# Understanding How Mitochondrial Damage Drives Fatty Liver Disease: A Patient's Guide to the Science

Fatty liver diseases, which now affect millions of people worldwide due to rising obesity and type 2 diabetes, are closely linked to the function of mitochondria — the tiny energy-producing power plants inside our liver cells. This review article explains how these cellular structures become damaged as fatty liver progresses, how certain medications and alcohol can harm them, and why new treatments targeting mitochondria offer hope for patients. The authors examine research showing that mitochondria can initially adapt to protect the liver, but eventually fail under sustained metabolic stress, driving inflammation, scarring, and disease progression.

# Understanding How Mitochondrial Damage Drives Fatty Liver Disease: A Patient's Guide to the Science

## Table of Contents

- Key Points
- Why This Research Matters: The Growing Problem of Fatty Liver Disease
- What Are Mitochondria and Why Do They Matter for Your Liver?
- How Do Researchers Study Liver Mitochondria?
- Key Finding #1: The Liver's Mitochondria Adapt in Early Obesity
- Key Finding #2: What Happens When Fat Accumulates (Steatosis)
- Key Finding #3: The Dangerous Transition to NASH
- How Medications and Toxins Damage Liver Mitochondria
- The Dangerous Combination: Metabolic Disease Plus Alcohol
- Emerging Treatments That Target Mitochondria
- What This Means for Patients
- What This Review Could Not Prove
- Practical Recommendations for Patients
- Frequently Asked Questions
- Source Information

## Key Points

- Mitochondria adapt in early obesity, increasing fat-burning capacity by about 85%, but this protection fails as fatty liver progresses.
- Transition to NASH involves impaired mitochondrial efficiency, oxidative stress, inflammation, and activation of liver scarring cells.
- Drugs like amiodarone and valproic acid can severely inhibit mitochondrial fat oxidation, increasing the risk of liver failure.
- Alcohol plus metabolic disease creates a 'double hit' on mitochondria, accelerating progression from steatosis to fibrosis.
- Weight loss, bariatric surgery, and emerging drugs like THRβ agonists improve fatty liver by restoring mitochondrial function.

## Why This Research Matters: The Growing Problem of Fatty Liver Disease

Fatty liver diseases have become a major health crisis worldwide. With vaccines and treatments now controlling viral hepatitis, the main causes of liver disease have shifted dramatically toward non-communicable factors — excessive alcohol consumption, common metabolic diseases, exposure to environmental toxins (called xenobiotics), and drug-induced liver injury.

The worldwide rise in obesity and type 2 diabetes mellitus (T2DM) has created what researchers call a **"syndemic"** — a synergy of epidemics that may drive worse liver disease outcomes across Europe and beyond. These metabolic conditions share key features: abnormal fat deposition in organs where fat doesn't belong (ectopic fat), altered metabolic fluxes, and insulin resistance.

In adipose tissue (body fat), altered mitochondrial function contributes to tissue dysfunction, with impaired insulin-mediated triglyceride storage leading to a "spillover" of fat into other organs, including the liver. This explains how hepatic (liver) lipid accumulation initiates dynamic changes in mitochondrial function and promotes the progression from simple fatty liver (steatosis, or NAFL) to the more dangerous non-alcoholic steatohepatitis (NASH) and ultimately to hepatic fibrosis and cirrhosis.

Importantly, decades of research on how medications and environmental chemicals affect liver mitochondria have dramatically improved our understanding of the role these organelles play in metabolic disease. This growing insight has sparked intense interest in **targeting mitochondria as a therapeutic strategy** for fatty liver diseases.

## What Are Mitochondria and Why Do They Matter for Your Liver?

Mitochondria are often called the power plants of the cell — and for good reason. Their major role in the liver is energy production, through the oxidation of fuels including amino acids, pyruvate, and fatty acids. The tight coupling between fuel oxidation and ATP (adenosine triphosphate, the body's energy currency) synthesis is called **oxidative phosphorylation (OXPHOS)**.

