Sometimes it seems as if there's a news announcement of some diabetes-related research almost every day. Some of them represent major advances or new theories that may eventually lead to cures.
Others are simply statistical analyses that show that food X or behavior Y increases or decreases diabetes risks by Z percent. I find these stories pretty dull, as we all have a pretty good idea of what is healthy and what is not, and many of these studies are sponsored by the manufacturers of the foods that are studied.
But sometimes studies are reported that are interesting, but probably not important enough to warrant an entire blog post. So I thought I'd give a roundup of some of those that have appeared in the past several months.
Mutations in a single gene makes mice eat more and get obese. We all know that mouse studies don't always translate into human studies. In fact, if you want to make sure you don't get diabetes in your next incarnation, the best way would be to try to come back as a mouse, as we can cure them in myriad ways.
The reason this study, which shows that mice with a particular gene eat more and become obese, is interesting is that approximately 25% of Americans carry a mutation in the analogous gene, called BDNF. It's an example of the fact that some people have a more difficult time avoiding obesity than others do. That's something many of us know intuitively, but others refuse to believe it.
Vinegar reduces blood glucose levels after meals. This is not really news; books on the glycemic index noted years ago that vinegar reduces the glycemic index. What I find interesting is that according to this report the vinegar increases the liver levels of a molecule called AMPK, which is the same molecule that metformin affects.
High-GI diets are linked to fatty liver disease. Paté de fois gras (or paté made from fatty goose livers) is made by force-feeding geese with grains. It seems that "fois gras" can also result in humans who eat too many high-GI, high-carb meals.
A study of Italians showed twice the rate of fatty liver disease in those with high-GI diets. But so-called subgroup analysis showed that this was true only in people with insulin resistance.
This is interesting because it shows that a diet that works for people without insulin resistance may be a disaster with those who do have insulin resistance.
Overweight people's brains don't respond to satiety signals as easily as brains of the nonobese. This is another illustration of the fact that obesity is not the result of a character flaw but can result when people's physiological controls are abnormal. The article includes links to other studies showing that various differences in the brains of obese people may cause them to eat more.
Decreases in the level of a protein called menin during pregnancy allow beta cells to multipy. At first, the results of this study sound wonderful. All we'd have to do is figure out how to block the protein menin and make our beta cells grow.
But there's a catch. The reason this protein exists in the first place is to keep the beta cells from growing too much, in other words, to help prevent pancreatic cancer, a deadly disease. During pregnancy, the controls are temporarily removed because the mother needs more insulin to cover the increased needs caused by the pregnancy. But after the baby is born, menin levels return to normal and the pancreas also returns to its former size.
Menin may also be involved in the increase in beta cell mass that usually occurs when people become overweight. In both pregnancy and overweight, when the pancreas fails to increase in size, diabetes results.
This is interesting because it is a good illustration of the delicate balance our bodies normally maintain. We want some organs to be able to grow, but not too much; cancer is uncontrolled growth. We want some insulin, but not too much or we'll go low. We want some glucagon, but not too much or we will go too high.
Diabetes means our bodies have become unbalanced. Fixing that balance is not a simple matter of finding some drug that will either create or destroy something in our bodies. It means finding some therapy that will mimic the delicate balance a healthy body maintains by itself. This is not easy.
Losing weight can restore healthy functioning of blood vessels. This study showed that when lean healthy young adults gained just 9 pounds, their endthelium, the lining of blood vessels, became impaired.
The impaired functioning was significantly correlated with an increase in visceral fat, the kind that accumulates in your abdomen, but not with an increase in subcutaneous fat, the kind that occurs under the skin. Impaired functioning of the endothelium can lead to cardiovascular events, or heart attacks and strokes.
But the good news is that losing that weight restored healthy functioning. Most of us would like to lose weight to help improve our blood glucose control. But this is evidence that the weight loss should improve our health even if it doesn't affect blood glucose levels.
Vitamin E reduces cardiac risk in some people with diabetes. Studies some time ago suggested that supplementing with vitamin E would be beneficial for people with diabetes. Then some recent studies suggested that supplementing with vitamin E had no effect at all and might actually increase cardiac events.
Now a study shows that people with diabetes who have a particular gene (Hp 2-2) had 50% fewer heart attacks and deaths when they took vitamin E than those who took a placebo. About 40% of people with diabetes carry this gene.
This is a good example of why we get conflicting results from all these megatrials of drugs and other treatments. The treatment may help one type of patient, not help another type, and actually harm another type. The overall results could depend on how many of each type were included in the trials. And if the researchers weren't aware of their differences, there's no way they could control for this.
Published On: January 22, 2008