Obesity Can Actually Scar Your Fat Tissue, Making Weight Loss Even Harder

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Our body’s fat-storing mechanisms – called adipose tissues – are very good at the job of taking our excess calories and storing them in the form of high-energy molecules called lipids.

But new research suggests their cells can expand to a size that literally suffocates them, triggering inflammation and making the adipose tissues less efficient. Not only is this bad news for losing weight, it also puts other organs at risk of critical damage.

Research led by the University of Exeter in the UK found that levels of an enzyme called lysyl oxidase increase in adipose tissues as an individual’s body mass index goes up, indicating the cells were being scarred as they expanded in size.

Lysyl oxidase – or LOX – crosslinks fibres of collagen, a tough protein that builds structures inside cells and helps connect tissue. Excess LOX can mean there’s too much fibrous structure surrounding cells, making the tissue rigid.

All of this adds up to fat cells that can no longer expand to fit more lipids, and change how fat is distributed around the body.

Scarred adipose tissue can see more fat distributed around organs and less under the skin, giving people an ‘apple’ shape with larger bodies and thinner limbs.

Since this visceral fat is more of a concern for our health than subcutaneous fat, it’s a serious problem that warrants addressing.

“One could have very little fat below the skin and still be at risk of diabetes due to a lot of fat within the abdomen and inner organs,” says physician Katarina Kos from the University of Exeter’s Medical School.

It also means there’s less room for fat to be stored inside the adipose tissue itself.

While you might imagine this to be a good thing, that fat doesn’t disappear – instead, it can be diverted into other tissues such as the liver and the heart, raising the risk of cardiovascular disease.

And if all that isn’t bad enough, stiffer adipose tissues also make it hard for the cells to release their stores of fat.

“Scarring of fat tissue may make weight loss more difficult,” says Kos.

Much of the problem starts with the cells in adipose tissue becoming starved of oxygen.

The researchers compared the levels of messenger RNA expressed for the LOX enzyme in adipose tissues from patients undergoing bariatric surgery, and again in samples collected over nine months later.

They also analysed LOX expression in response to mild inflammation in the fat tissues of healthy male volunteers, and compared levels in diabetic patients.

While having diabetes didn’t affect the levels of LOX, and therefore the scarring of the tissues, low levels of oxygen and inflammation had a significant impact on its expression.

This was taken to suggest that as the cells fill and expand, they’re deprived of the oxygen they need to survive. This triggers and inflammation process, increasing LOX levels and making the cells more fibrous.

Unfortunately weight loss surgery didn’t see the LOX levels decrease, making it unlikely that the tissues would become less scarred even with radical interventions.

The take-home message is to keep our adipose tissue in check before it gets to that stage.

“There is evidence that once fat tissue becomes scarred, despite weight loss, it may not recover fully,” says Kos.

“We need to look after our fat tissue which can cease to cope if it is overworked when being forced to absorb more and more calories.”

Kos’s advice is to exercise or at least take a walk after a meal. Weight loss is hard, and while a few people have the ability to keep at it, others face an uphill battle thanks to a mix of biology and habit.

But if knowing it could only get harder later gives some people that incentive to cut a few calories and walk after a meal, then this is one study to pay close attention to.

This research was published in Metabolism.

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Hepatitis-B vaccination at birth may not be necessary in India: ICMR funded study

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A large multi-centre study done in North India shows that many newborns are protected at birth by natural antibodies to hepatitis-B and so Hep-B vaccination at birth is not necessary. The study, whose findings have been published in the Indian Journal of Pediatrics, was done to look at whether hepatitis-B vaccination at birth was crucial for India.

Hepatitis-B virus (HBV) can cause chronic hepatitis, liver cirrhosis and lead to hepatocellular carcinoma (HCC) in susceptible persons.

The study, which was funded by the Indian Council of Medical Research (ICMR), involved 2671 children from participating centres in Delhi, Rajasthan, Uttar Pradesh, Uttarakhand, and Gujarat of whom 880 were fully immunised starting at birth and 686 were fully immunised but without the birth dose. The ICMR had launched this study to look at hepatitis-B infection rates in children vaccinated at birth compared to those vaccinated starting at six weeks.

The study found that infection rate was similar even in those babies not given the birth dose thereby supporting the government’s pragmatic programme. The study lends support to the government’s pragmatic approach to vaccinate babies born at home starting at six weeks instead of at birth.
“We found birth dose was not needed as infection rates were the same regardless of birth dose,” says Jacob Puliyel the study’s primary author and a pediatrician at St. Stephens Hospital in Delhi.

The researchers also found high protective antibodies in children before vaccination indicating that missing the birth dose does not cause much problem. “These natural antibodies may also be the reason why the hepatocellular carcinoma rate in India is very low,” says Puliyel who is also a member of the government’s technical advisory board on immunization. The conclusions of the study in North India support that of anther large ICMR study conducted in Andhra Pradesh in South India reported in 2014 which also reported the presence of hepatitis-B antibodies in children before vaccination.

