Category: Dermatology

Categories : DermatologyTags :

A New Insight into the Mechanisms of Epidermal Renewal

On By ModernMedia
Picture by Macrovector on Freepik

The mechanisms underlying skin renewal are still poorly understood, but interleukin-38 (IL-38), a protein involved in regulating inflammatory responses, could provide insights. Researchers observed it for the first time in the form of condensates in keratinocytes, the cells of the epidermis. The presence of IL-38 in these aggregates is enhanced close to the skin’s surface exposed to atmospheric oxygen. This process could be linked to the initiation of programmed keratinocyte death, a natural process in the epidermis. This study, from University of Geneva (UNIGE) researchers, could bring new perspectives for the study of human epidermis and the illnesses that affect it.

Renewal of the epidermis relies on stem cells located in its lowest layer, which constantly produce new keratinocytes. These new cells are then pushed to the surface, differentiating along the way and accumulating protein condensates. Once they reach the top of the epidermis, they undergo a programmed death, cornification, to create a protective barrier of dead cells.

“The way in which the epidermis constantly renews itself is well documented. However, the mechanisms that drive this process are still not fully understood,” explains Gaby Palmer-Lourenço, associate professor at the Faculty of medicine of UNIGE and principal investigator. The study is published in the journal Cell Reports.

An unexpected role

Interleukin 38 is a small messenger protein that ensures communication between cells. It is known for its role in regulating inflammatory responses and its presence in keratinocytes, the cells of the epidermis, was previously associated with the preservation of the skin’s immune balance. “In keratinocytes in vivo, we found that IL-38 forms condensates, specialized protein aggregates with specific biochemical functions, a behavior that was not known for this protein,” recounts Gaby Palmer-Lourenço. Even more curious, the closer the keratinocytes were to the surface of the skin, the greater the amount of IL-38 within these condensates.

A reaction to oxidative stress

Blood vessels stop in the skin layer located below the epidermis. Therefore, the quantity of oxygen available for the keratinocytes is lower in the basal layers of the epidermis compared to the top layers that are directly exposed to the air that surrounds us. However, even though it is necessary to maintain cell functions, oxygen also causes oxidative stress by forming free radicals, reactive molecules that endanger the cell. “We were able to show that oxidative stress does indeed cause IL-38 condensation under laboratory conditions,” confirms Alejandro Díaz-Barreiro, postdoctoral fellow at the UNIGE Faculty of medicine, and first author of the study.

“Our results lead us to believe that, as we move closer to the epidermal surface, the increasing oxygen concentration promotes the formation of protein condensates, indicating to keratinocytes that they are in the right place to enter cell death,” furthers Gaby Palmer-Lourenço. This hypothesis provides new leads to decipher the mechanisms of epidermal renewal. It could also pave the way for a better understanding of the pathological mechanisms underlying certain skin diseases, such as psoriasis or atopic dermatitis. These questions will be further examined by the research group in future studies.

Contributing to an alternative to animal models

Alejandro Díaz-Barreiro is already working on the next step: “In the model we used previously, the effects of oxidative stress were artificially induced in a single layer of keratinocytes, a scenario that differs from the actual situation in the skin. We are therefore developing a new experimental system to apply oxygen gradients to in vitro reconstituted human epidermis. In this model, only the skin surface will be exposed to ambient air, while the other layers will be protected. This will allow us to study in detail the effect of oxidative stress on epidermal renewal.” By enabling a more precise analysis of human cells, this new system will provide an alternative to animal models often used for the study of skin biology and disease.

Source: Université de Genève

Categories : Dermatology Environmental EffectsTags :

Air Pollution Exposure may be Associated with Eczema

On By ModernMedia

Data from hundreds of thousands of U.S. adults suggests that each zip code increase of 10 µm/m3 in PM2.5 levels is associated with a doubling in eczema rates among residents

Photo by Kouji Tsuru on Pexels

People living in areas with higher levels of air pollution are more likely to have eczema, according to a new study published November 13, 2024 in the open-access journal PLOS ONE by Dr Jeffrey Cohen of Yale School of Medicine, USA.

