�Terminally ill rodents with type 1 diabetes get been restored to good health with a individual injection of a substance other than insulin by scientists at UT Southwestern Medical Center.
Since the uncovering of insulin in 1922, type 1 diabetes (insulin-dependent diabetes) in humans has been treated by injecting insulin to lower high blood lucre levels and prevent diabetic coma. New findings by UT Southwestern researchers, which appear online and in a next issue of the Proceedings of the National Academy of Sciences, suggest that insulin isn't the only agent that is effectual. Leptin, a hormone produced by the body's fat cells, likewise lowers blood glucose levels and maintains them in a normal range for extended periods, they found.
"The fact that these animals don't kick the bucket and are restored to normal health despite a total want of insulin is hard for many researchers and clinicians to believe," aforesaid Dr. Roger Unger, professor of national medicine and senior author of the study. "Many scientists, including us, thought it would be a waste of time to give leptin in the absence of insulin. We've been brainwashed into thought process that insulin is the only heart that tin correct the consequences of insulin deficiency."
The mechanism of leptin's glucose-lowering action appears to involve the suppression of glucagon, a internal secretion produced by the pancreas that raises glucose levels. Normally, glucagon is released when the glucose, or sugar, level in the blood is low. In insulin lack, however, glucagon levels ar inappropriately high gear and cause the liver to exit excessive amounts of glucose into the bloodstream. This action is opposed by insulin, which tells the body's cells to bump off sugar from the bloodstream.
In type 1 diabetes, which affects about 1 zillion people in the U.S., the pancreatic islet cells that bring forth insulin ar destroyed. Type 1 diabetics must convey insulin multiple times a day to metabolize line glucose and regiment their diets. In comparison, patients with non-insulin dependent, or type 2, diabetes make insulin, but their bodies don't react well to it. Type 2 diabetes affects 'tween 18 one thousand thousand and 20 million mass in this country.
In the current cogitation, researchers tested for the first time whether a single injectant of the leptin gene given to insulin-deficient mice and rats on the verge of death from diabetic coma could reversal the dangerous condition and prevent the animals from dying. The animals that received the leptin factor began producing excessive amounts of leptin, which reversed all the measurable consequences of type 1 diabetes including weight loss, hyperglycaemia and ketoacidosis, a potentially fatal condition that develops when the body doesn't have sufficiency insulin to meet basic metabolic requirements. Much of the effect was mediated by make out suppression of the heights glucagon levels, said Dr. Xinxin Yu, assistant instructor of internal medicine and lead source of the study.
"These animals were in reality dying," Dr. Yu said. "But if we gave them the leptin factor, within two weeks, the terminally ill rodents were restored to full health without whatsoever other treatment."
Dr. Unger aforementioned it's to a fault premature to know whether leptin mightiness someday put back insulin as a treatment for diabetic patients, simply this survey demonstrates that leptin could at least handle some of insulin's job requirements and do it for longer periods of time. Injected insulin is biologically active for only trey to four hours.
"My hope is that you could give leptin for one type of action glucagon's suppression, for example and insulin for another. Or perhaps give a substance other than insulin entirely," Dr. Unger said. "What would be a awful advance would be the ability to give an oral federal agent that suppresses glucagon without injections."
Dr. Yu said the research team hypothesizes that leptin combats diabetes not only be suppressing glucagon's action on the liver, but likewise by boosting the insulin-like actions of IGF-1 (insulin-like growth factor-1), a endocrine that promotes growth and mimics insulin.
"One of the things that happens when a fry gets case 1 diabetes is their growth is stunted until they're minded insulin," Dr. Unger aforementioned. "The same is true with these mice. However, we set up that if you take aim a diabetic rat that's not receiving insulin and make it hyperleptinemic, it almost catches up growthwise."
While the treated animals' blood glucose levels inched back up over time, their hyperglycemia (heights blood sugar) consistently remained well down the stairs the elevated pre-treatment levels. The untreated rodents, on the other hand, died within deuce or trey days. The researchers tracked the treated rodents for 25 weeks.
The next step is to study other potential glucagon suppressants and begin leptin clinical trials within the next year.
Other UT Southwestern researchers involved in the study were Dr. May-Yun Wang, supporter professor of internal music; Dr. Zhao Wang, post doc researcher in internal medical specialty; and quondam postdoctoral
