The obesity paradox refers to extant evidence showing that obesity in older subjects or in patients with several chronic diseases may be protective and associated with decreased mortality. A number of mechanisms have been postulated to support the existence of obesity paradox; however, marked heterogeneity was found across studies and this has cast doubt on the actual presence of this phenomenon.
Obesity in childhood and adolescence continues to be a major health issue due to significant health implications and to the economic burden that arise from treating this disease and its complications. Current data show that childhood obesity is no longer just a concern for developed countries, but more significantly affecting developing countries. In adult population, cardiovascular disease is the main cause of mortality and morbidity among obese patients. It is therefore believed that risk factors found in adult patients could also be observed in obese youth.
The circadian clock coordinates behavioral and circadian cues with availability and utilization of nutrients. Proteasomal degradation of clock repressors, such as cryptochrome (CRY)1, maintains periodicity. Whether macroautophagy, a quality control pathway, degrades circadian proteins remains unknown. Here we show that circadian proteins BMAL1, CLOCK, REV-ERBα and CRY1 are lysosomal targets, and that macroautophagy affects the circadian clock by selectively degrading CRY1.
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