The prevalence of eczema has increased globally with industrialisation, suggesting a possible contribution from environmental factors. In the new study, researchers used data from the U.S. National Institutes of Health All of Us Research Program, covering hundreds of thousands of U.S. adults. The current study included 286 862 people for whom there was available demographic, zip code and electronic health record data.

Overall, 12 695 participants (4.4%) were diagnosed with eczema. After controlling for demographics and smoking status, people with eczema were more likely to live in zip codes with high levels of fine particulate matter, or PM2.5, in the air. For every increase of 10 µm/m3 in average PM2.5 air pollution in their zip code, people were more than twice as likely to have eczema.

The authors conclude that increased air pollution, as measured by PM2.5, may influence the risk of developing eczema, likely through its effects on the immune system.

The authors add: “Showing that individuals in the United States who are exposed to particulate matter are more likely to have eczema deepens our understanding of the important health implications of ambient air pollution.”

Provided by PLOS

Categories : DermatologyTags :

Has the Root Cause for Psoriasis Finally been Found?

On By ModernMedia
Photo: CC0

Scientists may have uncovered the root cause of psoriasis. New research published in Nature Communications strongly suggests the hormone hepcidin may trigger the onset of the condition. This marks the first time hepcidin has been considered a potential causal factor. In mammals, hepcidin is responsible for regulating iron levels in the body.

Psoriasis is a chronic and sometimes debilitating skin disease affecting 2-3% of the global population. The condition is characterised by red, scaly patches that impact the quality of a patient’s life and can sometimes be life-threatening.

The international research team behind this discovery – which includes Dr Charareh Pourzand at the University of Bath – hopes their finding will lead to the development of new drugs able to block the action of the hormone.

Those most likely to benefit from such a treatment are patients with pustular psoriasis (PP) – a particularly severe and treatment-resistant form of the disease that can affect a patient’s nails and joints as well as skin.

Dr Pourzand, who studies ways to mitigate iron imbalances in the skin, said: “Psoriasis is a life-changing dermatological disease. Patients face a potentially disfiguring and lifelong affliction that profoundly affects their lives, causing them both physical discomfort and emotional distress. The condition can also lead to other serious health conditions.

“A new treatment targeting iron hormone imbalance in the skin offers hope. This innovative approach could significantly enhance the quality of life for millions, restoring their confidence and wellbeing.”

We need skin iron – but not too much

Iron is an essential trace metal, not just for transporting oxygen through the body’s circulatory system but also for maintaining healthy skin: it’s involved in many essential cellular functions, including wound healing, collagen production and immune function. However, iron overload in the skin can be harmful, amplifying the damaging effects of UV sunlight and causing hyperproliferative chronic diseases (where cells grow and multiply more than normal), including psoriasis.

Studies going back 50 years have reported high iron concentrations in the skin cells of psoriatic patients, however the cause of this excess and its significance to the condition have remained unclear until now.

The new study is the first to name hepcidin as the likely link.

Hepcidin is responsible for controlling how much iron is absorbed from food and later released into the body. In healthy individuals, it’s produced exclusively in the liver, however the new study has found that in people with psoriasis, the hormone is also generated in the skin.

Exposure to hepcidin triggers iron overload

In the new study, mice (which have many genetic and physiological similarities to humans) developed a rodent form of psoriasis after being exposed to high levels of skin-produced hepcidin.

This over-abundance of the hormone caused the animals’ skin cells to retain far more iron than was required. In turn, this excess iron triggered both a hyperproliferation of skin cells and an abnormally high concentration of inflammation-inducing neutrophils (a type of immune system cell) in the topmost layer of skin.

These two outcomes – an overproduction of skin cells and an abundance of neutrophils – are main features of human psoriasis.

