Diabetes News - Dec. 17, 2000

Answer To Obesity May Be A Protein

Because obesity can lead to so many different health complications, scientists have been actively seeking an effective treatment for decades. A recent study conducted in mice offers a promising treatment involving the protein perilipin.

Perilipin is a protein that works by blocking the enzyme called hormone-sensitive lipase from interacting with fat in the diet. Ordinarily this enzyme breaks up fat, and converts it into energy. But when the enzyme can't get to the fat, the fat is burned up instead of being stored.

Doctors at Baylor College of Medicine in Houston recently conducted a study in which mice were bred to be missing the gene coding for perilipin. These perilipin-free mice had an increased metabolism, with half the body fat and 8% more muscle than control mice. In addition, the mice without the perilipin ate about 25% more calories per day, and had virtually no exercise, similar to lifestyles in developed countries.

The results, which can be found in Nature Genetics (December, 2000), also indicate that crossbreeding mice with a genetic predisposition for obesity with mice bred to have an absence of perilipin still resulted in lean mice. The research is promising for those struggling with obesity, but is not yet at the stage where it can be tested in humans.

Treating Diabetes With E. Coli?

E. coli ordinarily is associated with dire illness and death, but a recent scientific presentation indicates that it may actually be used to prevent certain autoimmune diseases such as diabetes.

In the first week of December, Harrogate was the site of the British Society for Immunology Congress 2000. One presentations was led by doctors at the University of Bristol, who discussed research involving E. coli bacteria. The researchers explained that this bacteria, which occurs naturally in human intestines, may produce a protein that inhibits autoimmune diseases from developing.

A protein found in E. coli, called the B-subunit, blocks autoimmune diseases by binding to immune system cells and changing their behavior. The B-subunit is nontoxic, and scientists believe that it may be used as a treatment in the form of a nasal spray. The researchers are now in the early stage of testing this on human study participants.

Inflammatory Triggers Identified As Causing Type 1

While there are numerous treatments for diabetes, there is still no cure, but recent research somewhat related to the study above, promises ways to stop the disease in its early stages. Scientists are beginning to clarify the steps by which Type 1 diabetes actually develops. 

In a recent issue of Diabetes (volume 49, pages 1801-1809, November 2000), scientists from Scripps Research Institute in La Jolla, California; the Walter and Eliza Hall Research Institute in Melbourne, Australia; and the Hagedorn Research Institute in Copenhagen, Denmark published the results of their study. The scientists were trying to isolate the exact cellular processes that are necessary to trigger destruction of pancreatic beta cells.

The researchers found that the autoimmune process typically blamed for destruction of beta cells is not actually sufficient by itself to cause cell death. Rather than being the real culprit, the activation of the autoimmune process triggers other truly destructive elements that cause beta cell death. 

One element now identified by this research as a primary cause of beta cell death is gamma-interferon. Mice which were bred to have defective gamma interferon receptors did not develop Type 1 diabetes. The researchers also found that other inflammatory cytokines, in addition to gamma-interferon, were necessary for beta cell destruction.

Another significant finding of this research was that if immune regulatory systems are corrected, even relatively late in the destructive process, beta cells can recover. Several treatments are suggested, such as the B-subunit treatment above, or using oral insulin which redirects the immune system toward a more protective cytokine profile. Oral insulin works by distracting the immune system so that an autoimmune reaction does not occur, and is currently being tested in the DPT1 Study. 

Other possibilities include reducing damaging cytokines with anti-inflammatory medications, or possibly by increasing anti-inflammatory prostaglandins via a greater intake of fish and seeds in the diet. As these damaging processes become clarified, better interventions to stop total destruction of the beta cells become possible, especially as earlier identification of those at risk becomes more widespread.

Lifescan Fined $60 Million For Defective Meter

The F.D.A. has come down hard on Johnson & Johnson and its susidiary, Lifescan, for failing to step in to correct problems with its SureStep meter, manufactured between May, 1996 and early 1998. A $60 million fine was imposed because Lifescan failed to respond to nearly 3,000 complaints that its meter gave inaccurate low readings and gave erroneous error messages when readings were exceedingly high. 

Court documents reveal that Lifescan first became aware of defective readings in 1993 but proceeded with development and manufacture. A physician who oversaw clinical evaluations at Lifescan recommended a recall of the meter in May, 1997, but the company did not act until the F.D.A. had already started its investigations in 1998. A class action suit has also been filed for millions of dollars in damages stemming from at least 61 complaints involving injury or illness, as well as three or more deaths possibly linked to defective readings.

Gene Study Suggests Gut For Islets

Recent scientific studies have shown a trend toward treating diseases at the most basic level--in the genes. One such study involves mice that were genetically engineered to produce insulin in cells in the stomach.

The study was led by doctors at the University of Alberta in Edmonton, Canada. The researchers began by transferring the gene for human insulin into K cells, which are found in the stomach and small intestine. Next, they bred mice to carry these K cells.

Results of the study, which are published in the journal Science (volume 290, pages 1959-1962, December 8, 2000), indicated that the mice were able to produce human insulin. Also, the K cells prevented the mice from developing diabetes, despite a destruction of beta cells.

The scientists believe that K cells are ideal substitutes for beta cells because they are able to store and secrete insulin. Also, K cells release the hormone GIP after a meal, so engineering the cells to release insulin instead would be a beneficial response to meal-time fluctuations in blood sugar levels. More research is necessary before the treatment may be attempted in humans.

Gene Mutation May Trigger Some Type 1

Although it is understood how Type 1 diabetes affects the body, it is not clear why it happens. A new study attempts to offer one explanation by way of a mutated gene.

Doctors from Washington University School of Medicine in St. Louis, Missouri recently conducted a study of the gene known as JM2. When this gene mutates, it causes the body to develop a disorder called X-linked autoimmunity-allergic disregulation syndrome (XLAAD). This disorder, which causes chronic diarrhea, eczema, and food allergies, can also cause Type 1 diabetes.

In the study, which can be found in the Journal of Clinical Investigation (December 15, 2000), the researchers compared blood samples from two families with children diagnosed with XLAAD and Type 1 diabetes. It is unclear how the disorder leads to diabetes, and scientists state that there are other ways that Type 1 diabetes may develop.

Diabetes Drug Submitted For FDA Approval

The drug company Amylin Pharmaceuticals Inc. has recently applied for FDA approval for its diabetes drug Symlin. This drug would be used in combination with insulin to treat people with Type 1 or Type 2 diabetes. The company also hopes to begin the process for regulatory submission in Europe in the first part of 2001.

      

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