Circadian clocks and insulin resistance

If nothing else, this article had great figures (Stenvers et al., 2018).

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Clock gene mutations, exposure to artificial light at night, disturbed sleep, shift work, social jet lag, etc., are factors that contribute to circadian disruption and insulin resistance.

Figure 1.

Figure 2. Clocks, clocks everywhere!

The human circadian timing system is not exactly 24 hours, therefore, it needs to be entrained every day. Environmental light is the most important zeitgeber for setting the central pacemaker, while that, food intake, physical activity, etc., contribute to setting peripheral pacemakers.

In humans, tissue-specific glucose tolerance, insulin sensitivity, and thus nutrient partitioning depend on the time of day. For example, glucose tolerance is higher in the morning than at night. And the effects of insulin on fat storage are greater at night than in the morning. Worded another way, adipose stores more fat with less insulin in the evening compared to morning.


Some of the most basic findings to support the role of circadian rhythms in insulin sensitivity come from rodent studies: damage to the central clock (SCN) results in insulin resistance within weeks independent from food intake or physical activity. In humans, observational studies on shift workers have been supported by intervention studies on intentional circadian disruption which show, collectively, insulin resistance and various aspects of metabolic syndrome.

Figure: muscle clock

Entraining and capitalizing on the muscle clock has been largely under-rated until very recently. Entrain the muscle clock indirectly via SCN with light in the morning and more directly with food intake and some sort of physical activity. Capitalize on this by front-loading calories, optimize by combining all 3 (and maybe more in the future, as more is uncovered).

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