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Study from Pennington Biomedical Reveals How Warm Temperatures Influence Appetite and Weight Gain

Scientists identified neurons that connect warm temperatures with appetite and energy expenditure

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LSU's Pennington Biomedical Research Center identified a key brain mechanism that connects environmental temperature with appetite and energy balance, offering new insight into how external conditions can shape body weight over time. (PBRC)

Researchers at Pennington Biomedical Research Center have identified a key brain mechanism that connects environmental temperature with appetite and energy balance, offering new insight into how external conditions can shape body weight over time.

The findings, published in the journal Communications Biology, highlight a group of neurons that act as a critical integration point between thermoregulation – the body's ability to maintain its internal temperature – and the systems that control hunger and metabolism.

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The study, "Obesogenic effects of warm temperature involve feeding adaptation by preoptic area leptin receptor neurons," focused on a region of the brain called the hypothalamus, which plays a central role in regulating body temperature and energy balance. Scientists identified a subset of neurons, specifically preoptic area leptin receptor neurons, that respond to warm temperatures.

Using advanced techniques in animal models, researchers found that warm temperatures activate these neurons, which reduce food intake and increase feelings of fullness. Since these neurons communicate with the brain's melanocortin system, a key pathway that controls hunger and satiety, activating this pathway mimics the appetite-suppressing effects of warmth.

At first glance, this might suggest warm environments help prevent overeating, but the story is more complex. Despite reducing how much is eaten, warm temperatures also lower the body's energy expenditure – meaning fewer calories are burned. Therefore, even though appetite decreases, the reduction in calorie burning can be greater, ultimately leading to weight gain over time.

Researchers describe this as an "obesogenic" effect of warm environments, highlighting that temperature is an important, often overlooked, factor in long-term weight regulation.

"These results challenge traditional thinking that focuses primarily on diet and physical activity by showing that the brain integrates environmental cues, like temperature, alongside metabolic signals," said lead author Laura Kaiser, who is senior PhD student in the Central Leptin Signaling Laboratory under the direction of Dr. Heike Muenzberg-Gruening. "Understanding how these systems work together gives us a more complete picture of what drives body weight over time."

These findings open the door to potential new approaches for addressing obesity by targeting the brain pathways that link environment and metabolism. This can help to explain how the brain coordinates competing demands, such as maintaining body temperature while also regulating energy intake, and why environmental conditions can have such a strong, lasting impact on body weight.

Dr. Muenzberg-Gruening, Director of the Central Leptin Signaling Laboratory, said, "Warm environments are shown to reduce how much energy the body burns. Even if appetite goes down slightly, the overall effect can still promote weight gain. That helps explain how modern, temperature-controlled environments may contribute to obesity in ways we are only beginning to understand."

Understanding how temperature affects energy balance could help explain rising obesity rates in climate-controlled, indoor environments; suggests that warm environments may support weight gain in underweight individuals despite a reduction in appetite due to lower energy expenditure; inform new therapeutic strategies that target these neural circuits; and provide a more complete picture of how lifestyle and environment interact to shape long-term health.

This work was supported by the following grants: P20 RR02195, P/F NORC #2P30-DK072476-06, 2R01DK092587, R01AT011683 and 1-OT2OD023864-01. This work utilized the facilities of the Cell Biology and Bioimaging Core and Animal Metabolism and Behavior Core that are supported in part by COBRE (P20-RR021945) and NORC (1P30-DK072476) center grants from the National Institutes of Health, an NIH Equipment Grant (S10OD023703) and NIH Virus Center grant no. P40RR018604.

For more information, see www.pbrc.edu.

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