CONSUMING WHEY PROTEIN BEFORE MEALS REDUCES BLOOD SUGAR SPIKES

A whey protein drink before breakfast can control erratic glucose levels associated with type 2 diabetes, say Tel Aviv University researchers

Blood sugar surges - after-meal glucose "spikes" - can be life threatening for the 29 million Americans with diabetes. Diabetic blood sugar spikes have been linked to cardiovascular disease, cancer, alzheimer’s diseases ,  , kidney failure, and retinal damage. Now a new Tel Aviv University study, published inDiabetologia, suggests a novel way to suppress these deadly post-meal glucose surges: the consumption of whey protein concentrate, found in the watery portion of milk separated from cheese curds, before breakfast.

According to TAU's Prof. Daniela Jakubowicz and Dr. Julio Wainstein of the Wolfson Medical Center's Diabetes Unit, Prof. Oren Froy of the Hebrew University of Jerusalem, and Prof. Bo Ahrén of Lund University in Sweden, the consumption of whey protein before meals may even keep diabetics' need for insulin treatment at bay.

"What's remarkable is that consuming whey protein before meals reduces the blood sugar spikes seen after meals. It also improves the body's insulin response, putting it in the same range or even higher than that produced by novel anti-diabetic drugs," said Prof. Jakubowicz. "High milk intake has long been associated with lower risk for type 2 diabetes and cardiovascular disease, and milk whey protein increases the production of a gut hormone called glucagon-like peptide-1 (GLP-1) that stimulates insulin secretion. This, in turn, reduces the blood glucose rise after meals."

"We hypothesized that stimulating GLP-1 production by consuming whey protein before a meal would enhance insulin secretion and have beneficial glucose-lowering effects in type 2 diabetes," Prof. Jakubowicz said.

The study was conducted on 15 individuals with well-controlled type 2 diabetes at Wolfson Medical Center. The participants were randomized to receive either 50 grams of whey in 250 ml water or a placebo, followed by a standardized high-glycemic index breakfast of three slices of white bread and sugary jelly - a meal designed to produce the maximum post-meal glucose spike.

Blood samples were taken 30 minutes before the meal, when the whey protein or placebo drinks were consumed. Further blood samples, assessing plasma concentration of glucose, intact GLP-1, and insulin concentrations, were taken when the breakfast was served and at 15, 30, 60, 90, 120, 150, and 180 minute intervals after the meal.

The researchers found that glucose levels were reduced by 28 percent after the whey pre-load over the 180-minute post-meal period, with a uniform reduction during early and late phases. With whey pre-load, insulin and GLP-1 responses also were significantly higher (105 and 141 percent, respectively), producing a 96 percent increase in early insulin response.

"The early insulin response that usually is deficient in type-2 diabetes was significantly higher after whey protein than with placebo, and the whey protein preload significantly reduced the elevation of blood glucose after breakfast," said Prof. Jakubowicz. "Whey protein could therefore represent a novel approach for enhancing glucose-lowering strategies in type 2 diabetes."

Based on the findings of this study, the authors are considering a long-term clinical trial to test the enduring benefits of whey protein consumption for diabetics.

SYNTHETIC SPERM PROTEIN RAISES THE CHANCE FOR SUCCESSFUL IN VITRO FERTILIZATION

Having trouble getting pregnant -- even with IVF? Here's some hope: A new research report published in October 2014 issue of The FASEB Journal, explains how scientists developed a synthetic version of a sperm-originated protein known as PAWP, which induced embryo development in human and mouse eggs similar to the natural triggering of embryo development by the sperm cell during fertilization

"We believe that the results of this study represent a major paradigm shift in our understanding of human fertilization by providing a precise answer to a fundamental unresolved scientific question in developmental biology," said Mahmoud Aarabi, M.D., Ph.D., a researcher involved in the work from the Department of Human Genetics at Montreal Children's Hospital Research Institute in Montreal, Canada. "Based on our findings, we envision that physicians will be able to improve their diagnosis and treatment of infertility, a problem that affects 10-15 percent of couples worldwide, and scientists will be able to finally resolve the signalling pathway leading to initiation of embryonic development in mammals."

To make their advance, Aarabi and colleagues injected transcripts coding for PAWP protein into human eggs, and the immediate fertilization events, including release of calcium inside the eggs, were investigated carefully. (The human eggs used in this study were donated by infertile women and consisted of immature eggs that were further matured in the laboratory and thus were not suitable for IVF.) The injected eggs were fixed before cell division. A similar protocol was used in mice where the PAWP protein was injected into the eggs. The scientists found that when PAWP inhibitors were injected with the sperm cell into the eggs, a procedure known as ICSI in human infertility therapy, they blocked the sperm-induced fertilization. This is the first time that any sperm protein is shown to be susceptible to such an important inhibition effect.

"Reducing the number of IVF cycles for couple would save them money and disappointment," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Equally important, this research helps us better understand the events that occur when an egg is first fertilized as well as what we can do to influence those events."

Its A Stress Protein That Makes Neuropathic Pain Worse Who Knew!

Today's post from sciencedaily.com (see link below) is another of those infuriating articles that highlight the discovery of yet another pain blocking or enhancing protein or molecule or genetic marker and offer hope that in the future, this knowledge will be used to produce drugs aimed at blocking pain signals. They're infuriating because we know that the end product is still years away and because we only ever partially understand the science but they're also essential in letting us know that progress is being made, however slowly and giving us a glimpse into the world where researchers are exploring ways to control chronic pain symptoms such as neuropathy produces.

