Latest news with #MASLD
Medscape
2 days ago
- Health
- Medscape
ADA Issues New MASLD Guidelines
A new consensus report from the American Diabetes Association (ADA) provides a practice-oriented framework for screening and managing metabolic dysfunction–associated steatotic liver disease (MASLD) in people with diabetes and prediabetes. Published online on May 28, 2025, in Diabetes Care, the report is a comprehensive update to the recommendations the ADA released in 2023. It is intended for clinicians treating patients with diabetes — primarily type 2 diabetes (T2D) — but also type 1 diabetes with obesity and prediabetes. Topics covered include the rationale for the recent change in terminology, epidemiology, fibrosis risk stratification, monitoring, treatment, and referral guidance, with interprofessional team management emphasized throughout. 'This will provide primary care doctors and anyone taking care of people with diabetes the tools to diagnose [MASLD] early and guide therapy…to prevent cirrhosis, and refer to the hepatologist as needed for additional therapy and monitoring,' lead author Kenneth Cusi, MD, professor of medicine at the Division of Endocrinology, Diabetes & Metabolism in the Department of Medicine at the University of Florida, Gainesville, Florida, told Medscape Medical News . The guidelines recommend that clinicians routinely screen people with T2D or prediabetes for MASLD. 'We explain that the liver should be incorporated into our management in the same way we do for chronic kidney disease, eye disease, and nerve disease as an end-organ damage that is particularly affected by diabetes,' Cusi said. In the United States, at least 70% of people with T2D have MASLD, about half of whom have the more progressive form termed metabolic dysfunction–associated steatohepatitis (MASH). About 1 in 5 with T2D have advanced liver fibrosis. The presence of MASH increases the risks for complications including cirrhosis, hepatocellular carcinoma, and overall mortality, according to the new consensus report. Liver disease has not been a focus of diabetes management until recently, Cusi noted. 'We didn't think about it. The epidemic of obesity, and with that, of diabetes, is driving this liver disease. The obesity epidemic has had a big worsening since the 1990s, so this damage in the past 20 or 30 years is just now becoming evident in the liver.' Terminology Change: Highlighting Insulin Resistance, Reducing Stigma The document reviews the current nomenclature for SLD, which was officially changed in 2023 to remove the words 'fatty' and 'alcoholic.' Now, MASLD is defined as the presence of SLD with at least one metabolic risk factor such as obesity, hypertension, prediabetes, high triglycerides, low high-density lipoprotein cholesterol, or T2D, with minimal or no alcohol consumption (< 20 g/d for women; < 30 g/d for men). The term 'MetALD' is used for those with MASLD who also have increased alcohol consumption (20-50 g/d for women; 30-60 g/day for men). Steatosis in the setting of alcohol consumption above those levels is termed 'alcohol-associated liver disease (ALD).' The term MASH is defined as steatohepatitis with at least one metabolic risk factor and minimal alcohol consumption. 'At-risk MASH' refers to steatohepatitis with clinically significant fibrosis (stage F2 or higher). Diagnosis: Staged Screening for Fibrosis The document recommends routine screening of people with T2D, prediabetes, and/or obesity with cardiovascular risk factors, with the goal of identifying those with high-risk MASH. Intervention is then aimed at preventing fibrosis progression and cirrhosis. A graphic diagnostic algorithm advises initial use of the noninvasive Fibrosis-4 (FIB-4) tool, which risk stratifies based on age, liver enzymes, and platelet count. 'The FIB-4 is composed of very simple things that are already in the electronic medical record of all patients. We also discuss the role of electronic medical records to improve implementation,' Cusi said. Those with a FIB-4 < 1.3 have a low risk for future cirrhosis and can be managed in primary or team care with optimized lifestyle and repeated FIB-4 every 1-2 years. If the FIB-4 is > 2.67, direct referral to a liver specialist is advised. If FIB-4 is between 1.3 and 2.67, a second risk-stratification test is recommended. Ideally, this would be a liver stiffness measurement (LSM), most commonly with transient elastography. If that is unavailable, an alternative is the noninvasive enhanced liver fibrosis (ELF) test. If the LSM is < 8.0 kPa or ELF is < 7.7, the fibrosis risk is low and routine management can continue with repeat testing in 1-2 years. But if higher, hepatology referral is recommended. Treatment: Lifestyle, Plus Old and New Drugs The report details lifestyle modification for MASLD, including nutrition plans; physical activity; behavioral health; and the role of diabetes self-management, education and support. The role of obesity treatment in people with MASLD, both metabolic surgery and pharmacotherapy, is also discussed at length. No current pharmacologic treatments have been approved for MASLD, but both semaglutide and tirzepatide have demonstrated benefit in treating MASH and are approved for treating T2D, obesity, and other related comorbidities. A thyroid hormone receptor beta agonist, resmetirom, was approved in early 2024 for the treatment of MASH with fibrosis stages F2 and F3, but is extremely expensive at about $50,000 a year, Cusi noted. An older, generic glucose-lowering drug, pioglitazone, has also shown benefit in reducing fibrosis and may be a lower-cost alternative. The document also includes a section on alcohol intake, which complicates the MASLD picture, Cusi noted. 'We think that this is going to help doctors to consider alcohol, which is often overlooked and under-reported. If patients have moderate fibrosis, they should completely quit alcohol.' Cusi has received research support (to his institution) from Boehringer Ingelheim, Echosens, Inventiva, Labcorp, and Perspectum, and has served as a consultant for Aligos Therapeutics, Arrowhead, AstraZeneca, 89bio, Bristol-Myers Squibb, Boehringer Ingelheim, Eli Lilly, GlaxoSmithKline, Novo Nordisk, ProSciento, Sagimet Biosciences, Siemens USA, Zealand Pharma, and Terns Pharmaceuticals.