Psoriasis runs in families though experts believe ‘environmental’ factors such as weight, infections and smoking are also triggers.

A disease with no cure

Currently there is no cure for psoriasis, though treatments that include topical creams, light therapy and oral drugs can help keep symptoms under control for patients with some forms of the condition. Recent treatments have focused on targeting the immune pathways that contribute to psoriasis developing.

Dr Pourzand believes a drug targeting hepcidin has the potential to dramatically improve treatment options for all psoriasis patients.

She said: “Our data strongly suggests hepcidin would be a good target for skin psoriasis treatment. A drug that can control this hormone could be used to treat flare-ups and keep patients in remission to prevent recurrence.

“Also, by adjusting the excess iron in psoriatic skin with customised iron chelators (substances that bind to excess iron in the body and help remove it), we would aim to halt the uncontrolled proliferation of psoriatic skin cells. This hyperproliferation is a major focus of our laboratory’s research on psoriasis therapy, conducted in collaboration with national and international scientists from the Skin@Bath Network, including those from this study.”

Source: University of Bath

Categories : Cancer DermatologyTags :

Common Skin Fungus Malassezia may Invade Tissue, Causing Breast Cancer

On By ModernMedia
Photo by National Cancer Institute on Unsplash

A common skin fungus, Malassezia globosa may invade deep tissues through the skin or by other means, then cause tumour growth, according to a new study. The study results appear in mBio, an open access journal of the American Society for Microbiology.

“It is important to take care of skin not only for beauty, but also for health,” said corresponding study author Qi-Ming Wang, PhD, a professor in the School of Life Sciences, Institute of Life Sciences and Green Development, Hebei University, Hebei, China. “As a factor promoting tumour growth, intertumoural microorganisms need to be paid more attention.” 

Recently, an increasing number of studies have shown a relationship between fungus and cancer. In the new study, Wang and colleagues subjected mouse breast cancer cells to tumour transplantation and then injected the M. globosa into the mammary gland fat pad. At the end of the experiment, they collected the tumour tissue to measure the tumour size and observe the content of intertumoral M. globosa. The researchers discovered that M. globosa colonises in breast fat pads leading to tumour growth. As a lipophilic yeast, the breast fat pad may provide an external source of lipids for the development of M. globosa, said the researchers. They also found that the pro-inflammatory cytokine interleukin (IL)-17a/macrophage axis plays a key role in mechanisms involved in M. globosa-induced breast cancer acceleration from the tumour immune microenvironment perspective.

“Although still controversial, the relationship between microbes and cancer is gaining attention. The imbalance of the microflora in the tumour may lead to disorder in the tumour microenvironment,” Wang said. “For example, Helicobacter pylori emerged as a potential cause of gastric cancer. In addition, Fusobacterium nucleatum has been identified as a potential colorectal cancer biomarker in stool and is predominantly found in the tumour microenvironment. Bacteria or fungi may play a direct (eg, toxins) or indirect (eg, inhibition of anti-tumoural immune responses) role in the tumorigenesis pathways of many of these risk factors. The imbalance of microbial homeostasis in tumours has a certain significance for cancer diagnosis, treatment and prognosis.” 

According to Wang, although the researchers found that M. globosa can promote the growth of tumours, the related transmission route is still unclear. 

Source: American Society for Microbiology

Categories : Cancer DermatologyTags :

Treating Radiation-induced Skin Injuries with Aspirin Hydrogels

On By ModernMedia
Photo by National Cancer Institute on Unsplash

Radiation is a powerful tool for treating cancer, but prolonged exposure can damage the skin. Radiation-induced skin injuries are painful and increase a person’s chances of infection and long-term inflammation. Now, researchers in ACS Biomaterials Science & Engineering report an aspirin-containing hydrogel that mimics the nutrient-rich fluid between cells and accelerates healing of skin damaged by radiation in animals. With further development, the new salve could provide effective and rapid wound healing for humans. 

