Tag: gastrointestinal

A Link Between Intestinal Changes, Diet and Disease

A new study published in Nature Metabolism has found a link between diet, intestinal cell changes and disease.

The intestine has to react quickly to changes in nutrition and nutrient balance. One of the ways it does so is with intestinal cells that are specialised in the absorption of food components or the secretion of hormones. In adult humans, the intestinal cells regenerate every five to seven days. The ability to constantly renew and develop all types of intestinal cells from intestinal stem cells is crucial for the natural adaptability of the digestive system. However, a long-term diet high in sugar and fat disrupts this adaptation and can contribute to the development of obesity, type 2 diabetes, and gastrointestinal cancer.

The molecular mechanisms behind this maladaptation are the research area of this study. Intestinal stem cells are thought to play a special role in maladaptation, and to investigate this, the researchers used a mouse model to compare the impacts of a high-sugar and high-fat diet and with a control group.

“The first thing we noticed was that the small intestine increases greatly in size on the high-calorie diet,” said study leader Anika Böttcher. “Together with Fabian Theis’ team of computational biologists at Helmholtz Munich, we then profiled 27 000 intestinal cells from control diet and high fat/high sugar diet-fed mice. Using new machine learning techniques, we thus found that intestinal stem cells divide and differentiate significantly faster in the mice on an unhealthy diet.” The researchers hypothesize that this is due to an upregulation of the relevant signaling pathways, which is associated with an acceleration of tumor growth in many cancers. “This could be an important link: Diet influences metabolic signaling, which leads to excessive growth of intestinal stem cells and ultimately to an increased risk of gastrointestinal cancer,” says Böttcher.

Using this high-resolution technique, the researchers have also been able to study rare cell types in the intestine, such as hormone-secreting cells. Among their findings, they were able to show that an unhealthy diet leads to a reduction in serotonin-producing cells in the intestine. This can result in intestinal inertia (typical of diabetes mellitus) or increased appetite. Furthermore, the absorbing cells were shown to adapt to the high-fat diet, increasing functionality and thus directly contributing to weight gain.

The study findings enable a new understanding of disease mechanisms associated with a high-calorie diet. “What we have found out is of crucial importance for developing alternative non-invasive therapies,” said study leader Heiko Lickert. 

Presently, there is no pharmacological approach to prevent, stop or reverse obesity and diabetes. Only bariatric surgery causes permanent weight loss and can even lead to remission of diabetes. However, these surgeries are invasive, non-reversible and costly to the healthcare system. Novel non-invasive therapies could happen, for example, at the hormonal level through targeted regulation of serotonin levels. This will be an avenue of future research for the group.

Source: EurekAlert!

1 in 10 Suffer Abdominal Pain After Meals

Photo by Vanessa Loring from Pexels

Around 11% of the global population frequently experience abdominal pain when they eat meals, according to a large online survey.

The research, presented at UEG Week Virtual 2021, found that was pain associated with eating is most common in those aged 18 to 28, with 15% of that age group affected. A gender split was seen, with 13% of women and 9% of men reporting eating-linked pain.

People experiencing frequent abdominal meal-related pain were also more likely to experience bloating, feeling full too soon, constipation and diarrhoea. The same group also had more severe psychological distress and non-gastrointestinal somatic symptoms.

A total of 36% of the people with frequent (>50% of the time) meal-related pain reported suffered from anxiety compared with 25% in the occasional (10-40% of the time) symptoms group and 18 % in those who never experienced meal-related pain. Those with frequent attacks also reported higher rates of depression (35%) compared to 24% in the occasional  symptom group and 17% in the group that never had meal-related pain.
The findings came from an online survey of 54 127 people across 26 countries.
Esther Colomier, study author and a joint PhD researcher at KU Leuven, Belgium, and the University of Gothenburg, Sweden, explained, “The take home message from this study is that people who experience meal-related abdominal pain more frequently experience other gastrointestinal symptoms and more regularly fulfil criteria for disorders of the gut brain interactions (DGBIs, formerly known as functional gut disorders), including common conditions such as irritable bowel syndrome (IBS), bloating and abdominal distension.”

“They also have a higher burden of psychological and somatic symptoms, such as back pain or shortness of breath, which are associated with major distress and functioning problems. These symptoms cause distress and disruption in daily life”, she added.

