Stress hormone timing creates a different kind of obesity, study suggests

A new preclinical study from Weill Cornell Medicine researchers suggests that disrupted glucocorticoid hormone rhythms can lead to a unique form of obesity that differs from that caused by a high-fat diet. Glucocorticoids, stress-related hormones, play a distinct role in obesity when their rhythms are flattened. In mice, flattening these hormone rhythms resulted in obesity comparable to a high-fat diet, but the fat stored was preferentially concentrated in skeletal muscle rather than liver.

This metabolic state was maintained even on a standard diet, while mice exposed to both a high-fat diet and flattened glucocorticoid rhythms accumulated the most fat. The study, published in Cell Reports, indicates that the timing of hormonal signals influences where the body stores excess calories and how insulin resistance develops.

The findings suggest that obesity and insulin resistance may depend not only on the amount of fat stored but also on where insulin resistance occurs and whether fat tissue remains capable of storing lipids instead of releasing them to other organs. This research challenges the notion that obesity is solely due to diet and highlights the potential impact of factors like sleep deprivation or stress on metabolic health.