The antioxidant MitoQ was seen to lower oxidative stress and inflammation in white blood cells from patients with type 2 diabetes. Since these factors are known contributors to heart disease, the findings suggest that mitochondrial supplements may be beneficial in preventing heart problems in these patients.
The study, “The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated from type 2 diabetic patients,” was published in the journal Redox Biology.
Studies indicate that type 2 diabetes is linked to a chronic low-grade inflammation that is present before the disease become apparent. Inflammatory cells, which are known to travel to the pancreas in diabetes, are sensitive to high blood sugar levels, and there are indications that the inflammation seen in diabetes may be caused by the effects of insulin resistance on such cells.
Other studies suggest that oxidative stress is involved in the processes that lead to diabetes. Studies show that high blood sugar levels cause an increase in the number of mitochondria, but this increase is not enough to deal with the rise in metabolic demand from diabetes.
Mitochondria — the cells’ energy factories — tend to produce excess amounts of oxidizing molecules under certain conditions. Obesity, which is tightly linked to type 2 diabetes, is one of those conditions. Oxidative stress is also a source of inflammation.
Given the bits and pieces of evidence that inflammation and oxidative stress contribute to type 2 diabetes, researchers at the Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO) in Spain examined how white blood cells, gathered from diabetes patients, react to the mitochondrial antioxidant MitoQ. The compound is a new generation of the mitochondrial antioxidant CoQ10.
The research team isolated white blood cells from 98 type 2 diabetes patients and 71 controls of the same age and sex. Cells from each patient were then divided into two parts — one was treated with MitoQ and the other was used as a control.
The patients had higher levels of certain blood fats and lower levels of good cholesterol, but since most patients were taking blood fat-lowering medications, the total and bad cholesterol levels were lower in patients than in controls. This did not prevent measures of inflammation to be higher in patients.
White blood cells from patients also produced more reactive oxygen species (ROS). While MitoQ did not have an impact on oxidative stress in inflammatory cells from controls, the treatment reduced oxidative stress in patient-derived cells to nearly normal levels.
During an inflammatory state, white blood cells get attached to the endothelial cell layer — the lining of the insides of blood vessels — which enables them to sneak between cells to enter the tissue. As this is the mechanism the cells use to get into the pancreas, researchers looked at the interactions between white blood and endothelial cells.
They noted that in diabetes patients, the inflammatory cells tended to stick more to endothelial cells. MitoQ normalized the interactions between the two cell types in patients, but again, did not disturb the healthy balance in controls.
The same thing was seen when researchers inspected the levels of inflammatory factors, which were higher in patients but normalized by MitoQ treatment.
The elevated ROS production in white blood cells in T2D patients is part of my new hypothesis just published in Medical Hypotheses: http://www.medical-hypotheses.com/article/S0306-9877(16)30451-0/abstract In my hypothesis, both WBC and platelets are induced to generate high levels of ROS by ultra-exogenous sulfide formation or USF. USF is caused by a diet rich in sulfur.
what is the therepeutic dose of co Q10.