Lower gastrointestinal symptoms such as constipation and diarrhoea were experienced in 30% of those who reported frequent meal-related pain, versus 20% in the group who reported occasional symptoms and 10 % in the no symptoms at all group. The same applied for bloating and abdominal distension symptoms, which were reported as often as once a week in the group who experienced frequent meal pain, compared to two or three days a month in the group with occasional pain and one day a month in the group who experienced no symptoms.

Esther Colomier concluded, “Considering meal-related symptoms in future diagnostic criteria for DGBIs should be encouraged. In clinical practice, assessing meal association in all patients with DGBIs could be of major importance for improving and individualising treatment. Here, patients could benefit from a multidisciplinary care approach, including dietary and lifestyle advice, psychological support and pharmacological therapy.

Source: EurekAlert!

Eight Factors Predict Gastrointestinal Bleeding Risk after Heart Attack

Using machine learning, researchers at Karolinska Institutet have identified eight primary factors that increase the risk of a common bleeding complication after heart attack.

Some of these factors had been known already, however, the researchers have found additional predictors, such as smoking, blood pressure and blood glucose. The study was published in the European Heart Journal – Cardiovascular Pharmacotherapy.

“If we can identify patients at high risk of upper gastrointestinal bleeding following heart attack, doctors will be able to take prophylactic measures to mitigate this risk,” said the study’s corresponding author Moa Simonsson, deputy consultant at Karolinska University Hospital and doctoral student. “There are, for instance, drugs that combat bleeding complications, gut bacteria tests that can be used on risk groups and other possibilities for personalised treatment for heart attack patients at high risk of bleeding complications.”

Upper gastrointestinal (GI) tract bleeding is one of the most common bleeding complications following acute myocardial infarction. The condition requires a lot of resources to treat, causes considerable suffering and increases mortality risk. Bleeding complications also limit antithrombotic use, which in turn can worsen the cardiovascular prognosis.

Over the past 20 years, a close focus on bleeding has resulted in several strategies for reducing the risk of upper gastrointestinal tract bleeding. However, few studies on this complication include a diverse population of heart attack patients.

For the current study, the researchers sourced data from the national SWEDEHEART registry on almost 150 000 patients with acute myocardial infarction between 2007 and 2016. Approximately 1.5 percent of these patients suffered GI bleeding within a year of their heart attack, and they also had an increased risk of death and stroke.
Several known factors that increase the risk of upper GI tract bleeding were confirmed by the analysis, including low levels of haemoglobin, previous upper GI tract bleeding, age and intensive antithrombotic treatment.

Using an algorithm, the researchers also identified additional risk factors, including smoking, blood pressure, blood glucose and previous treatment for stomach disorders, such as ulcers and acid reflux.

“If you combine traditional statistical models with machine learning methods, you can create unique opportunities to find key risk factors for previously unknown cardiovascular events,” explained co-author Philip Sarajlic, doctoral student at Karolinska Institutet. “This makes it possible for us to make effective use of valuable data from the medical quality registry by taking account of complex relationships between risk factors and outcomes in order to further optimise the current recommendations for patient care.”

The researchers will soon begin a major clinical study to explore the significance of diagnosis and treatment of a common infection in the upper GI tract.

“A pilot study last year showed a two-fold increase in the presence of Helicobacter Pylori in heart attack patients,” said last author Robin Hofmann, researcher and consultant at Karolinska Institutet. “We will now proceed with a large randomized study to ascertain whether a systematic screening of heart attack patients for Hp infection and, where relevant, its treatment, can reduce bleeding complications and improve prognosis after heart attack.”

Source: Karolinska Institute

A Leak-proof, Biocompatible Intestinal Patch

Researchers at Empa have developed a patch that stably seals two sutured pieces of intestine and thus prevents dangerous leaks.

A burst appendix or a life-threatening intestinal volvulus are emergencies that need to be treated by surgeons immediately. However, operations carry risks: highly acidic digestive juices and intestinal bacteria can leak out, causing peritonitis and sepsis.

Sealing sutured tissue with a plaster has already been tried, but the first were not well tolerated or were even toxic. Currently, these plasters are made of biodegradable proteins, which have variable clinical results. These is because they are mainly intended to support the healing process, and dissolve too quickly when in contact with digestive juices and don’t always hold tight. “Leaks after abdominal surgery are still one of the most feared complications today,” explained Empa researcher Inge Herrmann, who is also professor for nanoparticulate systems at ETH Zurich.

