Becoming obese or remaining lean can depend on the dynamics of the mitochondria, the body's energy-producing 'battery', say researchers.
Mitochondria are vital cellular organelles that generate and maintain proper energy levels in complex organisms. Using animal models, the Yale research team studied mitochondria in different populations of brain cells known to be involved in the regulation of appetite.
The team found that during the transition from a fasting to an over-fed state, mitochondria in neurons that promote hunger show dynamic changes that are the opposite of those found in neurons that control feelings of fullness.
Lead author Tamas Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine, said that they have found that mitochondrion need to have ongoing dynamic plasticity in order to support neurons, which are necessary for appetite and for the maintenance of life.
Horvath asserted that if these dynamic events - during which the mitochondria fuse to become more effective in generating energy - are disrupted, mitochondria become static, appetite-stimulating neurons become less active, and animals do not develop obesity when exposed to high-fat, high-calorie diets.
Yale co-lead author Marcelo O. Dietrich, M.D., said these same cellular events have different consequences in neurons that promote feelings of fullness. These consequences were described in a separate paper in the same issue of Cell, co-authored by Dietrich, Horvath, and a research team in Spain.
The study showed that similar molecular drivers control mitochondria-endoplasmic reticulum interactions and related stress. If the cellular events are disrupted in these mitochondria, animals become morbidly obese.
The study has been published in the journal Cell.