Blocking stress protein relieves chronic pain in mice  February 10, 2016 Source:University College London
 
Group of drugs being developed to treat mood disorders could also relieve chronic pain Date:

A group of drugs being developed to treat mood disorders could also relieve chronic pain, finds new UCL (University College London) research funded by the Medical Research Council.

The study, published in Science Translational Medicine, reveals how a protein that shapes the body's response to stress also drives chronic pain and so offers new targets for future pain treatments.

The researchers studied genetically modified mice that lacked a protein called FKBP51. This protein is very important for regulating stress. Variations in the human FKBP5 gene are linked to the risk of developing stress-related psychiatric disorders, such as major depression and post-traumatic stress disorder (PTSD).

Previous studies have shown that people with specific FKBP5 variations feel greater physical pain after serious trauma, and the UCL team have now discovered that mice without FKBP51 experience reduced chronic pain from nerve damage and arthritic joints.

"Inhibiting FKBP51 has a very powerful effect in mice with chronic pain," says lead author Dr Maria Maiarù (UCL Cell & Developmental Biology). "Not only does it block the pain from their injury without affecting their normal pain response, it also makes them more mobile. We did not find any negative side-effects."

The team then tested an FKBP51-blocking compound called SAFit2, developed by Dr Felix Hausch at the Max Planck Institute of Psychiatry to treat mood disorders by acting in the brain to reduce anxiety. By selectively blocking FKBP51 in the spinal cord, the UCL researchers were able to test its effects on chronic pain independently of its known effects on the brain. They found that SAFit2 substantially alleviated chronic pain in mice, making it a promising candidate for drug development.

"The compound was designed to have positive effects on mental health, but we have discovered that it also has significant benefits for physical pain syndromes," says senior author Dr Sandrine Géranton (UCL Cell and Developmental Biology). "Who wouldn't want a treatment that relieves chronic pain while also making you less stressed? This was an experimental study with mice, but if this could be successfully translated into a treatment for patients, it would be a win-win."

The study also showed that an injury can trigger long-term epigenetic changes in spinal cord sensory circuits. This in turn leads to increased production of FKBP51 which contribute to the body's pain response.

"FKBP51 in the brain can prolong the stress response after trauma and we have found that it also exacerbates the pain response," explains Dr Géranton. "Although this may have once had an evolutionary advantage in promoting survival, in our current lifestyles it can lead to chronic pain, depression and PTSD. Chronic pain affects 1 in 5 adults worldwide and there are currently no effective treatments, so we are extremely excited to have identified a new treatment target."

Story Source:

The above post is reprinted from materials provided by University College London. Note: Materials may be edited for content and length.

Journal Reference:
M. Maiaru, K. K. Tochiki, M. B. Cox, L. V. Annan, C. G. Bell, X. Feng, F. Hausch, S. M. Geranton. The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling. Science Translational Medicine, 2016; 8 (325): 325ra19 DOI: 10.1126/scitranslmed.aab3376

https://www.sciencedaily.com/releases/2016/02/160210165713.htm

FIRST PICTURES OF BRCA2 PROTEIN SHOW HOW IT WORKS TO REPAIR DNA

Scientists have taken pictures of the BRCA2 protein for the first time, showing how it works to repair damaged DNA

Mutations in the gene that encodes BRCA2 are well known for raising the risk of breast cancer and other cancers. Although the protein was known to be involved in DNA repair, its shape and mechanism have been unclear, making it impossible to target with therapies.

Researchers at Imperial College London and the Cancer Research UK London Research Institute purified the protein and used electron microscopy to reveal its structure and how it interacts with other proteins and DNA. The results are published today in Nature Structural and Molecular Biology.

Around one in 1000 people in the UK have a mutation in the BRCA2 gene. The lifetime risk of breast cancer for women with BRCA2 mutations is 40 to 85 per cent, depending on the mutation, compared with around 12 per cent for the general population. Many women who test positive for BRCA1 and BRCA2 mutations choose to undergo surgery to reduce their risk of breast cancer. Mutations can also raise the risk of other cancers, such as ovarian, prostate and pancreatic cancer.

The BRCA1 and BRCA2 genes encode proteins involved in DNA repair. The DNA in our cells undergoes damage thousands of times a day, caused by toxic chemicals, metabolic by-products and ultraviolet radiation. Repair mechanisms correct most of this damage, but unrepaired damage can lead to cancer.

The study was led by Professor Xiaodong Zhang from the Department of Medicine at Imperial College London and Dr Stephen West at the London Research Institute.

"This study improves our understanding of a fundamental cause of cancer," said Professor Zhang, a Wellcome Trust Senior Investigator. "It's our first view of how the protein looks and how it works, and it gives us a platform to design new experiments to probe its mechanism in greater detail.

"Once we have added more detail to the picture, we can design ways to correct defects in BRCA2 and help cells repair DNA more effectively to prevent cancer. We can also think about how to make the repair process less effective in cancer cells, so that they die."

The study found that BRCA2 proteins work in pairs -- which the researchers found surprising since BRCA2 is one of the largest proteins in the cell.

BRCA2 works in partnership with another protein called RAD51. BRCA2 helps RAD51 molecules to assemble on strands of broken DNA and form filaments. The RAD51 filaments then search for matching strands of DNA in order to repair the break.

The findings showed that each pair of BRCA2 proteins binds two sets of RAD51 that run in opposite directions. This allows it to work on strands of broken DNA that point in either direction. They also show that BRCA2's job is to help RAD51 form short filaments at multiple sites along the DNA, presumably to increase the efficiency of establishing longer filaments required to search for matching strands.