| Article 238 |
A Study Warns The Spread Of Type 2 Diabetes (T2D) Through The Toxic Meat Or Blood Transfusions
A study has found the spread of type 2 diabetes (T2D) through the blood transfusions or toxic meat as a result of misshapen protein bodies. The protein seeds are similar in those proteins associated with the spread of mad cow disease to the humans from the cattle. The authors say that type 2 diabetes (T2D) is easier to spread compared to the brain diseases (such as the mad cow disease) with the consumption of "rogue" proteins present in the animal products. The spread of brain diseases is not an easy task as the brain contains the blood-brain barrier (BBB), which can separate the fluid in the central nervous system and the brain from the circulating blood.
The islet amyloid polypeptide (IAPP) present in the cattle and other large animals are structurally similar to the humans. An earlier study has found the deposits of misshapen protein or islet amyloid polypeptide (IAPP) in more than 90 percent of the patients with diabetes. The researchers speculate that the spread of rogue proteins in species.
The researchers have conducted experiments on genetically modified mice models by injecting the mice models with the toxic clusters. They have observed the signs (symptoms) of type 2 diabetes (T2D) within weeks. They also observed the signs of type 2 diabetes when toxic clusters were added to pancreatic tissue of a healthy human in a dish. There is no evidence that shows type 2 diabetes (T2D) is contagious and the mechanism behind the development of type 2 diabetes (T2D) in the mice models will apply to the humans. Now the research team is investigating the possibility of acquiring type 2 diabetes (T2D) with the consumption of "rogue" proteins present in the animal products.
The senior author of the study was Christopher J. Soto, Associate Professor of Psychology, Colby College, Waterville, Maine, the United States. The study was published on August 1, 2017, in the Journal of Experimental Medicine. Title of the article was "Induction of IAPP amyloid deposition and associated diabetic abnormalities by a prion-like mechanism."
Treatment Of Parkinson's Disease With Exenatide, A Drug For The Treatment Of Type 2 Diabetes (T2D)
A study at University College London, the United Kingdom, shows the prevention of Parkinson's disease with the type 2 diabetes drug exenatide. A 48-week study with either placebo or with a weekly injection of exenatide was conducted on 62 patients with Parkinson's disease. The participants did not stop the regular treatment of Parkinson's disease. A 12 week washout period was included in the trial.
The study shows a significant improvement in the severity scores of the Parkinson's disease in patients under the treatment of type 2 diabetes drug exenatide and worsening disease severity scores in patients under the treatment of placebo. This study shows a promising treatment option for Parkinson's disease with diabetes drug exenatide. As the current study was small, researchers say that a long-term study is required with more participants before the approval of the type 2 diabetes drug exenatide as a viable treatment option for Parkinson's disease.
The study was funded by the Michael J. Fox Foundation for Parkinson's Research, New York, the United States. The co-author of the study was Dr. Thomas Foltynie, Ph.D., Professor of Neurology, National Hospital for Neurology and Neurosurgery, University College London. The study was published on August 3, 2017, in The Lancet journal. Title of the article was "Exenatide once weekly versus placebo in Parkinson's disease: a randomised, double-blind, placebo-controlled trial."
Exenatide: Once-Weekly type 2 diabetes drug exenatide is marketed as Bydureon or Byetta. It is a glucagon-like peptide-1 receptor agonist (GLP-1), used to lower the high blood sugar level in patients with type 2 diabetes (T2D). Exenatide can lower the blood sugar (glucose) levels by increasing insulin secretion, reducing the appetite and preventing the action of glucagon.
| Published on September 5, 2017 |
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