Biological Clock May Influence Obesity and Diabetes
By: Almas Eftekhari
Most organisms have an internal cycle, known as a circadian clock, which regulates important biological processes at the appropriate points throughout a 24-hour period. Circadian rhythms are driven by a set of clock “machinery” proteins that are present in every cell type, influencing sleep-wake cycles, body temperature, hormone levels, and numerous other important functions. The circadian clock can be modified to adjust to changes in the environment, by cues such as light or darkness.
Disruptions in circadian rhythms, resulting from activities such as shift work or frequent jet lag, have been linked to various health risks, including sleep disorders, hormone imbalances, and even cancer progression. Circadian rhythms also play a critical role in the pathways that regulate energy and metabolism, and growing evidence suggests that circadian disruptions can also contribute to obesity and type 2 diabetes.
“Obesity and the resultant type 2 diabetes have become an epidemic in our modern society, and our lifestyle of frequent circadian clock alteration may contribute greatly to this problem,” said Ke Ma, MD, PhD, from the Methodist Hospital Research Institute in Houston, TX.
Dr. Ma is exploring the relationship between metabolism and circadian rhythms, and she has recently discovered a novel mechanism that could be involved in a circadian disruption-induced development of obesity. In her presentation at the Association’s 73rd Scientific Sessions, Dr. Ma described a previously unknown role of circadian rhythms in the early stages of brown fat cell development.
Brown fat is the “good” type of fat, densely populated with mitochondria, which are structures inside the cell that burn energy to generate heat and maintain body temperature. Studies suggest that individuals with more brown fat tend to have lower BMI and may be protected against weight gain. Dr. Ma has discovered that a gene that helps activate the clock rhythm, called Bmal1, prevents the formation of brown fat.
When Dr. Ma blocked the Bmal1 gene in mice, they developed greater amounts of brown fat tissue and showed significantly increased energy expenditure and cold tolerance. They also had improved thermogenic capacity, meaning that they were more metabolically active and burned more energy than control mice. On the other hand, mice overexpressing the Bmal1 gene had significantly less brown fat and had lower metabolic activity.
“Our research may help to find specific ways to manipulate the biological clock to combat obesity and thus to prevent the development of diabetes,” said Dr. Ma.
Dr. Ma presented her results on June 22, 2013 at the 73rd American Diabetes Association Scientific Sessions in Chicago, IL.