Slim or obese? Brain decides
IN WHAT can pave the way for obesity treatment, scientists have decoded a key mechanism through which insulin controls a part of brain that manages body’s energy balance. They have shown how insulin in the satiety centre of the brain—known as the ventromedial hypothalamus (VMH)—can lead to obesity. VMH controls our appetite and energy expenditure.
Consumption of high-fat food causes more insulin to be released by the pancreas. Over the course of several intermediary steps, the insulin inhibits the transmission of nerve impulses in such a way that the feeling of satiety is suppressed and energy expenditure reduced. This promotes obesity.
To find out how insulin acts in the brain, researchers at University of Cologne, Germany, compared mice that lacked an insulin receptor in VMH with mice whose insulin receptors were intact.
With normal food consumption, the researchers discovered no difference between the two groups.
When the rodents were fed high-fat food, those with the defective insulin receptor remained slim, while their counterparts with functional receptors rapidly gained weight. The researchers found that the weight gain was due to both an increase in appetite and reduced calorie expenditure. The study was published in June 5 issue of Nature Neuroscience. The research opens avenues for obesity management. Earlier studies have shown how two hormones leptin and ghrelin influence energy balance and control obesity, says Anoop Misra, head of the Department of Diabetes and Metabolic Diseases at Fortis Hospital, Delhi. It can also help develop drugs for obesity control by hampering the insulin mediated pathway, he adds.