The ability of some biological systems to sense light—such as the visual and circadian systems—is both logical and well understood. In contrast, a recent finding made when researchers were studying how mice control their body temperature, found that light exposure regulates the function of adipocytes. More specifically, the team uncovered how light modulates how brown and white adipocytes, located deep in the body, work together during metabolism.

The study, which has implications far beyond describing how mice stay warm, noted that disruptions to this fundamental metabolic process appear to reflect an unhealthy aspect of modern life—spending too much time indoors.

Graphical abstract [Nayak et al.]

The work is published in Cell Reports, in a paper titled, “Adaptive Thermogenesis in Mice Is Enhanced by Opsin 3-Dependent Adipocyte Light Sensing.

The authors describe “a light response pathway in mice that employs encephalopsin to regulate the function of adipocytes” and establish “a key mechanism in which light-dependent, local regulation of the lipolysis response in white adipocytes regulates energy metabolism.”

“This paper,” noted Richard Lang, PhD, director of the visual systems group at the Cincinnati Children’s Hospital Medical Center, “represents a significant change in the way we view the effects of light on our bodies.

“Our bodies evolved over the years under the sun’s light, including developing light-sensing genes called opsins,” added Lang. “But now we live so much of our days under artificial light, which does not provide the full spectrum of light we all get from the sun.”

Many people understand that certain wavelengths of light can be harmful, such as ultraviolent light. This study describes a different, healthy role for light exposure. Despite the fur of a mouse, or the clothing of a person, light does get inside our bodies. Photons may slow down and scatter around once they pass the outer layers of skin, Lang said. But when they do enter, they affect how cells behave.

“This idea of light penetration into deep tissue is very new, even to many of my scientific colleagues,” Lang said. “But we and others have been finding opsins located in a variety of tissue types. This is still just the beginning of this work.”

These images show expression of the OPN3 gene (in blue) in white fat cells of mice in two locations. The upper panel shows interscapular white adipocytes (above a layer of muscle and above brown adipose tissue). The lower panel shows white adipocytes from the inguinal adipose depot. [Cincinnati Children’s Hospital Medical Center]

How light ignites an internal fire

The research team studied how mice respond when exposed to cold temperatures—about 40°F. They already knew that mice, much like humans, use both a shivering response and an internal fat-burning response to heat themselves.

Deeper analysis revealed that the internal heating process is compromised in the absence of the gene OPN3 and exposure specifically to a 480-nm wavelength of blue light. This wavelength is a natural part of sunlight but occurs only in low levels in most artificial light.

When the light exposure occurs, OPN3 prompts white fat cells to release fatty acids into the bloodstream. Various types of cells can use these fatty acids as energy to fuel their activities. But brown fat literally burns the fatty acids (in a process called oxidation) to generate heat that warms up the chilly mice.

When mice were bred to lack the OPN3 gene, they failed to warm up as much as other mice when placed in cold conditions. Surprisingly, even wild type mice failed to warm up when they were exposed to light that lacked the blue wavelength.

These data prompted the team to conclude that sunlight is required for normal energy metabolism. At least in mice. While the scientists strongly suspect that a similar light-dependent metabolic pathway exists in humans, more experimentation is necessary.

“If the light-OPN3 adipocyte pathway exists in humans, there are potentially broad implications for human health,” the study stated. “Our modern lifestyle subjects us to unnatural lighting spectra, exposure to light at night, shift work, and jet lag, all of which result in metabolic disruption. Based on the current findings, it is possible that insufficient stimulation of the light-OPN3 adipocyte pathway is part of an explanation for the prevalence of metabolic deregulation in industrialized nations where unnatural lighting has become the norm.”

In theory, “light therapy” could become a method for preventing metabolic syndrome from developing into diabetes. Replacing indoor lights with better, full-spectrum lighting systems also could improve public health, Lang said.

However, more study is needed to pin down the potential therapeutic value of light therapy. Questions to answer include determining how much sunlight is needed to support a healthy metabolism and whether people battling obesity might lack a functional OPN3 gene in their fat cells. For now, however, “if people want to take anything personal away from this, you likely can’t go wrong by spending more time outside,” Lang said.

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