Searching for a material that could reliably seal intestinal injuries and surgical wounds, Hermann’s team found a synthetic composite material made up of four acrylic substances that, together, form a chemically stable hydrogel. Additionally, the patch actively cross-links with the intestinal tissue until it is fluid-tight. The quadriga of acrylic acid, methyl acylate, acrylamide and bis-acrylamide works in perfect synergy, as each component conveys a specific feature to the final product: a stable bond to the mucosa, the formation of networks, resistance to digestive juices and hydrophobicity. This new technology is detailed in Advanced Functional Materials.

In lab experiments, the researchers found the polymer system met their expectations. “Adhesion is up to ten times higher than with conventional adhesive materials,” said researcher Alexandre Anthis from Empa’s Particles-Biology Interactions lab in St. Gallen. “Further analysis also showed that our hydrogel can withstand five times the maximum pressure load in the intestine.” The material’s design uses its tailored effect: The rubbery composite selectively reacts with digestive juices that might leak through intestinal wounds, expands and closes all the more tightly. The inexpensive, biocompatible super glue, could thus shorten hospital stays and save healthcare costs, and Anthis is making plans to bring it to market.

Source: Empa

Common Gut Bacteria Could Inhibit SARS-CoV-2

Bifidobacterium eriksonii, stained with fluorescent antibodies. Source: Public Health Image Library

South Korean researchers have found that certain common gut bacteria produce compounds that inhibit SARS-CoV-2. 

The research was presented on June 20 at World Microbe Forum, an online meeting of the American Society for Microbiology (ASM), the Federation of European Microbiological Societies (FEMS), and several other societies that taking place online June 20-24.

Previous clinical findings had shown that some patients with moderate to severe COVID experience gastrointestinal symptoms, while others show signs of infection in the lungs only.

“We wondered whether gut resident bacteria could protect the intestine from invasion of the virus,” said Mohammed Ali, a PhD student in Medicine at Yonsei University in South Korea.

To investigate this hypothesis, the researchers screened dominant bacteria inhabiting the gut for activity against SARS-CoV-2. Their efforts revealed that Bifidobacteria, already shown to suppress other bacteria such as H. pylori and have proven active against irritable bowel syndrome, had such activity, said Ali. Bifidobacteria are common in the guts of breast fed infants, which is partly driven by the bifidogenic activities of specific mother milk-derived oligosaccharides

The researchers also searched for potential illness-fighting compounds in databases containing microbially produced molecules, and discovered some that might also be useful against SARS-CoV-2. “To train our model we leveraged previous coronavirus datasets in which several compounds were tested against targets from coronaviruses,” explained Ali. “This approach seems to be significant as those targets share features in common with SARS-CoV-2.”

Ali emphasised the ecological nature of his approach to this work, pointing out that numerous existing antibiotics and cancer therapies are themselves compounds that bacteria use to compete with each other within the gastrointestinal tract, and that these were initially purified from microbial secretions.

“Finding microbes that secrete anti-coronavirus molecules will be a promising method to develop natural or engineered probiotics to expand our therapeutics prevention techniques, to provide a more sustainable way to combat the viral infection,” said Ali.

Source: American Society for Microbiology

High Risk for Upper GI Bleeding Developed During Hospital Stay

Photo by Anna Shvets from Pexels

Patients who developed upper gastrointestinal (GI) bleeding during a hospital stay experienced worse adverse outcomes than those admitted for upper GI bleeding alone, according to a new study from France.

Currently hospitalised patients (inpatients) with upper GI bleeding showed a significantly higher mortality rate at 6 weeks than patients hospitalised for GI bleeding alone (outpatients), at 21.7% versus 8.8%, respectively, as well as increased frequency of rebleeding .

Upper GI bleeding is a common problem that occurs in 80 to 150 out of 100 000 people annually, with mortality rates between 2 and 15%. The condition is described as blood loss from a gastrointestinal source above the ligament of Treitz. 

Though upper GI bleeding in patients has fallen over the past decades, rates of rebleeding and mortality remained stable or risen slightly. The authors said that modifiable risk factors need to be identified to help reduce this.

Researchers investigated the outcomes among inpatients and outpatients with upper GI bleeding, collecting data on 2498 patients with upper GI bleeding from 46 hospitals. Inpatients were defined as patients who developed variceal or non-variceal bleeding at least 24 hours after hospitalisation, and outpatients (75% of participants) were defined as presenting with bleeding upon admission.