Health Line
6 days ago
- Health
- Health Line
Can Statins Reverse Fatty Liver Disease?
There is no evidence to show that statins can reverse fatty liver disease, also known as metabolic dysfunction-associated steatotic liver disease (MASLD). However, they may be able to help prevent the progression of the condition. Statins are medications typically used to lower cholesterol and reduce the risk of heart disease. A 2025 review found that, as statins have anti-inflammatory properties, they may be able to prevent the progression of MASLD by: reducing fat around the liver decreasing inflammation improving scarring and damage of the liver improving liver function It's important to remember that statins are not the standard treatment option for MASLD and should not be used in place of a prescribed treatment. How can fatty liver be reversed? Fatty liver can be reversed if it is in its early stages before any liver damage has occurred. There are several ways to reduce fatty liver during this period, such as: Lifestyle measures. Making lifestyle adjustments during the initial stages of MASLD is vital to slowing down the progression of the condition and potentially reversing the condition. This includes: following a healthy diet getting regular exercise avoiding or limiting alcohol consumption losing weight if you have overweight or obesity Treating underlying conditions. Several conditions, such as diabetes and high cholesterol, can lead to fat accumulating around the liver. Addressing these underlying conditions may help to manage symptoms and potentially reverse MASLD. Early diagnosis.
Time of India
21-05-2025
- Health
- Time of India
Why liver function tests are key for people with diabetes and obesity
Conceived as a princely minister of warmth and life, the liver is often overlooked in diabetes and obesity , whereas the organ is a prime regulator in metabolism. In recent times, a plethora of evidence has begun linking decreased liver performance with metabolic disorders. Thus stands the Liver Function Test ( LFT ) as an important investigative tool for all, ranging from diabetes to obesity or a combination of the two. The Link Between Liver, Diabetes, and Obesity The liver controls lipid metabolism and glucose metabolism. In type 2 diabetes patients, this equilibrium is lost because of insulin resistance, which generally leads to fat accumulation in the liver by a mechanism independent of alcohol, i.e., Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). Likewise, obesity leads to excess fat deposition around organs, such as the liver, and sets them up for inflammation and fibrosis. Without treatment, these disorders progress to cirrhosis and ultimately, even liver cancer in certain situations. What Liver Function Tests Tell Us Proceeding with LFTs, the following enzymes and proteins are measured: ALT (SGPT)- a liver enzyme that helps detect liver damage or inflammation, especially in conditions like fatty liver , diabetes, and obesity. ALP (Alkaline Phosphatase) - reports bile duct function Bilirubin - the liver's power to clear waste Albumin and Total Protein - the capacity of the liver to synthesise proteins Elevated liver enzymes in patients with diabetes or obese individuals often indicate silent liver damage before the appearance of signs and symptoms. by Taboola by Taboola Sponsored Links Sponsored Links Promoted Links Promoted Links You May Like Sente dores nas articulações? Este simples hábito pode mudar sua vida! AlwaysFit Saiba Mais Undo Why Routine Monitoring Is Important Diabetes and obesity are chronic conditions . As a rule, and when patients with diabetes have a higher than normal BMI or altered lipid profile, LFTs must be checked, Black Book Reference American Diabetes Association. Similar recommendation in Indian guidelines. With obesity rates running at 12% in India and more than 100 million cases of diabetes recorded as per the ICMR-INDIAB study 2023, the burden of liver-related comorbidities is something one can only imagine. Liver abnormalities alter drug metabolism, thereby possibly affecting diabetic treatment. In a diseased liver, drugs like metformin or statins undergo altered metabolism, which predisposes one to side effects. Fibroscan and Ultrasound Liver Advanced liver fibrosis occurs more frequently in people with type 2 diabetes, often being caught late or never at all. FibroScan and ultrasound liver imaging are two such non-invasive methods for assessing liver stiffness with high accuracy, thus providing an early diagnosis. On the Defensive Good news is that the liver is mostly reversible in early stages. When combined with lifestyle changes (weight loss, low-carb diet, physical activity, and diabetes management), LFTs may be reversible in fatty liver conditions. Also, avoiding alcohol, good hydration, and paying attention to liver health every 6–12 months, provide good points of prevention against the long-term establishment of the disease. Liver health is closely linked with diabetes and obesity, and often acts as a silent alarm system. Hence, regular liver function tests should be considered more of a preventive than just a diagnostic tool. For anyone struggling with blood sugar and weight issues, keeping an eye on their liver will be the key to keeping the metabolic system healthy throughout a long life. Authored by: Dr. Sameer Bhati, Public health expert Study shows why obese people shouldn't consume too much alcohol One step to a healthier you—join Times Health+ Yoga and feel the change