Most people undergoing radiotherapy for cancer will experience radiation-induced skin injury that can include redness, pain, ulcers, necrosis and infection. There are few treatments for these wounds, with the most common methods being debridement and hyperbaric oxygenation. Wound dressings made from hydrogels are gaining popularity because they are easy to apply and provide a wet environment for healing that is similar to the inside of the body. Glycopeptide-based hydrogels are especially promising: In laboratory and animal studies, the nanofibre structures have promoted cellular growth and regulated cell adhesion and migration. A research team led by Jiamin Zhang, Wei Wang, Yumin Zhang and Jianfeng Liu proposed loading aspirin, a common anti-inflammatory drug, into a glycopeptide-based hydrogel to create a multifunctional wound dressing for radiation-induced skin injuries.       

In lab tests with cultured cells, the researchers found that the aspirin-contained hydrogel scavenged reactive oxygen species, repaired DNA double-strand breaks and inhibited inflammation caused by radiation exposure without affecting cellular growth. In mouse models of radiation-induced skin injury, the researchers found that dressing wounds for three weeks with the salve reduced acute injuries and accelerated healing – results that the team says point to its potential as an easy-to-administer, on-demand treatment option for reducing radiation damage and promoting healing in humans.

Source: American Chemical Society

Categories : DermatologyTags :

Starvation and Adhesion Drive Formation of Keratinocyte Patterns in Skin

On By ModernMedia
Skin cell (keratinocyte) This normal human skin cell was treated with a growth factor that triggered the formation of specialised protein structures that enable the cell to move. We depend on cell movement for such basic functions as wound healing and launching an immune response. Credit: Torsten Wittmann, University of California, San Francisco

Fingerprints are one of the best-recognised examples of pattern formation by epithelial cells. The primary cells in the epithelium are the keratinocytes, and they are known to form patterns at the microscopic and macroscopic levels. While factors affecting this pattern formation have been reported, the exact mechanisms underlying the process are still not fully understood.

A team of researchers, led by Associate Professor Ken Natsuga at the Faculty of Medicine, Hokkaido University, have revealed that cell-cell adhesion governs pattern formation in keratinocytes. Their findings were published in the journal Life Science Alliance.

“In this study, we used an immortalised keratinocyte cell line, called HaCaT, which retains all the properties of normal keratinocytes,” Natsuga explained. “In order to ensure that our findings were accurate, we established single-cell cultures from this cell line.”

The team observed pattern formation in both the original heterogeneous cell line, as well as in single-cell-derived cultures. During culturing, the keratinocytes moved randomly and spontaneously formed high- and low-density regions, leading to pattern formation.

The pattern formation was markedly influenced by starvation. When the culture medium was renewed, patterns were obscured, but reappeared as the nutrients in the culture medium were consumed by the keratinocytes.

The team then examined the gene expression in the keratinocytes, which revealed that cell adhesion proteins and keratinocyte differentiation proteins were upregulated in high-density regions. “As cell adhesion is necessary for the development of high-cell-density regions, we specifically investigated the expression of adherens junction (AJ) molecules such as E-cadherin and actin,” Natsuga elaborated. “We found that these molecules were localised at the intercellular junctions of high-density regions.”

The authors then used a mathematical model to confirm that, under spatially uniform density and stress, strong cell adhesion leads to the formation of density patterns. They were also able to demonstrate that the keratinocyte patterns influenced cell proliferation and differentiation, and that serum starvation influences epidermal stratification (a type of differentiation) in skin cells from mice.

“Our study presents a novel and robust model of cell–cell adhesion-induced patterning (CAIP),” concludes Natsuga. “We have deepened our mechanistic insight into cellular organization and its consequences for cell fate decisions and epithelial stratification.”  The team demonstrated that epithelial cell–cell adhesion is essential and sufficient for patterning. Future work will focus on adding more variables to the model to understand other processes that occur concurrently during development.