The fact that a good number of unvaccinated babies had high levels of antibody suggest it could be protecting some babies early in life, at a time when they are vulnerable to develop chronic hepatitis. Most babies are naturally immune to hepatitis-B infection due to passive transfer of antibodies from the mother.

India started vaccinating children against hepatitis-B in 2011. It is given at birth to babies born in hospitals. However, because many babies are delivered at home, outside of healthcare settings, the government introduced the pragmatic programme schedule of HBV vaccination, wherein the vaccine is given starting at six weeks to children born outside such health-care settings.

However mothers in highly immunized communities have lower hepatitis-B antibody levels as vaccine induces lower antibody levels than natural infection and the antibody levels of vaccinated cohorts are no longer boosted by exposure to wild-type infection. Babies born to these mothers will correspondingly have lower levels of antibodies, says Puliyel. “Therefore, paradoxically, nation-wide Hepatitis-B vaccination may reduce natural antibody transfer to newborns and there is a possibility it may increase incidence of HCC instead of reducing it.”

He however cautions that more studies are needed to confirm this before changes in immunization practice can be recommended.

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Bacteria Living in Our Gut Are Hijacking And Controlling Our Genes

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Your gut microflora isn’t just sitting silently waiting for you to wolf down your next meal – it turns out there’s a constant conversation going on between these bacteria and your body’s genetic code.

New research has found a chemical produced by ‘good’ bacteria in our digestive system has an unusual effect on the chromosomes in nearby cells, a discovery that could help us better understand links between our diet and the development of one of the world’s most deadly cancers.

A team led by scientists from the Babraham Institute in the UK that discovered DNA in the epithelial tissues of the human colon contain an unusual level of a chemical known to act as an epigenetic switch, turning genes on and off.

What’s more, they found these levels were elevated in just one other part of the body: our brain.

Crotonylation is a recently discovered genetic editing process not unlike the more familiar form of genetic manipulation called methylation.

Both processes change how genes are expressed by tweaking the surrounding chemistry, without altering the actual code itself.

While methylation involves the addition of a methyl group (CH3) to a nucleotide base – usually cytosine (C), but occasionally adenosine (A) – crotonylation clips an acetyl group onto proteins called histones that help keep strands of DNA neatly ordered.

Finding crotonylated histones in gut tissue suggests something is preventing the body from removing those acetyl groups. And the researchers suspected they knew what it could be.

Small organic molecules called short-chain fatty acids (SCFA) are produced when the fibre in our fruit in veg is fermented by our resident microbes.

Previous research had suggested there were links between the cell’s metabolism and crotonylation, pointing to SCFAs as the culprit.

The researchers analysed tissue from the colon, brain, liver, spleen, and kidney, and found higher levels of histone crotonylation in the brain and colon.

Why this occurs in the brain but not the other organs is still something of a mystery.

Yet this new study demonstrates it’s the bacteria that are ultimately responsible for the modification.

“Short chain fatty acids are a key energy source for cells in the gut but we’ve also shown they affect crotonylation of the genome,” says lead author Rachel Fellows from Babraham Institute.

Specifically, SCFAs produced by the kinds of bacteria found in a healthy human colon promote crotonylation by preventing an enzyme called histone deacetylase 2 (HDAC2) from removing the markers.

To confirm bacteria were indeed responsible, the researchers dosed mice with a cocktail of antibiotics to wipe out most of the bacterial microflora in their guts. Not only did the SCFAs drop, so too did the crotonylation of the histones in their gut lining.

Exactly what benefits the bacteria might get – if any – wasn’t addressed by the study.

But the research could have implications in how our genes are affected by our diet, which could go some way to help flesh out the links between dietary fibre and bowel cancer.

With around 770,000 deaths from colorectal cancer each year, finding more ways to prevent and treat the disease is a high priority for researchers.

Meanwhile, it’s a good reminder for us to check our diet and make sure it’s not just our bodies that are being well fed, but our tiniest citizens as well.

“Our intestine is the home of countless bacteria that help in the digestion of foods such as plant fibres,” says the study’s lead scientist, Patrick Varga-Weisz.

“They also act as a barrier to harmful bacteria and educate our immune system. How these bugs affect our cells is a key part of these processes.”

This research was published in Nature Communications.

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India and Germany to begin joint research in the area of ‘Bioinformatics in Health Research’

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To facilitate bilateral cooperation in biotechnology between the scientific communities of India and Germany, the Department of Biotechnology (DBT) will soon begin collaborative research in the identified priority area of ‘Bioinformatics in Health Research’ under the programme of Indo-German Cooperation in Health Research.

The purpose of the programme is to stimulate new collaborations, e.g. the preparation of joint projects under national funding programmes. The programme facilitates bilateral cooperation in biotechnology between the scientific communities of India and Germany by way of joint research projects which will encompass bilateral workshops/seminar and exchange visits of scientists.

