Mice with a mutation in a gene called "Clock," which helps drive circadian rhythm, ate significantly more and gained more weight.
The finding could help explain why disrupted sleep patterns, particularly when combined with a high-fat diet, are associated with excessive weight gain and the onset of metabolic syndrome in some people.
The National Cholesterol Education Program defines metabolic syndrome as having at least 3 of the following risk factors: high blood pressure, high glucose levels, high triglyceride levels, low levels of HDL cholesterol, and a large waist circumference.
Scientists have found that circadian rhythms ( which control the sleep/wake cycle and other biological processes ), hunger, and satiety are all regulated by centers within hypothalamus. And previous studies in humans have suggested that disrupted sleep patterns may contribute to the development of obesity, diabetes, and metabolic syndrome.
A study, led by Fred W Turek Northwestern University in Evanston, found that mutant mice were more active during times when rodents usually sleep.
They also had less fluctuation in blood levels of leptin, a hormone that transmits a satiety signal to the brain.
The researchers also found that Clock mutant mice had reduced levels of the hormone ghrelin within the hypothalamus, indicating that ghrelin may participate in the neuronal relay linking sleep, wakefulness, and appetite.
Together, these alterations in neural and peripheral hormones suggest that a number of previously undetected brain circuits may exist that are common to sleep and eating.
The mice with a mutation in the Clock gene fed a regular diet gained about as much weight as normal mice that were fed a high-fat diet.
The mice with a mutation in the Clock gene showed even greater weight gain and changes in metabolism when fed a high-fat diet.
They developed a wide range of conditions associated with obesity, diabetes, and the metabolic syndrome, such as high levels of cholesterol, triglycerides, and glucose, and insulin resistance.
The National Institute on Aging ( NIA ), the National Heart, Lung and Blood Institute ( NHLBI ), and the National Institute of Diabetes and Digestive and Kidney Diseases ( NIDDK ) supported this work. The NIA, NHLBI and NIDDK are components of the National Institutes of Health ( NIH ).
Source: NIH, 2005