Source: Hokkaido University

Categories : Dermatology Diet and NutritionTags :

Can Omega-3 Fatty Acid Intake Affect Acne Severity?

On By ModernMedia
Picture by Macrovector on Freepik

In a study in the Journal of Cosmetic Dermatology that included 60 individuals with mild to moderate acne, following the Mediterranean diet and taking omega-3 fatty acid supplements led to significant reductions in inflammatory and non-inflammatory skin lesions, as well as improved quality of life.

Notably, 98.3% of participants had omega-3 fatty acid deficits at the start of the study. Acne severity lessened significantly in those who reached target omega-3 fatty acid levels during the study.

“Lifestyle interventions, including dietary recommendations, should not be considered in opposition to prescription medications, but rather as a valuable adjunct to any modern acne treatment plan,” said corresponding author Anne Guertler, MD, of the Ludwig Maximilian University of Munich, in Germany. “Future studies should build on the foundation laid by our current findings in a randomised, placebo-controlled design to improve dietary recommendations for acne patients.”

Source: Wiley

Categories : Dermatology Environmental EffectsTags :

Toxic Chemicals from Microplastics can be Absorbed through Skin

On By ModernMedia
Photo by FLY:D on Unsplash

Toxic chemicals used to flame-proof plastic materials can be absorbed into the body through skin, via contact with microplastics, new research shows. The study offers the first experimental evidence that chemicals present as additives in microplastics can leach into human sweat, and then be absorbed through the skin, into the bloodstream.

Many chemicals used as flame retardants and plasticisers have already been banned, due to evidence of adverse health effects including damage to the liver or nervous system, cancer, and risks to reproductive health. However, these chemicals are still present in the environment in older electronics, furniture, carpets, and building materials.

While the harm caused by microplastics is not fully understood, there is increasing concern over their role as conduits of human exposure to toxic chemicals.

The research team demonstrated in a study published last year, that chemicals were leached from microplastics into human sweat. The current study now shows that those chemicals can also be absorbed from sweat across the skin barrier into the body.

In their experiments, the team used innovative 3D human skin models as alternatives to laboratory animals and excised human tissues. The models were exposed over a 24-hour period to two common forms of microplastics containing polybrominated diphenyl ethers (PBDEs), a chemical group commonly used to flame retard plastics.

The results, published in Environment International, showed that as much as 8% of the chemical exposed could be taken up by the skin, with more hydrated – or ‘sweatier’ – skin absorbing higher levels of chemical. The study provides the first experimental evidence into how this process contributes to levels of toxic chemicals found in the body.

Dr Ovokeroye Abafe, now at Brunel University, carried out the research while at the University of Birmingham. He said: “Microplastics are everywhere in the environment and yet we still know relatively little about the health problems that they can cause. Our research shows that they play a role as ‘carriers’ of harmful chemicals, which can get into our bloodstream through the skin. These chemicals are persistent, so with continuous or regular exposure to them, there will be a gradual accumulation to the point where they start to cause harm.”

Dr Mohamed Abdallah, Associate Professor of Environmental Sciences at the University of Birmingham, and principal investigator for the project, said: “These findings provide important evidence for regulators and policymakers to improve legislation around microplastics and safeguard public health against harmful exposure.”

Professor Stuart Harrad, co-author of the paper, added “the study provides an important step forward in understanding the risks of exposure to microplastics on our health. Building on our results, more research is required to fully understand the different pathways of human exposure to microplastics and how to mitigate the risk from such exposure.”

In future research, the team plan to investigate other routes through which microplastics could be responsible for toxic chemicals entering the body, including inhalation and ingestion.

