Posted by: Glow-worm PJ16 JAN 2013
In a study published recently in Nature Medicine, a team from the University of Pennsylvania showed that the deletion of a gene contained in fat cells, which influences the mammalian circadian clock, can cause mice to become obese without any change in calorific intake.
The daily rhythms of most organisms are controlled by a master clock, the circadian oscillator, which tracks time and co-ordinates biological processes with relation to day and night. In mammals it is located in an area of the hypothalamus of the brain known as the “superchiasmatic nucleus” (SCN). Normally the SCN exerts overall control over peripheral food clocks found in the tissues, but researchers were surprised to find that when a peripheral “clock gene”, known as BMAL1, was deleted from fat cells, a change in ing habits occurred in the normally nocturnal mice, causing them to become obese. It appears that a slight shift of ing times into what would be a rest period leads to increased energy storage. This behavioural change resembles a phenomenon found in humans known as night-eating syndrome, which leads to obesity caused by altered metabolism.
The food clock’s purpose is to help our bodies make the most efficient use of nutritional intake, and it controls genes involved in digestion and absorption of nutrients and their distribution to the tissues, by adapting to anticipate eating patterns.
Separate research has demonstrated the influence on the BMAL1 gene of a gene known as PKC-gamma, which allows readjustment of the food clock over time, in response to changes in ing habits. Animals with deleted PKC-gamma genes were unable to readjust their food clock.
The above findings could have implications for understanding the molecular basis of obesity and diabetes, since desynchronised food clocks might influence the development of these disorders.