Primary outcomes included mortality and rebleeding rates, assessed at 6 weeks from onset. Hospital stay duration, and the requirement for radiological or surgical intervention were secondary outcomes.

Outpatients were younger (average age 67), more likely to be smokers and consumed more alcohol than inpatients. Inpatients had a significantly higher rate of comorbidities (39% vs 27%, respectively), and more inpatients had a Charlson score above 3 than outpatients (38.9% vs 26.6%). There was no difference in sex or body weight.

Outpatients had a shorter hospital stay of 9 days compared to 16 for inpatients. The  authors noted that the groups did not differ in needing radiological or surgical intervention.

More inpatients were taking aspirin, steroids, and heparin, while more outpatients were taking oral anticoagulants and NSAIDs. At bleeding onset, more inpatients were on proton pump inhibitors (PPIs) than outpatients (41.6% vs 27.5%). However, more outpatients received intravenous PPIs than inpatients (87% vs 79%).

“Despite the more prevalent use of PPI among inpatients, their [upper gastrointestinal bleeding] was mainly related to peptic ulcer disease (PUD) and [esophagitis],” the authors explained. “This may be explained by the higher intake of aspirin and steroids, known to increase PUD-related haemorrhage risks especially in the elderly and hospitalized patients.”

For all patients, risk factors associated with 6-week mortality were rebleeding, Charlson score > 3, haemodynamic instability, pre-Rockall score > 5 and being an inpatient.

Independent  mortality risk factors for inpatients were prothrombin < 50% and rebleeding, though bleeding-related mortality was lower among inpatients compared to outpatients (10.8% vs 20.6%).

“We found that mortality in outpatients was more likely to be directly related to [upper gastrointestinal bleeding] as opposed to inpatients where death resulted more commonly from other causes,” the authors stated.

When looking at patient groups separately, cirrhosis and antiplatelets were independent outcome predictors among outpatients, in addition to rebleeding, comorbidities, haemodynamic instability and severity of bleeding.

Difficulty in comparability of results to previous studies is a limitation to this study due to the 6-week mortality timeline versus the 28-day one for previous studies. The reason for inpatient hospitalisation also was not recorded, which could impact the results.

Source: MedPage Today

Journal information: El Hajj W, et al “Prognosis of variceal and non-variceal upper gastrointestinal bleeding in already hospitalised patients: Results from a French prospective cohort” United European Gastroenterol J 2021; DOI: 10.1002/ueg2.12096.

Lenvatinib Produces Impressive Results Against Tough Tumours

Image by doodlartdotcom from Pixabay

Lenvatinib, a multitargeted tyrosine kinase inhibitor (TKI) induced a strong tumour response in patients with advanced gastrointestinal or pancreatic tumours, according to results from a phase II trial.

The study focused on previously treated advanced gastroenteropancreatic neuroendocrine tumors (GEP-NETs). An overall response rate (ORR) of 29.9% was seen in the trial, with a particularly high ORR — 44.2% — in patients with pancreatic NETs. 

“This study provides novel evidence for the efficacy of lenvatinib in patients with disease progression following treatment with other targeted agents, suggesting the potential value in the treatment of advanced GEP-NETs,” wrote Jaume Capdevila, MD, PhD, of Vall Hebron University Hospital in Barcelona, and colleagues.

TKIs are a group of pharmacologic agents that disrupt the signal transduction pathways of protein kinases by several modes of inhibition. Since sunitinib maleate (Sutent), another multitargeted TKI, was approved ten years ago, investigators have been evaluating newer-generation TKIs that target VEGF receptors (VEGFRs), among other receptors, both in pancreatic and non-pancreatic NETs.

Lenvatinib targets VEGFR 1-3, fibroblast growth factor receptors (FGFR) 1-4, and platelet-derived growth factor receptor alpha.

The researchers noted that studies have demonstrated its particular effectiveness against FGFR-1, which is a key driver of resistance to antiangiogenic drugs, “suggesting that it could potentially also reverse primary and acquired resistance to anti-VEGFR treatments or to other targeted agents.”

A total of 111 patients were enrolled in the study; 55 had histologically confirmed grade 1-2 pancreatic NETs, while 56 had gastrointestinal NETs. Patients were administered 24-mg lenvatinib once daily until disease progression or treatment intolerance. Median follow-up was 23 months.