Medscape
19-05-2025
- Health
- Medscape
Novel Genetic Variant May Drive MASLD
A novel genetic variant may be a driving force behind the development of metabolic dysfunction–associated steatotic liver disease (MASLD) in some cases, according to researchers at the Mayo Clinic in Rochester, Minnesota. In an article published in Hepatology , Filippo Pinto e Vairo, MD, PhD, and colleagues described their discovery of a single inherited variant of the mesenchymal-epithelial transition ( MET ) gene in a familial case of MASLD involving a father and daughter with no apparent additional risk factors. MASLD remains one of the world's most common diseases and will likely become the leading cause of liver cirrhosis worldwide, the researchers wrote. MASLD, formerly known as nonalcoholic fatty liver disease (NAFLD), likely stems from a combination of genetic and environmental factors, they said. Their discovery of the gene variation prompted the researchers to investigate whether that variation and others on the MET gene were linked to steatotic liver disease. They used Mayo Clinic's Tapestry study, a large-scale genetic sequencing project, to analyze the exome sequencing data of 3904 adults with MASLD to identify other cases and analyze them. About 1% (45 individuals) had rare variants of the MET gene potentially associated with MASLD, and 8 of the 45 (18%) had genetic variants in the same area as the index patient and her father. Pinto e Vairo, medical director of the Program for Rare and Undiagnosed Diseases in the Mayo Clinic's Center for Individualized Medicine, explained the potential implications of the findings in a Q&A with Medscape Medical News . What prompted you to conduct this research? How did you identify the original patient? Pinto e Vairo: The original patient was identified through clinical care and underwent liver biopsy due to elevated liver enzymes. Her histology confirmed MASH [metabolic dysfunction–associated steatohepatitis], and subsequent exome sequencing revealed a novel heterozygous MET variant, inherited from her affected father, which led to a deeper investigation into the genetic basis of her condition. Were you surprised by any of the findings? Why or why not? Pinto e Vairo: The findings were surprising in several ways. First, variants in MET had not previously been implicated as a germline monogenic cause of MASLD or MASH in humans. Its known roles had largely been confined to cancer. Second, the discovery that rare, loss-of-function variants in the MET kinase domain could underlie liver steatosis and inflammation ran counter to the usual oncogenic MET variants, which are typically gain-of-function. The confirmation that the MET variants impaired downstream signaling further reinforced a novel mechanism. The lack of high polygenic risk scores in patients with these MET variants also highlighted that monogenic drivers might be underrecognized contributors to MASLD/MASH. Based on your research and other research, how might genetics play into MASLD? Pinto e Vairo: Genetics play a significant role in MASLD by modulating both susceptibility and disease progression. While large-scale genome-wide association studies have identified common variants — such as those in PNPLA3 , TM6SF2 , GCKR , MBOAT7 , and HSD17B13 — that confer risk or protection, this study adds evidence that rare monogenic variants can also independently drive the disease. This suggests a genetic spectrum in MASLD, ranging from polygenic, environmentally modulated forms to monogenic cases with high penetrance. The interplay between these rare variants and broader metabolic context will be crucial to understand personalized risk. Is there a practical application for this research now? What might the future clinical applications be? Pinto e Vairo: The immediate practical application lies in the potential for early identification of individuals at high risk for MASLD/MASH through exome or genome sequencing, particularly in families with a strong history of liver disease. Clinically, this could justify enhanced surveillance or earlier lifestyle and therapeutic interventions in at-risk individuals. In the future, this research may support the development of targeted therapies that can restore or bypass defective MET signaling. Moreover, it opens the door to personalized medicine strategies that consider a patient's unique genetic profile when choosing interventions or preventive strategies. What are the next steps? Pinto e Vairo: The next steps include functional validation of other rare MET variants to better understand their pathogenic potential and variability in phenotypic expression; longitudinal cohort studies to monitor disease progression in individuals with MET variants and to define genotype-phenotype correlations more precisely; and ultimately therapeutic exploration, including in vitro and in vivo modeling, to determine whether restoring MET signaling could reverse or mitigate disease.
