Researchers have found that a drug called ‘Liraglutide’ that is meant for diabetes control can also non-diabetes but obese people to lose weight as well as keep off diabates.
Researchers from the Columbia University Medical Centre found that 63% of participants who were given liraglutide for 56 weeks lost at least 5% of their body weight whereas just 27% of the group not given or the placebo group lost that much.
“It adds another possibility for doctors to treat patients who are having trouble either losing weight or maintaining weight loss once they get the weight off,” said study first author Dr Xavier Pi-Sunyer from the Columbia University Medical Centre.
Liraglutide, developed by the company Novo Nordisk, mimics natural hormone glucagon-like peptide 1, which reduces hunger, increases satiety and slows the rate at which the stomach empties its contents into the small intestine. The US Food and Drug Administration has approved liraglutide for obesity but in a higher dose than it is for diabetes.
In theri experiment, Pi-Sunyer and his team assigned 2,500 men and women with a body mass index (BMI) of at least 30, or a BMI of at least 27 if they also had high cholesterol or high blood pressure, to receive a 3.0-milligram dose of liraglutide daily, and 1200 with a placebo treatment.
After 56 weeks, those on liraglutide lost an average of 8.3 kg, compared with 2.9 kg for the people on the placebo. However, the cost of the medication is too high at $1,000 for a month’s treatment. The study has been published in the New England Journal of Medicine.
The new research finding follows the Clumbia University Medical Center’s finding in April that cellular defect that can impair the body’s ability to handle diabetes. The CUMC team found that ryanodine receptor type 2 (RyR2) calcium channels in insulin-producing cells play an important and previously underappreciated role in glucose balance.
The CUMC researchers were initially studying a rare form of exercise-induced arrhythmia called catecholaminergic polymorphic ventricular tachycardia (CPVT), which can be caused by mutations in the RyR2 gene.
“When we generated murine models of CPVT that harbor mutations in the RyR2 channels that make them leaky, we observed that they weren’t secreting enough insulin in response to glucose,” said lead author Gaetano Santulli. “Since RyR2 channels are also expressed in pancreatic cells, we wondered whether they were mechanistically contributing to the glucose imbalance.”
When the researchers performed glucose tolerance tests on 27 CPVT patients with known mutations that make the RyR2 channels leaky, many of them exhibited reduced serum insulin levels and higher-than-normal blood sugar following a glucose challenge.
“This was completely unexpected, and it suggested we were on to something important in terms of understanding diabetes,” said Dr. Marks.