The ORR was 16.4% for patients with gastrointestinal NETs, and median duration of response was 19.9 months for patients with pancreatic NETs and 33 months for gastrointestinal NETs. The median progression-free survival (PFS) for both groups was 15.7 months.

These results compare well with PFS outcomes reported in phase III trials, including those evaluating sunitinib and surufatinib, the authors noted.

“Interestingly, the ORR in pancreatic NETs was 44%, a rate not seen before with targeted agents,” Jonathan Strosberg, MD, head of the neuroendocrine tumor division at Moffitt Cancer Center in Tampa, told MedPage Today.

Dr Strosberg, who was not involved with this research, noted that the study group had been heavily treated beforehand, and that 29% had received prior sunitinib. “In contrast, the response rates with other TKIs have been <20% in this population, even in less heavily treated populations. The ORR for gastrointestinal NETs was more modest, but still impressive,” he added.

The most common grade 3/4 adverse events was hypertension (22.7%), while a majority of patients needed either a dose reduction or a pause.

“This suggests that lower starting doses might be considered in this population, and that particularly close monitoring of blood pressure is necessary,” said Dr Strosberg.

The study results “suggest that lenvatinib is more than just a ‘me-too’ competitor to sunitinib,” he noted. “It actually seems to have superior activity, potentially due to its ability to target both the VEGF and FGF receptors. Moreover, it appears to have activity in patients who have progressed on sunitinib. Randomized phase III studies with this drug are warranted, both for pancreatic and GI/lung NETs.”

Source: MedPage Today

Journal information: Capdevila J, et al “Lenvatinib in patients with advanced grade 1/2 pancreatic and gastrointestinal neuroendocrine tumors: results of the phase II TALENT trial (GETNE1509)” J Clin Oncol 2021; DOI: 10.1200/JCO.20.03368.

Woman Suffered ‘Excruciating’ Pain From Rare Gastrointestinal Condition

An undiagnosed, rare gastrointestinal condition left a 32-year old UK woman in “excruciating” pain for 16 months before a life-saving emergency operation.

In January 2020,  Rebecca Bostock started to experience stomach swelling and had difficult keeping her food down. After she was rushed into hospital on Good Friday this year, her mysterious illness was found to be Superior Mesenteric Artery Syndrome (SMAS).

“I don’t want anyone to go through what I went through,” she said.

Ms Bostock, 32, underwent an emergency operation at Gloucestershire Royal Hospital. Nurses there told her they had only treated three cases of SMAS in 27 years. She was also told that she likely survived because she had been rushed into hospital on that day.

“My stomach was swollen so much that I couldn’t breathe, I was being sick and couldn’t keep any medication down,” Ms Bestock said. “I was on a downward spiral. They took me into imaging and diagnosed SMAS and I was taken away for the operation. They said I needed the operation straight away or I wouldn’t survive even a couple more hours.”

Ms Bostock said she had been experiencing pain for 16 months, with stomach swelling, fever, sickness, diarrhoea and dizziness, and visited the GP and emergency departments several times. She was told there that the pain was likely to be caused by endometriosis or irritable bowel syndrome. 

“I was referred to a gynaecologist around the time of the first lockdown but everything shut down and I didn’t see one for months,” she said. “I was advised to change my diet, which seemed to help at first, but then the symptoms deteriorated again to the point where I struggled to walk and couldn’t breathe.”

SMAS is a rare disease, affecting some 0.1 to 0.3% of the population, and is defined as compression of the third portion of the duodenum between the abdominal aorta and the superior mesenteric artery. It is now mostly treated by laparoscopic duodenojejunostomy. The operation released the blockage, “re-plumbing” her stomach as the surgeon told her.

She is still unable to eat solid foods but hopes to introduce them to her diet soon and wants to raise awareness of the rare condition so that others can learn to spot the signs earlier.

“I want to tell my story to raise awareness I feel blessed and relieved,” she said. “I’m so thankful to the doctors and nurses who saved my life. I get so emotional thinking about it and I can’t thank them enough. It is so rare and even doctors don’t know about it, so helping people to spot the signs and be able to rule it out is so important.”

Source: BBC News

A Fungus in Certain Foods Slows Intestinal Healing

A study has found that a fungus found in certain foods such as cheese and processed meats can cause intestinal injuries in humans and mice with Crohn’s disease to fester and impeding healing.

