Examining the Role of Exercise Timing in Weight Management: A Review

Many adults cite exercise as a primary strategy for losing weight, yet exercise alone is modestly effective for weight loss and results in variable weight loss responses. It is possible that some of the variability in weight loss may be explained by the time of day that exercise is performed. Few studies have directly compared the effects of exercise performed at different times of the day (i. e., morning versus evening exercise). Results from these existing studies are mixed with some studies demonstrating superior weight and fat mass loss from morning exercise, while other studies have found that evening exercise may be better for weight management. Exercise timing may alter modifiable lifestyle behaviors involved in weight management, such as non-exercise physical activity, energy intake, and sleep. The purpose of this review is to summarize evidence for and against time-of-day dependent effects of exercise on weight management. Although limited, we also review studies that have examined the effect of exercise timing on other lifestyle behaviors linked to body weight regulation. While exercise at any time of day is beneficial for health, understanding whether there is an optimal time of day to exercise may advance personalized treatment paradigms for weight management.

Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity

Pro-opiomelanocortin (POMC) neurons form an integral part of the central melanocortin system regulating food intake and energy expenditure. Genetic and pharmacological studies have revealed that defects in POMC synthesis, processing, and receptor signaling lead to obesity. It is well established that POMC is extensively processed by a series of enzymes, including prohormone convertases PC1/3 and PC2, and that genetic insufficiency of both PC1/3 and POMC is strongly associated with obesity risk. However, whether PC1/3-mediated POMC processing is absolutely tied to body weight regulation is not known. To investigate this question, we generated a Pomc-CreER T2; Pcsk1 lox/lox mouse model in which Pcsk1 is specifically and temporally knocked out in POMC-expressing cells of adult mice by injecting tamoxifen at eight weeks of age. We then measured the impact of Pcsk1 deletion on POMC cleavage to ACTH and α-MSH, and on body weight. In whole pituitary, POMC cleavage was significantly impacted by the loss of Pcsk1, while hypothalamic POMC-derived peptide levels remained similar in all genotypes. However, intact POMC levels were greatly elevated in Pomc-CreER T2; Pcsk1 lox/lox mice. Males expressed two-fold greater levels of pituitary PC1/3 protein than females, consistent with their increased POMC cleavage. Past studies show that mice with germline removal of PC1/3 do not develop obesity, while mice expressing mutant PC1/3 forms do develop obesity. We conclude that obesity pathways are not disrupted by PC1/3 loss solely in POMC-expressing cells, further disfavoring the idea that alterations in POMC processing underlie obesity in PCSK1 deficiency.