Time of India
15-05-2025
- Health
- Time of India
Can a hormone reverse fatty liver disease? Here's what experts think
Researchers at Oklahoma University found that the hormone FGF21 can reverse fatty liver disease. The hormone signals the brain to improve liver function. It lowers liver fat and reverses fibrosis. The hormone also lowers cholesterol. This discovery could lead to new drugs for treating fatty liver disease. Clinical trials are showing good therapeutic benefits. Fatty liver disease is rising as a global health concern. Often considered a 'silent' disease as it shows few or no symptoms, fatty liver disease, however, can get serious, depending on its cause and progression. A new study has found that a certain hormone can reverse fatty liver disease . A groundbreaking study by the researchers at the University of Oklahoma found that a hormone can reverse the effects of fatty liver disease in mice. The study is published in Cell Metabolism . What is fatty liver disease? Fatty liver, medically known as hepatic steatosis, is a condition in which fat builds up in the liver. There are two major types of fatty liver disease: alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD). AFLD, as the name suggests, occurs in people who drink large amounts of alcohol. NAFLD, on the other hand, affects people who drink little or no alcohol. Though the cause of nonalcoholic fatty liver disease (NAFLD) is unknown, people who have type 2 diabetes, or prediabetes, obesity, are middle-aged or older, have high blood pressure, are prone to the disease. How does the hormone control fatty liver disease? The researchers found that the hormone FGF21 (fibroblast growth factor 21) can reverse fatty liver disease . The hormone works primarily by signaling the brain to improve liver function . Sponsored Links Sponsored Links Promoted Links Promoted Links You May Like Google Brain Co-Founder Andrew Ng, Recommends: Read These 5 Books And Turn Your Life Around Blinkist: Andrew Ng's Reading List Undo They delved into how FGF21 acts on the brain to influence liver metabolism. Understanding the mechanism of action of the hormone could become instrumental as a target for a new class of highly anticipated drugs that are in Phase 3 clinical trials. 'Fatty liver disease, or MASLD (metabolic dysfunction-associated steatotic liver disease), is a buildup of fat in the liver. It can progress to MASH (metabolic dysfunction-associated steatohepatitis) during which fibrosis and, ultimately, cirrhosis can occur. MASLD is becoming a very big problem in the United States, affecting 40% of people worldwide, and there is currently only one treatment approved by the Food and Drug Administration to treat MASH. A new class of drugs, based on FGF21 signaling, is showing good therapeutic benefits in clinical trials, but until now, the mechanism for how they work has been unclear,' Matthew Potthoff, Ph.D., the lead author and a professor of biochemistry and physiology at the University of Oklahoma College of Medicine and deputy director of OU Health Harold Hamm Diabetes Center said in a statement. Fatty liver diet: Best and worst foods for your liver The findings showed that FGF21 was effective at causing signaling in the model species that changed the liver's metabolism. The researchers found that this process lowered the liver's fat, and the fibrosis too was reversed. The hormone also sent a separate signal directly to the liver, specifically to lower cholesterol. 'It's a feedback loop where the hormone sends a signal to the brain, and the brain changes nerve activity to the liver to protect it. The majority of the effect comes from the signal to the brain as opposed to signaling the liver directly, but together, the two signals are powerful in their ability to regulate the different types of lipids in the liver,' Potthoff added. Similar to the GLP-1s (glucagon-like peptide 1) weightloss drugs that regulate blood sugar levels and appetite, FGF21 acts on the brain to regulate metabolism. Interestingly, both are hormones produced from peripheral tissues: GLP-1 from the intestine and FGF21 from the liver, and both work by sending a signal to the brain. 'It is interesting that this metabolic hormone/drug works primarily by signaling to the brain instead of to the liver directly, in this case. FGF21 is quite powerful because it not only led to a reduction of fat, but it also mediated the reversal of fibrosis, which is the pathological part of the disease, and it did so while the mice were still eating a diet that would cause the disease. Now, we not only understand how the hormone works, but it may guide us in creating even more targeted therapies in the future,' the lead author added. Future-Proof Your Child with AI Skills | Limited Early Bird Seats – 33% OFF! | WhatsApp: 9560500838