The programme is being implemented within the agreement of Indo-German cooperation in S&T of 1974, under which the Department of Biotechnology, Government of India and Forschungszentrum Julich BMBH (FZJ), Federal Republic of Germany, have agreed for cooperative programme in biotechnology.

DBT of the Ministry of Science & Technology, Government of India and the Project Management Agency at the German Aerospace Center (DLR-PT, European and International Cooperation), Bonn are the nodal implementing agencies from the Indian and German side respectively.

Through this programme, it is expected that the funded cooperation enables the partners to develop applicable scientific results which can be published and/ or could be commercialised and may lead to formation of joint ventures. All publications, patents coming out of these projects, need to be jointly authored by both Indian and German scientists. All necessary approvals like ethical clearance, HMSC approval from Indian point of view as well as EU, if applicable, from German point of view, e.g. before conducting animal experimentation if any needs to be obtained by PIs before undertaking the project.

Now, both the nodal agencies have invited research proposals in identified priority area of ‘Bioinformatics in Health Research’ from eligible scientists. Joint research projects are required to be submitted to both the nodal agencies by 15 January 2018. Scientists/faculty members working in regular capacity in universities, national R&D laboratories/institutes and private R&D institutes can be part of this joint research programme. For the private sector, partners from all kind of private sectors are eligible, but financing is limited. For Indian scientists from the private sector, only local hospitality in Germany as part of the exchange visit is available from the German side. For German scientists from the private sector, only travel costs are available for small and medium size enterprises (for definition of SME ref. to 2003/361/EC) as well as local hospitality in India will be borne by themselves.

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Scientists Just Changed Our Understanding of How Anaesthesia Messes With The Brain

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It’s crazy to think that we still don’t quite understand the mechanism behind one of the most common medical interventions – general anaesthetic.

But researchers in Australia just got a step closer by discovering that one of the most commonly used anaesthetic drugs doesn’t just put us to sleep; it also disrupts communication between brain cells.

The team investigated the drug propofol, a super-popular option for surgeries worldwide. A potent sedative, the drug is thought to put us to sleep through its effect on the GABA neurotransmitter system, the main regulator of our sleep-and-wake cycles in the brain.

But anyone who’s been “put under” will know that waking up from a general anaesthetic feels rather different from your usual morning grogginess.

On top of that, some people can experience serious side-effects, so scientists have been trying to figure out what else the drugs might be doing in the brain.

Using live neuron cell samples from rats and fruit flies, the researchers were able to track neurotransmitter activity thanks to a super-resolution microscope, and discovered that propofol messes with a key protein that nerve cells use to communicate with each other.

This protein, called syntaxin1A, isn’t just found in animal models – people have it, too.

“Every neuron communicates with other neurons by way of syntaxin1A-mediated neurotransmission, which is highly conserved from worms to humans,” the team writes in the study.

And it looks like the anaesthetic drug puts the brakes on this protein, making otherwise normal brain cell connections sluggish, at least for a while.

“We found that propofol restricts the movement of [syntaxin1A], required at the synapses of all neurons. This restriction leads to decreased communication between neurons in the brain,” says lead author of the study, PhD student Adekunle Bademosi from Queensland Brain Institute (QBI) at the University of Queensland.

The researchers think this disruption could be key to how propofol allows for pain-free surgery to take place – first it knocks us out as a normal sleeping pill would, and then takes things up a notch by disrupting brain connectivity.

The team’s results are a significant step up in what we know about the workings of general anaesthetic – a long-standing medical mystery.

“It is indeed a 180-year-old question, one of the unresolved mysteries in medicine,” senior author of the study, Bruno van Swinderen from QBI, told ScienceAlert.

“I think it has been a hard problem to solve because our hypotheses for explaining general anaesthesia have largely paralleled our growing understanding of how the brain works.”

To be able to track down the movements of a protein in the synapses – the connecting points between nerve cells – scientists needed to know how this synaptic process even works, a discovery that was only awarded a Nobel Prize as recently as 2013.

But now that imaging techniques are advancing, we can likely expect researchers to unravel the anaesthetic mystery even further.

More research will be needed to establish a causal link between propofol’s disruption of the syntaxin1A protein and its anaesthetic effects – and then there are also other anaesthetic drugs to be tested.

Still, van Swinderen thinks it’s possible that all general anaesthetics work in this particular manner, because they all share an important characteristic – they all bind to fats, and fats are found at crucial neurotransmitter exchange points in our synapses.

“The discovery has implications for people whose brain connectivity is vulnerable, for example in children whose brains are still developing or for people with Alzheimer’s or Parkinson’s disease,” says van Swinderen.

“It has never been understood why general anaesthesia is sometimes problematic for the very young and the old. This newly discovered mechanism may be a reason.”

The research has been published in Cell Reports.

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