Fatty liver breakthrough: A common vitamin shows promise in the study

Metabolic-associated fatty liver disease (MASLD( impacts roughly 30 % of people globally and has long lacked effective, targeted therapies. Now, researchers have uncovered a key genetic factor that worsens the condition. Even more surprising, the most effective way to target this factor may be an already and widely available treatment: Vitamin B 3.

An international research team has identified micro RNA-93 (miR-93) as a central regulator in MASLD. This marks the first time this molecule has been early linked to how the disease develops and progresses.

How miR-93 Disrupts Liver Function

MiR-93 is a small RNA molecule found in liver cells that controls the activity of certain genes. The researchers discovered that levels of miR-93 are unusually high in both people with fatty liver disease and in animal models. Their analysis showed that miR-93 drives fat buildup, inflammation, and scarring in the liver by suppressing SIRT1m a gene that plays a key role in managing fat metabolism inside liver cells.

To better understand its role, the team used gene editing to stop the production of miR-93 in mice. These animals showed significantly less fat accumulation in the liver, along with improved insulin sensitivity and better overall liver function. In contrast, mice engineered to produce excess miR-93 experiences more severe metabolic problems in the liver.

Vitamin B3 Emerges as a Potential Treatment

The researchers then screened 150 FDA-approved drugs to see if any could reduce miR-93 levels. Niacin ( Vitamin B3) stood out as the most effective option. In mice treated with niacin, miR-93 levels dropped sharply, while SIRT1 activity increased. This helped restore normal fat-processing pathways I the liver and improved overall lipid balance.

The research team explained, “ This study precisely elucidates the molecular origin on MASLD and demonstrates the potential for repurposing an already approved vitamin compound to modulate this pathway, which has high translational clinical relevance”.

They added, “ Given that niacin is a well-established and safe medication used to treat hyperlipidemia, it holds promise as a candidate for combination therapies targeting miRNA pathway in MASLD.”

 

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Some COVID-19 patients experience persistent chronic fatigue six months after infection, finds study

A team of scientists from Germany has recently revealed that almost 50% of patients present with moderate to severe chronic fatigue syndrome six months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. 

Background

Infection with SARS-CoV-2 is associated with a wide variety of symptoms, ranging from mild fever and cough to severe pulmonary and cardiovascular complications. Although almost 80% of coronavirus disease 2019 (COVID-19) patients remain asymptomatic or mildly symptomatic, a growing pool of evidence indicates that a significant fraction of COVID-19 patients present with persistent symptoms referred to as ‘long COVID’. Most commonly reported symptoms of long COVID are fatigue, cognitive impairment, and post-exertional malaise (worsening of symptoms after minor physical or mental exertion).

In the current study, the scientists have investigated mild to moderate COVID-19 patients who present with persistent fatigue and other related symptoms. They have also investigated whether these patients meet the diagnostic criteria for chronic fatigue syndrome/myalgic encephalomyelitis (ME/CFS), which is a neurological disease characterized by severe mental and physical fatigue, chronic pain, and sleep disorder.

Study design

A total of 42 COVID-19 patients presented with moderate to severe intensity chronic fatigue, exertion intolerance, cognitive dysfunction, and pain six months after SARS-CoV-2 infection were investigated in the study. All participants were diagnosed with mild to moderate COVID-19. A team of experienced clinical immunologists, rheumatologists, neurologists, and cardiologists was involved for an accurate diagnosis of ME/CFS in these patients based on the Canadian Consensus Criteria. The intensity and duration of post-exertional malaise (symptoms lasting for more than 14 hours) was considered to be the main diagnostic criterion for ME/CCFS.

Important observations

Of all enrolled patients, 32 had mild COVID-19 and 10 had moderate COVID-19 because of pneumonia. The numbers of male and female patients were 29 and 13, respectively, and the average age of the patients was 36 years (age range: 22 – 62 years).

Of 42 enrolled patients, 19 met the diagnostic criteria for ME/CFS and were found to have severe fatigue and functional impairment, severe stress intolerance, and hypersensitivity to noise, light, and temperature. The scientists categorized these patients as Chronic COVID-19 Syndrome/Chronic Fatigue Syndrome (CCS/CFS). The rest of the patients who were not diagnosed with ME/CFS mainly because of the relatively shorter duration of post-exertional malaise (2 – 10 hours) were referred to as CCS. The patients with ME/CFS showed significantly reduced hand grip strength than those without ME/CFS.

After 6 months of SARS-CoV-2 infection, all participants were found to have fatigue with different intensities. The most commonly observed symptoms were post-exertional malaise, cognitive impairment, and muscle pain. Although patients without ME/CFS exhibited less severe symptoms, most of them had severely impaired daily life activities. The majority of enrolled patients (n=28) were either unable to work or required a reduced work schedule because of post- Covid-19 symptoms.

In the study cohort, autonomic dysfunction was observed in most of the patients, with no significant difference in symptom intensity between patients with and without ME/CFS. The increase in systolic and diastolic blood pressure at standing position was significantly lower in patients with ME/CFS than those without it. Among patients with ME/CFS, four were diagnosed with postural tachycardia syndrome.         

Regarding biochemical parameters, only two patients in the entire study cohort showed mildly elevated C-reactive protein levels, indicating the absence of robust inflammatory response. Almost 50% of patients showed increased levels of interleukin 8 (IL-8), which is a clinical feature of severe COVID-19 patients. Moreover, a low level of mannose-binding lectin was observed in 22% of patients, indicating impaired immune functioning. An indication of autoimmune disorder was noticed in the study cohort as elevated levels of antinuclear antibody were found in 3 ME/CFS patients and 6 non-ME/CFS patients.

Study significance

The study reveals that even mildly affected COVID-19 patients can develop a severe chronic syndrome characterized by moderate to severe fatigue and exertion intolerance. Because most of the post-COVID symptoms considered in this study did not differ significantly between patients with and without ME/CFS, the scientists suggest that chronic COVID-19 syndrome is a more appropriate terminology than ME/CFS in defining long-term symptoms related to SARS-CoV-2 infection.

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