These findings, from researchers at Washington University School of Medicine in St. Louis and the Cleveland Clinic, suggest that there is potentially a diet-based way to treat Crohn’s disease.

“We’re not suggesting that people stop eating cheese and processed meat; that would be going far beyond what we know right now,” said first author Umang Jain, PhD, an instructor in pathology & immunology at the School of Medicine. “What we know is that this foodborne fungus gets into inflamed, injured tissue and causes harm. We’re planning to perform a larger study in people to figure out if there’s a correlation between diet and the abundance of this fungus in the intestine. If so, it is possible dietary modulation could lower levels of the fungus and thereby reduce symptoms of Crohn’s disease.”

Crohn’s disease is driven by chronic inflammation in the gastrointestinal tract and immunosuppressive medication is the usual treatment. Crohn’s patients endure flare-ups where digestive tracts are dotted with inflamed, open sores that can persist for up to months.

To understand why intestinal ulcers heal so slowly in some people, the researchers studied mice with injured intestines. By sequencing microbial DNA at the site of injury, they discovered that the fungus Debaryomyces hansenii was abundant in wounds but not in uninjured parts of the intestine. D. hansenii can be found in all kinds of cheeses, as well as sausages, beer, wine and other fermented foods.

Introducing D. hansenii into mice with injured intestines slowed down the healing process, and eliminating the fungus with amphotericin B sped it up. In humans, the researchers discovered  D. hansenii in seven out of seven of people with Crohn’s disease, and another analysis of Crohn’s patients found D. hansenii present but only in sites of injury and inflammation. 

“If you look at stool samples from healthy people, this fungus is highly abundant,” Jain said. “It goes into your body and comes out again. But people with Crohn’s disease have a defect in the intestinal barrier that enables the fungus to get into the tissue and survive there. And then it makes itself at home in ulcers and sites of inflammation and prevents those areas from healing.”

Their results suggest that elimination of the fungus could allow wounds to heal normally again, and minimise flare-ups. In mouse studies, amphotericin B eliminated the fungus but it is of limited use in people since it can only be administered intravenously, therefore an oral antifungal is being researched.

“Crohn’s disease is fundamentally an inflammatory disease, so even if we figured out how to improve wound healing, we wouldn’t be curing the disease,” Jain said. “But in people with Crohn’s, impaired wound healing causes a lot of suffering. If we can show that depleting this fungus in people’s bodies—either by dietary changes or with antifungal medications—could improve wound healing, then it may affect the quality of life in ways that we’ve not been able to do with more traditional approaches.”

Source: Medical Xpress

Journal information: U. Jain et al., “Debaryomyces is enriched in Crohn’s disease intestinal tissue and impairs healing in mice,” Science (2021). science.sciencemag.org/cgi/doi … 1126/science.abd0919

Eating Saturated Fats can Cut Symptoms of Pancreatitis


A study has found that symptoms of pancreatitis are less severe when foods with saturated fats are eaten.

The study, by researchers from Mayo Clinic, the Saint Louis University School of Medicine and the Washington University School of Medicine, examines the obesity paradox in which obese patients had better results when being treated for certain conditions, compared to non-obese patients.

Pancreatitis is the leading cause of hospitalisation from gastrointestinal disorders in the United States. It can have a variety of causes, such as gallstones, having abdominal surgery or overconsumption of alcohol.
Saturated fats are found in meat and dairy, while unsaturated fats are found in plants and fish, and in general consumption of unsaturated fats over saturated fats is encouraged as it is associated with reduced risk of heart disease and other conditions. However, exceptions such as the obesity paradox exist.

To delve into this question, the researchers examined 20 clinical reports from 11 countries, where fat intake in obese patients was monitored. They found that among obese patients who developed pancreatitis, those who ate a diet heavy in saturated fats had less severe symptoms than those who did not. 

To determine the cause of this protective effect, the researchers fed mice a diet rich in either saturated or unsaturated fats, and then induced pancreatitis in them. Those fed saturated fats developed less severe symptoms. On closer examination, they found that saturated fat did not interact well with pancreatic triglyceride lipase, reducing production of long-chain non-esterified fatty acids, which reduced the symptoms of pancreatitis.  

Source: Medical Xpress

Journal information: Biswajit Khatua et al. Adipose saturation reduces lipotoxic systemic inflammation and explains the obesity paradox, Science Advances (2021). DOI: 10.1126/sciadv.abd6449