Source: University of Birmingham

Categories : DermatologyTags :

Linked Biological Pathways Drive Skin Inflammation

On By ModernMedia
Picture by Macrovector on Freepik

A certain biological pathway involving interleukin-17 drives the inflammation seen in the skin disease psoriasis, according to a new study published in the journal Immunity. The work could lead to improved therapies for all inflammatory skin diseases, including atopic and allergic dermatitis and a type of boil called hidradenitis suppurativa, say the study authors.

Led by researchers at NYU Langone Health, the new study found that the interleukin-17 (IL-17) pathway, whose activity is blocked by existing anti-inflammatory drugs, activates a protein called hypoxia inducible factor 1-alpha (HIF-1-alpha) in psoriasis. Researchers say that IL-17 has long been known to be active in inflammation, but the role of HIF-1-alpha has until now been unclear.

The research team also found that HIF-1-alpha let inflamed skin cells more actively break down sugar for energy, supporting their metabolism and leading to the production of a waste product called lactate. When consumed by inflammatory T cells, lactate triggered production of IL-17, fuelling even more inflammation.

The findings show that in human skin tissue samples from psoriatic patients, measures of gene activity around IL-17 and HIF-1-alpha were similar, suggesting that these factors are interconnected. Experiments in mice treated to develop psoriasis found that subsequent treatment with an experimental drug that blocks the action of HIF-1-alpha, called BAY-87-2243, resolved inflammatory skin lesions.

Further, skin samples from 10 patients successfully treated with anti-inflammatory drug etanercept showed diminished activity for both IL-17 and HIF-1-alpha, suggesting to researchers that when IL-17 is blocked, so is HIF-1-alpha.

“Our study results broadly show that activation of HIF-1-alpha is at the crux of metabolic dysfunction observed in psoriasis and that its action is triggered by IL-17, another key inflammatory-signaling molecule,” said corresponding study author Shruti Naik, PhD, associate professor at NYU Grossman School of Medicine.

Further experiments were performed on skin samples from five patients with psoriasis whose healthy and inflamed skin was separately treated with either BAY-87-2243 or an existing combination of topical drugs (calcipotriene and betamethasone dipropionate). Researchers then compared differences in inflammatory gene activity as a measure of impact and found that the HIF-1-alpha inhibitor had a greater effect than existing topical drugs. Specifically, skin samples that responded to HIF-1-alpha therapy had 2,698 genes that were expressed differently, while standard-of-care-treated samples had 147 differently expressed genes.

Genetic analysis of skin samples from another 24 psoriatic patients treated with the IL-17A-blocking drug secukinumab showed only decreased, not heightened, gene activity connected to HIF-1-alpha when compared to HIF-1-alpha gene activity in nine healthy patients with no psoriatic disease. Researchers say this indicates HIF-1-alpha’s blocked action was codependent on blockage of IL-17.

Additional experiments in mice showed that blocking glucose uptake in the skin slowed psoriatic disease growth by limiting glucose metabolism, or glycolysis. Both the number of immune T cells tied to inflammation and the cell levels of IL-17 also decreased. The researchers found further that levels of lactate, the main byproduct of glycolysis, in psoriatic skin cell cultures dropped once exposed to the glycolysis-inhibiting drug 2-DG.

Directly targeting lactate production in psoriatic mice using a topical skin cream containing lactate dehydrogenase, which breaks down lactate, also slowed disease progression in the skin, with reduced numbers of inflammatory gamma-delta T cells and reduced IL-17 activity. Gamma-delta T cells were shown to take up lactate and use it to produce IL-17.

“Evidence of HIF-1-alpha’s depressed action, or downregulation, could also serve as a biomarker, or molecular sign, that other anti-inflammatory therapies are working,” said study co-senior investigator Jose U. Scher, MD, professor at NYU Grossman School of Medicine.

Scher, who also serves as director of NYU Langone’s Psoriatic Arthritis Center and the Judith and Stewart Colton Center for Autoimmunity, says the team plans to develop experimental drugs that can block HIF-1-alpha and lactate action in the skin “to end the underlying vicious cycle of IL-17-driven inflammation in skin disease. Our research fundamentally expands the scope of feasible therapeutic options.”

