As a sugar-rich foodstuff, jelly is not often seen as a good thing for diabetics. But a new gel-based method for administering drugs could cut back on injections for diabetics and virtually eliminate their blood sugar highs and lows. Scientists have come up with a new gelatinous drug form that releases a slow but regular dose of an insulin-regulating hormone. In mice, it kept glucose levels down for five straight days—120 times longer than the hormone alone. And the method could be used to deliver drugs to treat cancer and other diseases as well.
Peptide drugs are an up-and-coming method used to treat a number of diseases. There are currently 40 peptide drugs on the market, and 650 more are being clinically tested, so the pharmaceutical industry is investing a lot in the future of these treatments. One peptide drug, used to treat diabetes, relies on weekly injections of tiny plastic capsules filled with the peptide that causes
insulin to be released slowly over the course of the week. This means far fewer injections than diabetics’ typical insulin regimen, but the injections are painful due to the large needles required to fit the capsules. Side effects like nausea are common. Plus the production is complicated because the drug and its capsule must be synthesized separately and then combined.
Camels are known for their humps, which store fat and allow camels to survive long periods of time without food or water. But camels have also developed other traits like insulin resistance and salt tolerance to help them feel more at home in extreme environments. Scientists are now working to determine what these adaptations look like on the genetic level, and they hope their results, published in Nature Communications this week, may eventually shed some light on metabolism-related diseases in humans, too.
Diabetes has become a common condition around the country, affecting about one in six Americans. But in Appalachia, the rate is twice that: One person of every three in the region is diabetic—and many people believe there’s no way they can avoid it. Over at Salon, Frank Browning details how diabetes has become an all-too-familiar part of life in the region:
[Health worker Lora Hamilton] says most people are resigned — and believe there’s nothing they can do. “They tell me, ‘I’ve got diabetes or I’m going to get it. I’m just gonna have to live with it. My granddad lost a leg. My grandmother was on dialysis.’ And what I say is, ‘Well, you know you can keep that from happening by taking care of yourself.’”
This is what Michael Snyder’s diabetes onset looked like.
What’s the News: Have you ever wondered what is going on in your body at the molecular level when you’re sick? If you could see which medications, whether for treating cold symptoms or cancer, had an effect on you, and whether changing your diet, exercise, or some other factor would increase their effectiveness, you’d gain a lot of power over your body.
This kind of detailed information would start with getting your genome sequenced, but it wouldn’t stop there. It would require a constant stream of information about which genes are being expressed, at what levels, and in what tissues, and what else is going with your metabolism. That level of granularity has been the goal of geneticist Michael Snyder’s work and it has yielded a striking new paper: Snyder’s team analyzed samples of his own blood, taken over the course of 14 months, and were able to watch in real-time as the geneticist developed type 2 diabetes and successfully arrested its progress.
We all know that slouching in chairs and sitting in cars all day is no good for our bodies. But can even a little laziness—a few days off from the gym, a weekend of lounging—cause problems? It appears so: A new study suggests healthy people will develop higher blood sugar after only three days of a sedentary lifestyle.
Most studies that just compare sedentary people with active ones don’t tell us much about whether sedentary living actually causes the problems—diabetes, high blood pressure, and so on—associated with it. The inactive people with health problems might have genetic or other reasons for them, and it could be that their illnesses are causing their lack of exercise, rather than the other way around. But this study is pretty clever: it compares people against themselves before and after forced laziness, so differences can be pinned to reduced activity.
Researchers have long suspected that living in a bad neighborhood can be hazardous to your health—whether because of poor access to health care and a paucity of areas to exercise in and stores that sell healthy food, or some combination of other factors, living in a poor area means you have a disproportionate chance of becoming ill and obese. But how can you tell whether that effect is intrinsic to poverty, or whether it can be reversed if people move into more well-off neighborhoods? With a giant, long-term study that gives families in poor neighborhoods a chance to move to other areas.
The results of such a study, conducted by the US Department of Housing and Urban Development, have now been published, and they show that moving from low-income housing projects to a neighborhood with less than 10% of people living below the poverty line does have a positive effect on health. Read More
What’s the News: Scientists found that periodic fasting may decrease the risk of coronary artery disease and diabetes, and also causes significant changes in heart-disease risk factors like cholesterol, blood-sugar, and triglyceride levels, which hadn’t been linked to fasting before. “We’ve shown it is not a chance finding. Fasting is not just an indicator for other healthy lifestyles,” says lead researcher Benjamin Horne of the Intermountain Medical Center Heart Institute. “It is actually the fasting that is working to reduce the risk of disease.”
They’re about three and a half feet tall and their origins are mysterious, but an isolated group of Ecuadorians with a genetic mutation causing dwarfism are making news for another reason: They hardly ever get cancer or diabetes. Medical researchers say the villagers’ genetic protection from these diseases could lead to preventative treatments for the general population–and could therefore increase human longevity.
The villagers’ condition is called Laron syndrome, which is caused by an insensitivity to growth hormone.
Laron syndrome results from a mutation in the gene that codes for growth hormone receptor (GHR), a protein that binds with the human growth hormone and ultimately results in the production of the insulin-like growth factor 1 (IGF1), causing cells to grow and divide. When a person has two of these mutated and non-working genes, they can develop the disease. [LiveScience]
Jaime Guevara-Aguirre, the leader of the study about the Ecuadorians appearing in Science Translational Medicine, has been looking into their condition and extraordinary resistance to age-related diseases for more than two decades, since his serendipitous discovery of the people while riding horseback in Ecuador.
“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.” [The New York Times]
In an attempt to find a cure for type 1 diabetes, researchers are looking to an unlikely source: testicles. In a new study, researchers extracted stem cells drawn from human testes and reprogrammed them to produce insulin. When implanted into diabetic mice, the altered cells brought down the mice’s blood glucose levels, temporarily curing their diabetes.
In type 1 diabetes, the body’s immune system mistakenly destroys the pancreatic beta and alpha cells, which regulate blood glucose levels. Without the insulin created by their beta cells, diabetics experience high glucose levels that cause serious health problems.
Lead researcher G. Ian Gallicano and his colleagues took human spermatogonial stem cells–precursor cells that give rise to sperm–and reverted them to an embryonic state. Then the researchers coaxed them to develop into insulin-producing cells that resemble beta cells. Finally, they injected these pseudo-beta cells into the pancreases of mice with type 1 diabetes.
In a presentation on Sunday at the American Society for Cell Biology annual meeting, Gallicano said the graft was able to produce enough insulin to “cure” the mice of their diabetes for a week, though insulin levels were not high enough to treat humans this way.
Scientists knew that overweight mothers tend to have more overweight children. But is the same true for fathers? This week in Nature, Margaret Morris and her team demonstrated this effect in male rats, the first time it’s been shown to work in males. The findings are another example of how non-genetic factors, like how much a parent eats, can have a biological impact on offspring.
The researchers put one of their two groups of male rats on a high-fat diet, the other on a normal one. Unsurprisingly, the high-fat rats put on a lot of weight and began to show symptoms of type II diabetes, like insulin resistance and struggles with metabolizing glucose. And then there were their kids:
The real surprise came when Morris’s team went on to examine the obese rats’ female offspring. These too had problems regulating insulin and glucose levels. The healthy fathers, however, had correspondingly healthy daughters. Whether similar defects emerge in sons remains to be seen. [Nature News]