Bones affect appetite and metabolismApart from providing structure to support muscles and tissues, the skeleton produces hormones, too. One of them, is known as osteocalcin – and researchers have found that they play a key role in the metabolism of sugar and fat.
Mathieu Ferron, a researcher at Montréal Clinical Research Institute (IRCM) and professor at Université de Montréal's Faculty of Medicine, alongwith his team have spent the last decade studying how osteocalcin works. Their discovery has led them to boldly state that the hormone might be the answer the prevention of type 2 diabetes and obesity.
“One of osteocalcin’s functions is to increase insulin production, which in turn reduces blood glucose levels,” explained Ferron. “It can also protect us from obesity by increasing energy expenditure.”
Separate studies have shown in some cases, that changes in blood concentrations of osteocalcin may even prevent the development of diabetes. These protective properties sparked Ferron's interest in how this hormone actually works.
"When it is first produced in osteoblasts, osteocalcin is in an inactive form," noted Ferron. "What interested us was understanding how osteocalcin becomes active so as to be able to play its role when released into the blood.
The IRCM team found their answer: Furin.
Furin causes osteocalcin to become active before it released into the blood. They also found that Furin causes a decrease in appetite – an unexpected effect. To support the result, the team also demonstrated that osteocalcin itself has no effect on appetite. They further suggested the existence of a new bone hormone is that controls food intake.
The team hopes to determine whether Furin is associated with another protein incolved in appetite regulation.
Diet no more: Bacterial fats may be blamed for heart diseaseIt is known that heart attacks and strokes result from prolonged atherosclerosis (hardening and clogging of the arteries with fatty substances called lipids). However, recent evidence suggests that the culprit behind the fatty clogs is not only from food – but, from the bacteria in the mouth.
Previously, doctors and researchers assumed that the lipids came from consumption of fatty-rich food. But, they also noted that some people who eat these foods do not necessarily develop heart disease.
Based on the study by UConn researchers, they found strange lipids that come from a specific family of bacteria with a chemical signature unlike those from animals.
The bacteria, called Bacteroidetes make distinctive fats which are not typical for mammals.
The Bacteroidetes themselves are not the actual cause of this as they are typically located in our mouth and gut. It is the lipids they produce that can pass easily through cell walls and into the bloodstream which causes the most fatty clogs, as compared to those from food.
The team also revealed that the immune system also sees the lipids as a signal of bacterial invasion and reacts against it. However, although recognised as foreign, the lipids can still be broken down by an enzyme in the body to make inflammation-enhancing molecules.
This means Bacteroidetes create more trouble for the blood vessels as they attack the lipids and enhance the inflammation at the same time.
The researchers hope to identify exactly where the bacterial lipids accumulate next. This could provide convincing evidence that these unusual lipids are associated with atheroma formation, and in turn provide solutions to tackle heart disease.
Smoking now associated with inflammatory bowel diseaseSmoking has been long been associated with respiratory diseases and cancers. However, for the first time, a South Korean study has shown a direct effect of cigarette smoke on intestinal inflammation.
The researchers from Kyung Hee University, reported that their results suggest that cigarette smoking activates specific white blood cells in the lung, which might later move to the colon, triggering bowel inflammation.
"The airways and the intestinal system have a lot in common," says Hyunsu Bae, of Kyung Hee University in South Korea. "Interestingly, in Traditional Korean Medicine, a connection between the lung and the large intestine has long been emphasised. Crohn's disease is more likely to occur in people with airway diseases, suggesting that inflammation in the lungs is linked with inflammation in the gut."
From their study on mice, the researchers found increased levels of mucus and inflammation in the colon, and blood in the faeces of smoke-exposed mice. They also found increased levels of CD4+ T cells, a type of white blood cell, which releases a pro-inflammatory protein called interferon-gamma.
The team is confident that CD4+ T cells were responsible for the cigarette smoke-induced colitis. To support this, they even tested the isolated cells by injecting them on mice which were free from smoke exposure. It revealed that the injected cells migrated to the colon, and the non-smoke-exposed mice developed colitis shortly after.
The researchers hope the study could help scientists to develop new treatments for inflammatory bowel diseases such as Crohn's disease – and increase awareness among smokers of their risk for colitis. MIMS
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