Naik points out that while many available therapies for psoriasis, including steroids and immunosuppressive drugs, reduce inflammation and symptoms, they do not cure the disease. She said further experiments are needed to refine which experimental drug works best, with respect to HIA-1-alpha inhibition, before clinical trials could start.

Source: NYU Langone Health / NYU Grossman School of Medicine

Categories : Dermatology Diet and NutritionTags :

UV Exposure Increases Appetite but Suppresses Weight Gain

On By ModernMedia
Photo by Julian Jagtenberg on Pexels

In a novel study, a team of dermatologists evaluated the effect of ultraviolet (UV) exposure on appetite and weight regulation. They found that UV exposure raises norepinephrine levels, decreases leptin levels, and induces the browning of subcutaneous fat, thereby increasing energy expenditure. These results potentially pave the way for new approaches to prevent and treat obesity and metabolic disorders. Their findings appear in the Journal of Investigative Dermatology, published by Elsevier.

Co-first authors Qing-Ling Quan, MD, PhD, and Eun Ju Kim, PhD, Department of Dermatology, Seoul National University Hospital, explained, “Recent evidence has suggested that UV exposure limits body weight gain in mouse models of obesity. Subcutaneous fat is a critical organ in regulating energy homeostasis. Alongside previous studies on the effects of UV exposure on obesity and metabolic disorders, our team was inspired by our prior discovery that, although UV rays do not directly reach subcutaneous fat when exposed to the skin, they can regulate the metabolism of subcutaneous fat. This led us to hypothesise that skin exposure to UV rays could play a significant role in systemic energy homeostasis, prompting this research.”

Investigators discovered that when exposed to UV radiation consistently, mice fed a normal diet and those on a high-fat diet exhibited increased appetite due to a decrease in leptin, a key hormone in appetite regulation. But there was no weight increase – they found that UV radiation inhibits weight gain by enhancing secretion of the neurotransmitter norepinephrine, which not only decreases leptin but also increases energy expenditure through the “browning” of subcutaneous fat.

The increased energy intake, driven by heightened appetite, is converted to heat and burned before it can accumulate in subcutaneous fat, thus preventing weight gain.

This research provides new insights into the impact of UV exposure on appetite and weight regulation, opening possibilities for novel approaches in the prevention and treatment of obesity and metabolic disorders. Specifically, uncovering the mechanism by which UV radiation prevents weight gain could offer new approaches to dietary regulation and weight loss, providing innovative insights into health and obesity management that could positively impact human health.

Lead investigator Jin Ho Chung, MD, PhD, Department of Dermatology, Seoul National University Hospital, Seoul National University College of Medicine, explained, “This study elucidates the mechanism by which UV exposure can increase appetite while inhibiting weight gain. These findings contribute significantly to understanding the effects of UV radiation on energy metabolism and homeostasis and open new avenues for exploring prevention and treatment strategies for obesity and metabolic disorders. Notably, the fact that UV radiation lowers leptin levels and increases norepinephrine, thereby promoting the browning of subcutaneous fat and increasing energy expenditure, provides a groundbreaking clue for the development of obesity treatment strategies. This research demonstrates that UV exposure not only affects the skin but also plays a deep role in our body’s energy metabolism and homeostasis processes. However, further research is needed on the long-term effects and safety of UV exposure, and there should be significant interest in developing new therapeutic approaches that utilise the efficacy of UV radiation.”

However, as co-corresponding author Dong Hun Lee, MD, PhD, Institute of Human-Environment Interface Biology, Seoul National University, noted, “Because UV exposure can accelerate skin aging and promote skin cancer, it is advisable to minimise UV exposure and protect the skin with sunscreen. Thus, our research team plans to conduct follow-up studies to develop new strategies that could mimic the effects of UV radiation for obesity and metabolic regulation.”

Source: Elsevier