This process is finely regulated by many circulating and intrahepatic factors. Researchers measure how efficiently this works using something called the **respiratory control ratio (RCR)** — the ratio of ADP-stimulated respiration (when energy is being made) to resting respiration. A high RCR means the mitochondria are working properly.

Here's a simplified overview of how liver mitochondria process fuel:

-
**Pyruvate** (from carbohydrate breakdown) enters the tricarboxylic acid (TCA) cycle after being converted to acetyl-coenzyme A
-
**Fatty acids** are broken down through a process called **β-oxidation**, which requires coenzyme A and L-carnitine and involves several enzymes with specific activities depending on the fatty acid's chain length
- During **fasting**, fatty acid oxidation generates **ketone bodies**, which are released into the bloodstream and used by other tissues for energy
- The process produces NADH and FADH₂, which feed electrons into the **electron transport chain (ETC)** to create the electrochemical potential needed for ATP production

Notably, 13 polypeptides of the ETC are encoded by **mitochondrial DNA (mtDNA)**, while the rest are encoded by nuclear DNA. Liver mitochondria contain all the components needed for mtDNA replication, transcription, and translation, as well as enzymes involved in DNA repair.

Mitochondria are not static structures. They constantly undergo **mitochondrial biogenesis** (creation of new mitochondria), a complex program orchestrated by key transcription factors including NRF1, NRF2, and PGC1α/β. Another important regulator is **AMPK**, which activates PGC1α. Mitochondria also undergo **fusion and fission** (dynamics) and **mitophagy** — a selective recycling process that specifically eliminates damaged mitochondria.

Beyond energy production, liver mitochondria play several other critical roles:

-
**Gluconeogenesis**: During fasting, they help produce glucose from precursors like alanine, pyruvate, and lactate, using mitochondrial enzymes pyruvate carboxylase and malate dehydrogenase
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**Fatty acid synthesis**: After feeding, the TCA cycle metabolite citrate leaves the mitochondria to serve as a carbon source for new fat production
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**Bile acid synthesis**: From cholesterol, via the enzyme CYP27A1
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**Cell signaling**: They generate **reactive oxygen species (ROS)** via ETC complexes I and III and some enzymes of the fatty acid oxidation pathway. ROS activate protective transcription factors like Nrf2, which boost antioxidant responses and mitochondrial biogenesis
-
**Toxin metabolism**: They contain CYP1A2 and CYP2E1, enzymes that metabolize acetaminophen (paracetamol), ethanol, fatty acids, and ketone bodies

## How Do Researchers Study Liver Mitochondria?

Studying mitochondria in the human liver is challenging. Many methods are invasive or technically complex, which limits large-scale investigations. However, recent advances have enabled researchers to gain meaningful insight into mitochondrial function in human livers. The authors summarize a range of methods used in human studies:

-
**Transmission electron microscopy**: The gold standard for assessing mitochondrial content, area, and number — but invasive and time-consuming
-
**Protein expression and proteomics**: Measures ETC complexes I–IV, cardiolipin, and mtDNA content — but no single accepted marker exists for liver
-
**High-resolution respirometry (HRR)**: A quasi-gold standard that measures oxygen flux in liver tissue or isolated mitochondria — but requires invasive biopsy samples
-
**Liver ³¹P magnetic resonance spectroscopy (MRS)**: Measures ATP and phosphate levels in vivo, in intact tissue — ideal for repeated clinical studies but requires specialized expertise
-
**Liver ¹³C MRS**: Tracks mitochondrial oxidation by measuring how labeled acetate or lactate is incorporated into hepatic glutamate and alanine
-
**PET imaging**: Uses radiolabeled fatty acids to measure fatty acid oxidation — but involves radiation exposure
-
**Breath tests**: Using ¹³C-labeled metabolites — indirect and not yet validated

## Key Finding #1: The Liver's Mitochondria Adapt in Early Obesity

A landmark study by Koliaki and colleagues used ex vivo high-resolution respirometry to measure oxygen fluxes in whole-liver tissue and isolated liver mitochondria from lean and obese individuals with different stages of biopsy-proven NAFLD. The results were striking: contrary to what happens in skeletal muscle, **maximal uncoupled respiration related to β-oxidation and TCA cycle activity was approximately 85% higher in livers from obese individuals without steatosis compared to lean controls**.

