Societes Nordiques

This is one of those stories that we hope will continue to provide answers, results and hope to people living with Type I diabetes. Shan Wolff has gained a little bit more of his life back since having an islet-cell transplant at Baylor University Medical Center. It is not a cure, and it does not make his life perfect again. There are drawbacks such as the hassles and risks of living with a suppressed immune system now. Nevertheless, we have to say: Go Shan!!!!

ED - Newest Marker for Diabetes and Heart Disease We all know that people who are overweight, have high blood pressure and cholesterol levels face a substantial risk of developing heart disease and diabetes. Well, researchers from Boston recently found out that the decrease in blood flow that contributes to eretile dysfunction or impotence can be a marker as well.

Chinese Medicinal Medicine, Berberine - For Now Its a Theory There are a few stories out there in the news today about a plant-based substance, berberine. Traditional Chinese medicine claims that it lowers glucose levels. It turns out that a group of Asian scientists were able to show that it indeed works in animals. Now they plan to turn to human experiments.

It would be exciting news if it works in humans, too. However, right now it is still a theory or hypothesis. Lets save the PR energy for the results. :)

Accumulation of lipid in the liver tissue has been variously referred to as fatty infiltration, fatty degeneration, and liposis. Liposis refers to excessive accumulation of fat or lipid material predominantly consisting of triglycerides and fatty acids. Normal liver may contain as much as 5% of its weight as fat. Lipidotic liver may contain as much as 50% of its weight as fat, most of it being triglycerides. Under conditions of hepatic triglyceride accumulation, lipid droplets appear surrounded by membranes to form liposomes. Hepatic triglycerides seem to be contained in two separate pools, which mix poorly. Only one of these pools is involved actively in secreting triglycerides into the plasma. Many models of drug-induced lipidosis have been described. These include CCU, ethionine, orotic acid, ethanol, tetracycline antibiotics, corticosteroids, and yellow phosphorus. Lipidotic liver is also observed in hepatic resection and in disease states such as diabetes. Choline-deficient diet has also been used to produce fatty liver, and this model has been studied extensively.

The plasma concentration of triglycerides can be reduced to half the normal value within ½ h after CCI administration in fasted animals. Abnormal accumulation of triglycerides in the hepatic cells has been demonstrated as early as 2 h after the administration of this hcpatotoxic compound. Such accumulation of fat has been documented by following the incorporation of labeled fatty acids, measuring freshly secreted triglycerides, by morphometric analysis of appropriately stained liver sections, and trapping with the use of detergents in intact animals as well as in perfused liver preparations. There is also evidence for the blocked release of triglycerides from the liver. Hepatic accumulation of fat after ingesting alcohol has been well documented. This can be attributed to the introduction of physiological lesions at multiple sites of lipid metabolism. No only can individual factors be evoked to explain the abnormal accumulation of fat in alcoholic liver—the problem may be compounded by indirect effects mediated via nutritional imbalances such as choline deficiency. Moreover, such effects may also be mediated via hormonal mechanisms such as the effects of catecholamines on mobilization of body fat.

Ethionine-induced and orotic acid-induced accumulation of fat in the liver is a result of striking reduction in the transport of lipid from the liver. Depressed plasma levels of very-low-density lipoprotein (VLDL) have been attributed either to defective glycosylation or to impaired synthesis of the phospholipid component of VLDL. The initial biochemical event triggering the accumulation of fat in the liver tissue in response to orotic acid appears to be related to deficiency of ATP consequent to the acceleration of uridine synthesis. Ethionine also causes a decrease in ATP, which leads to accumulation of fat in the liver. The complex biochemical manifestations of ethionine include depressed serum triglycerides, phospholipids, cholesterol, cholesterol esters, lipoproteins, and glucose. Changes in hepatic function include impaired excretion of sulfobromophthalein (BSP) and mild elevation of serum bilirubin. Several other experimental models of fatty liver have been studied extensively. Administration of large intravenous doses of tetracycline and its derivatives is associated with the fine fatty vacuolization of the liver. Corticosteroid administration also results in fatty infiltration of the liver. Injection of a large dose of yellow phosphorus, a component of many rat poisons, results in fatty infiltration of the liver. Hepatic lipid increases twofold within 10 h after partial hepatectomy in experimental animals. The majority of the lipid accumulating after this surgical practical removal of the liver is in the form of triglycerides. After the resection recovers to normal size, the triglycerides fall to normal levels, indicating that the elevation of liver fat is a specific response to partial hepatectomy.