scientists were able to prompt beige fat production in aged animals that otherwise would not.

Reference: “Age-dependent Pdgfrβ signaling drives adipocyte progenitor dysfunction to alter the beige adipogenic niche in male mice” by Abigail M. Benvie, Derek Lee, Benjamin M. Steiner, Siwen Xue, Yuwei Jiang and Daniel C. Berry, 1 March 2023, Nature Communications.
DOI: 10.1038/s41467-023-37386-z

The study was co-authored by master’s student Derek Lee, Benjamin M. Steiner, Ph.D. ’22, and doctoral student Siwen Xue, along with Yuwei Jiang from the University of Illinois at Chicago. The research was funded through a $2.2 million, five-year grant from the National Institutes of Health. The grant also will enable Berry’s lab to delve deeper into the role of the pathway it has identified, as well as other molecular regulators of beige fat formation and elucidate how their levels and activity change during the aging process.

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