This elevated oxidative capacity — occurring even when intrahepatic triglyceride levels are still low — strongly supports the concept of **mitochondrial adaptation**. In other words, the mitochondria are working overtime to burn off excess fat and protect the liver. This protective response has been confirmed in animal studies: high-fat intake induced transient upregulation of 13 OXPHOS genes and mitochondrial respiration in steatosis-resistant A/J mice.

Similarly, lean humans without steatosis who were given a high-fat diet showed **16% increased hepatic ATP content**, measured in vivo by ³¹P MRS. These findings suggest that the absence of liver fat accumulation results from **mitochondrial adaptation or plasticity** — a state that may characterize a moderately insulin-resistant obese phenotype, or an early stage of obesity that could eventually lead to NAFLD.

## Key Finding #2: What Happens When Fat Accumulates (Steatosis)

Despite the upregulated oxidative capacity seen in non-steatotic obesity, studies in obese people who already have fatty liver (NAFL) show **heterogeneous results** — likely due to differences in obesity grade and duration, age, liver fat content, and whether liver histology was available.

Here's what the studies found:

-
**No change in ATP content or production**: Non-invasive ³¹P MRS detected no difference in hepatic ATP content or ATP synthase flux rates (V_ATP) between elderly obese people with NAFL and young lean volunteers
-
**No change in citrate synthase flux**: Using [1-¹³C]acetate infusion, researchers found no difference in hepatic citrate synthase flux (V_CS) between young lean or overweight individuals with or without NAFL
-
**Increased TCA cycle flux**: In contrast, [U-¹³C]propionate administration revealed increased hepatic TCA cycle flux rates (V_TCA) and anaplerotic flux in middle-aged obese people with steatosis. Greater V_TCA has been repeatedly found in other cohorts and is associated with a switch from lactate to glycerol as the substrate for gluconeogenesis
-
**Increased respiration in isolated mitochondria**: High-resolution respirometry showed a comparable **4–5-fold increase** in malate-, glutamate-, and malate-octanoylcarnitine-stimulated respiration, as well as maximal uncoupled respiration, in hepatic mitochondria from both steatotic and non-steatotic livers of obese individuals compared to non-steatotic livers of lean individuals
-
**Recent confirmation**: Newer high-resolution respirometry studies reported increased maximal coupled respiration (statistically significant) and uncoupled respiration (p = 0.054, a statistical trend) from malate-glutamate-octanoylcarnitine in livers of obese individuals with NAFL vs. lean individuals without steatosis

Interestingly, hepatic oxidative capacity correlated with **hepatic triglycerides, plasma free fatty acids, and insulin resistance** in isolated mitochondria — but only with **body mass index** when measured in liver tissue. This suggests that the upregulation of oxidative capacity in obesity is independent of steatosis.

However, the authors note that some mitochondrial abnormalities may occur early in NAFL, including **lower hepatic respiratory control ratio (RCR)** and reduced expression of genes involved in mitochondrial quality control — early warning signs that the adaptive phase is beginning to fail.

## Key Finding #3: The Dangerous Transition to NASH

The transition from simple fatty liver (NAFL) to the inflammatory condition NASH marks a critical turning point. Here's what happens at the cellular level:

**In the adaptive phase (obesity without or with NAFL):** Greater availability of free fatty acids (FFAs) increases the intracellular pool of fatty acyl-CoA, which stimulates mitochondrial fatty acid oxidation and may increase TCA cycle and ETC activity. This upregulated oxidative capacity temporarily protects against lipotoxic insulin resistance and triglyceride accumulation. Meanwhile, any excess reactive oxygen species produced are scavenged by increased catalase and GPX1 (glutathione peroxidase 1) activity.

**But with the onset of steatosis**, mitochondrial biogenesis and quality control begin to decline — the first signs that the protective adaptation is starting to fail.

