More data released on key diabetes genes
A Kansas State University graduate student has found a correlation between childhood obesity and asthma. Sara Rosenkranz, doctoral student in human nutrition, Manhattan, conducted research that found that healthy children with higher levels of body fat and lower levels of physical activity had greater amounts of airway narrowing after exercise. “Kids who are overweight and
Full Post: Link between childhood obesity and asthma
One of the most reliable indicators to predict that a person will develop type 2 diabetes is the presence of insulin resistance.
Insulin is produced in the pancreas and is the hormone responsible for ensuring that glucose reaches several tissues and organs in the body, such as muscles. Insulin resistance is characterized by the lack of tissue response to insulin and is counteracted by a greater production of insulin by the pancreas. When the pancreas does not have the capacity to produce the amount of insulin required for tissues to receive glucose, glucose in blood increases to pathological levels and the individual goes from being insulin-resistant to suffering type 2 diabetes. Although it is unclear what makes people develop insulin resistance, several studies report that resistant subjects show functional alterations in mitochondria. These intracellular organelles are responsible for transforming glucose into energy that the cell will then use to perform several functions. A study performed by the researcher Marc Liesa, a member of Antoni Zorzano’s lab at the Institute for Research in Biomedicine (IRB Barcelona), describes a new control pathway of a gene responsible for mitochrondrial fusion, a process that contributes to the correct function of these organelles. This pathway could therefore be a key component in the development of insulin resistance. The results of this study have been published in the scientific journal PloS One .
Diabetes: a complex genetic map
Previous studies demonstrated that people resistant to insulin have altered mitochondrial capacity to “generate” energy through a process called oxidative phosphorylation. In a study performed in 2003, two possible main actors were identified, the genes PGC1-beta and PGC1-alpha. These two genes are responsible for regulating the whole cascade of genes and proteins that allow mitochondria to produce energy by means of oxidative phosphorylation. Now, for the first time, a study has shown that another gene, called Mitofusin 2 (Mfn2), which is decreased in diabetic patients, is also controlled by PGC1-beta. This information is highly relevant because until now it was considered that PGC1-beta controlled the production of energy only by regulating the expression of mitochondrial genes responsible for oxidative phosphorylation. “We have discovered what the cell does to regulate this mitochondrial fusion gene and we explain why this gene is decreased in diabetes, as it is regulated by PGC1-beta, which in turn is affected by this disease. However, although this evidence allows us to propose interesting hypotheses as to the role of Mfn2, its exact role remains unknown”, explains the first author of the study, Marc Liesa.
Key or secondary role in diabetes?
One of the hypotheses is that mitochondrial fusion is crucial for the correct function of these organelles and when the gene that regulates this fusion is decreased, the function of mitochondria is also impaired. But where is Mfn2 situated in the genetic map of diabetes? Is the decrease in mitochondrial fusion related directly to the appearance of insulin resistance? The researchers have obtained the first data that support the notion that Mfn2 plays a key role.
In 2005, in experiments in vitro using rat skeletal muscle cells, the scientists removed the expression of only the Mfn2 gene without touching PGC1-beta, and confirmed that the decrease in mitochondrial fusion affected the capacity to generate energy, “regardless of whether PGC1-beta is functioning correctly”, stresses the head of the group, Antonio Zorzano. “What we are proposing is that the alteration in the fusion alters mitochondrial activity. Observation that the removal of only Mfn2 produces insulin resistance in later experiments in a simple living model - not only in individual cells - , would imply that modulation of this gene contributes to this pathology, thereby making Mfn2 a therapeutic target of interest”, concludes Zorzano.
Type 2 diabetes currently affects 6.5% of the populated aged between 30 and 65 in Spain and recent years have witnessed an increasing incidence of this disease among adolescents and children.
A new study by Narendra et al. suggests that Parkin, the product of the Parkinson’s disease-related gene Park2, prompts neuronal survival by clearing the cell of its damaged mitochondria. “[This is] an exciting new discovery that links the fields of mitochondrial quality control and the genetics of Parkinson’s disease (PD),” writes Heidi McBride of the
Full Post: Researchers shed new light on genetics of Parkinson’s
German scientist Otto H. Warburg’s theory on the origin of cancer earned him the Nobel Prize in 1931, but the biochemical basis for his theory remained elusive. His theory that cancer starts from irreversible injury to cellular respiration eventually fell out of favor amid research pointing to genomic mutations as the cause of uncontrolled cell
Full Post: New evidence in support of Warburg theory of cancer
An important piece in the diabetes puzzle which has perplexed scientists for decades has been uncovered by a Sydney PhD student at Sydney’s Garvan Institute of Medical Research. The novel finding by Freddy Yip has revealed how insulin works and brings researchers one step nearer to understanding just how insulin prompts fat and muscle cells
Full Post: Sydney student solves piece of the diabetes puzzle
In a finding that could significantly influence the way type 1 diabetes is treated, researchers at Albert Einstein College of Medicine of Yeshiva University have developed a technique for transplanting insulin-producing pancreatic cells that causes only a minimal immune response in recipients. At present, cell transplantation therapy is limited because transplant recipients are forced to
Full Post: Researchers engineer pancreatic cell transplants to evade immune response
Vitamin K slowed the development of insulin resistance in elderly men in a study of 355 non-diabetic men and women ages 60 to 80 who completed a three-year clinical trial at the Jean Mayer Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA). “Men who received vitamin K supplementation had less progression in
Full Post: Vitamin K appears to slow development of insulin resistance in elderly men