Sunlight can stimulate men to eat and gain weight

Sunlight exposure stimulates eating and weight gain in men, but not women, through a hormone secreted by adipose tissue within the skin. The study, published in Nature Metabolism (UK), reveals how sunlight can affect eating behavior and whole-body energy balance, a grossly neglected process.

  The need to eat is largely controlled by communication between peripheral tissues and the brain. Hormones released from multiple organs (such as the intestines, adipose tissue and liver) reach specific brain regions, such as the hypothalamus, and in turn issue instructions to eat or stop eating, depending on the body’s energy level at the time.

  A team of researchers at Tel Aviv University in Israel analyzed epidemiological evidence from about 3,000 individuals in Israel over a three-year period and found that men, but not women, increase their eating in the summer, which is also the most intense period of the year for solar radiation. This result was supported by animal studies on male mice, which found that daily exposure to ultraviolet light for ten weeks stimulated the release of “hunger hormone” from the adipose tissue of their skin. When the hunger hormone reaches the hypothalamus, it turns on the appetite of these male mice, which in turn promotes eating and weight gain. However, this effect is not significant in female mice because estrogen interferes with the release of hunger hormone from adipocytes in the skin. In addition, in one experiment, human male skin samples increased expression of hunger hormone after five days of UV exposure, which is consistent with the increased feeding behavior observed after sunlight exposure.

  The researchers said the discovery of skin fat may be a mediator of feeding behavior through sunlight exposure, or add a new adipose tissue subtype to the energy balance equation. In a concurrent “News & Views” article, the scientists noted that “this study certainly lays the groundwork for subsequent studies on the role of skin in energy and metabolic homeostasis.

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