Knocking out the gene for a peptide associated with insulin was shown to protect mice against the harmful effects of a high-fat diet. Urocortin 3 plays a role in the increased production of insulin in response to high caloric intake in animals.

Scientists found that by removing the urocortin 3 gene from mice, they did not develop the age-related insulin resistance and high blood sugar observed in the normal control mice. The metabolisms of normal mice were compared to the metabolisms of those without the urocortin 3 gene. When placed on a high caloric diet for three months, the mice without the urocortin 3 gene packed on the same amount of weight but had lower insulin levels. But these mice also had lower blood sugar, improved glucose tolerance curves and they did not develop the fatty livers the control mice experienced.

Scientists hypothesize that by curtailing the abnormally high insulin levels, they were able to manipulate insulin sensitivity and avoid some of the untoward consequences of the high food intake and weight gain. Like many of us diabetics already know too well - while insulin is effective at lowering blood sugar it also promotes fat storage. This is a natural protective response to prepare for times when food may not be available. When insulin is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organs.

Urocortin 2 and urocortin 3 are part of the system that governs the body's response to insulin. Scientists already know that mice on a high-fat diet do better if either urocortin 2 or urocortin 3 is removed. Now they want to know if the mice will respond even better if both are missing. Such results may instruct us how best to develop therapeutic means to exploit these powerful effects.

A Harvard Medical School scientist's experiments with fish discarded along the coast near Boston have led to a new class of diabetes drugs. The latest, from Novartis, may get U.S. approval this week.

In the late 1970s, Habener, a doctor specializing in diabetes care, began buying discarded fish to learn about the ways animals controlled blood sugar. By 1987 Habener discovered a protein in the pancreas of anglerfish that tells the pancreas to produce insulin. He called it glucagon-like peptide-1, or GLP-1. In 1995, researchers uncovered another use for Habener's discovery to treat diabetes. The scientists found an enzyme that digests GLP. By blocking the enzyme, they could increase the body's reserves of GLP, thereby raising insulin levels. Twenty years later, we will soon have the pleasure of meeting Novartis' concept for this chronology of discoveries in the form of liraglutide.

In clinical trials, patients taking liraglutide attained normal blood sugars without the common side effect of weight gain. In fact, liraglutide was more likely to make the patients slightly leaner. Depending on dosage and length of treatment, it may help patients to lose weight. The drug does not cause a change in appetite. Furthermore, none of the liraglutide patients experienced episodes of low blood sugar levels throughout the trials.

I'm no fisherman, but if all the seagulls of Big Pharma are swarming overhead - there's bound to be a school of fish below. However, this school is quite competitive. At last count, the five largest diabetic drug makers are using Habener's findings to create new medicines.

A study conduced by the Howard Hughs Medical Institute found that people with insulin resistance have higher levels of fat inside their muscle cells.

A mitochondrial impairment inside muscle cells result in a buildup of fats that can cause insulin resistance, contributing to the development of diabetes. Intramuscular fat interferes with the ability of insulin to effectively enter the cell. It was found that the rate of ATP production in the muscles of those who are insulin-resistant was decreased by 30% compared to normal subjects without signs of insulin-resistance.

A little, yellow flower has shown promise in overcoming the obstacle of insulin resistance. Studies show that berberine activates an enzyme in the muscle and liver tissues that improve insulin sensitivity.. It lowers blood sugar by inhibiting absorption of sugars from the intestine and enhancing production of insulin. If that wasn't enough - berberine has been shown to reduce body weight, too. This pretty little flower may be worth a look-see after all.

The website YubaNet is running a report on a traditional Chinese medicine that some believe could treat Type 2 diabetes. The medicine is called berberine. It is derived from the roots and bark of various plants (including Goldenseal, pictured) and has traditionally been used in China to treat a number of health complaints, including diarrhea. Claims have also been made in the past that berberine lowers blood glucose. Well, it turns out there may be something to this claim: a research project conducted by researchers at Sydney's Garvan Institute, involving scientists from China, Korea and Australia, suggests berberine could be effective in this capacity. Lab experiments found that berberine activates an enzyme that is found in the muscle and liver. This enzyme is known to improve the body's sensitivity to insulin, thereby helping to lower blood sugar levels.

Why would anyone have a need for berberine? Well, I was interested to learn that many Type 2 diabetics cannot tolerate metformin, the drug often prescribed as a blood sugar lowering medicine. In addition, another common group of drugs, known as TZDs, can cause weight gain. Therefore, the hunt is very much on for alternative meds that lower blood sugar. Berberine may fit the bill because it's known to have few side effects.

Researchers have found that an extract from the Gardenia fruit can reverse some of the pancreatic dysfunctions that cause Type 2 diabetes. The extract has long been used in traditional Chinese medicine for that very purpose. This research proves that the extract is effective, but it also tells us why it is effective: there is a chemical contained in the extract known as "genipin." In Type 2 diabetes, a high concentration of an enzyme called uncoupling protein 2 (UCP2) appears to inhibit insulin secretion from the pancreas. Genipin blocks this enzyme, thereby protecting normal pancreatic function.

This is potentially big news for diabetes sufferers. The researchers say that there is at present no therapy available to treat the underlying cause of diabetes. That could change, however, if scientists are able to harness genepin into some sort of treatment option for Type 2 diabetics.