Regularly consuming whole grain foods such as barley, brown rice, millet, oatmeal and rye may help lose weight
It also decreases the risk of heart disease and diabetes, a study has claimed.
Why should you eat more whole grains? Here is all you need to know
The findings showed that study participants who ate whole grains had less inflammation, particularly in overweight people, which increases the risk of developing Type 2 diabetes.
Further, participants were also found to eat less when whole grain products were on the menu because whole grain consumption causes satiety.
Importantly, having a whole grain diet helps lose weight, as compared to refined grains — rich in starch, gluten and devoid of natural fiber.
“Our analysis confirmed that there is a sound scientific basis for the dietary recommendation to eat whole grains. This may particularly apply to people who are at increased risk of developing cardiovascular disease or Type 2 diabetes,” said Tine Rask Licht, professor at the Technical University of Denmark.
Additionally, the researchers used DNA sequencing to analyze stool samples from the participants in order to examine whether the different diet types affected the participants’ gut bacteria composition.
Overall, the analysis did not show major effects of the dietary grain products on the composition of the lose weight.
“However, even though the analysis did not reveal significant changes in the average gut microbiota after whole grain consumption, it may well be that the individual components of our gut microbes has an impact on the individual reaction of our body to dietary whole grains,” Licht explained.
For the study, described in the journal Gut, the team included adults at risk of developing cardiovascular disease or Type 2 diabetes. The participants were divided randomly into two groups, with whole grain diet and refined varieties for eight weeks.(IANS)
Drugs for diabetes, inflammation, alcoholism — and even for treating arthritis in dogs — can also kill cancer cells in the lab, according to a new health news and study.
The researchers systematically analysed thousands of already developed drug compounds and found nearly 50 that have previously unrecognised anti-cancer activity.
The findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.
“We thought we’d be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many,” said study researcher Todd Golub from Harvard University in the US.
The study, published in the journal Nature Cancer, yet to employ the Broad’s Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs).
Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin’s cardiovascular benefits.
“We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way,” said study first author Steven Corsello, from Dana-Farber Cancer Institute and founder of the Drug Repurposing Hub.
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad’s Cancer Cell Line Encyclopedia (CCLE).
Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment.
The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.
They found nearly 50 non-cancer drugs — including those initially developed to lower cholesterol or reduce inflammation — that killed some cancer cells while leaving others alone.
Some of the compounds killed cancer cells in unexpected ways.
“Most existing cancer drugs work by blocking proteins, but we’re finding that compounds can act through other mechanisms,” said Corsello.
Some of the four-dozen drugs researchers identified appear to act not by inhibiting a protein but by activating a protein or stabilising a protein-protein interaction.
For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilising the interaction between PDE3A and another protein called SLFN12 — a previously unknown mechanism for some of these drugs.
These unexpected drug mechanisms were easier to find using the study’s cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target.
For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs. (IANS)