**In NASH:** Continuous excess fatty acid overload progressively impairs the efficiency of mitochondrial oxidative capacity. This leads to:

1. Accumulation of lipotoxic metabolites (such as ceramides and diacylglycerols/DAGs), which induce insulin resistance
1. Augmented gluconeogenesis (GNG) and de novo lipogenesis (DNL)
1. Decreasing antioxidant activity, so increasing ROS production oxidizes membrane lipids, proteins, and DNA
1. Impaired mitochondrial biogenesis and quality control
1. Activation of JNK and NF-κB inflammatory pathways
1. Ongoing oxidative stress, hyperglycemia, and dyslipidemia activate Kupffer cells and stellate cells (the liver's immune and scarring cells), which via cytokines (TNF-α, IL-1β, and IL-6) drive inflammation, fibrosis, and disease progression

The authors present a helpful concept: **mitochondrial oxidative capacity varies broadly across the spectrum of obesity and NAFLD**, influenced mainly by body mass, but also age, insulin sensitivity, concomitant type 2 diabetes, chronic alcohol abuse, and possibly genetic variants. Oxidative capacity can transiently increase with longer duration of obesity, stimulating fatty acid oxidation and thereby limiting triglyceride deposition. However, this very process generates oxidative stress, which gradually exhausts the liver's antioxidative capacity. This explains the progressive mitochondrial abnormalities observed in NASH and fibrosis, followed by local (intrahepatic) and later systemic inflammation.

## How Medications and Toxins Damage Liver Mitochondria

One of the most valuable contributions of this review is its synthesis of what we've learned from xenobiotics — foreign chemical compounds like drugs and environmental toxins. These substances can impair mitochondrial function through different mechanisms, and understanding them has profound implications for patients.

**Microvesicular steatosis** (a form of fatty liver where tiny fat droplets accumulate) induced by xenobiotics such as **amiodarone** (a heart medication) or **valproic acid** (a seizure medication) results from **severe inhibition of mitochondrial fatty acid oxidation**. This condition carries a real risk of lethal liver failure.

**Macrovacuolar steatosis** (where larger fat droplets accumulate, displacing the nucleus) involves milder but chronic abnormalities of mitochondrial function. This state favors oxidative stress and progression to steatohepatitis and cirrhosis.

Specific examples of medications and toxins that target mitochondria at different points in the energy production pathway include:

-
**Amiodarone**: Impairs fatty acid oxidation and the electron transport chain/OXPHOS
-
**Valproic acid**: Depletes L-carnitine, impairs PPARα signaling, and reduces mtDNA — affecting multiple steps
-
**Ibuprofen and mildronate**: Impair fatty acid oxidation
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**Clozapine and bisphenol A**: Affect fatty acid oxidation and the ETC
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**Stavudine and linezolid**: Deplete mtDNA and impair OXPHOS
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**Troglitazone**: Impairs the ETC and OXPHOS
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**Alcohol intoxication**: Affects nearly every aspect of mitochondrial function — FAO, mtDNA homeostasis, ETC, OXPHOS, and activation of mitochondrial fission
-
**Hypoglycin A** (found in unripe ackee fruit): Impairs fatty acid oxidation

These examples highlight that **drug-induced mitochondrial dysfunction is a major mechanism of liver injury** — and that careful monitoring of liver function is essential for patients taking these medications.

## The Dangerous Combination: Metabolic Disease Plus Alcohol

A critical emerging concern highlighted in this review is the **joint presence of metabolic disease-related (lipotoxic) and alcohol-related liver diseases**. The authors emphasize that increasing awareness of this overlap highlights the need to better understand how these two insults interact and potentiate each other in disease progression.

Alcohol intoxication affects nearly all aspects of mitochondrial function — inhibiting fatty acid oxidation, depleting mtDNA, impairing the ETC and OXPHOS, and activating mitochondrial fission. When combined with the metabolic stress of obesity and type 2 diabetes, the result can be a **"double hit"** to already-strained mitochondria, accelerating progression from steatosis to steatohepatitis and fibrosis.

This is particularly relevant because even moderate alcohol consumption may be more dangerous in patients with underlying metabolic disease — a finding with important implications for patient counseling. **Hepatic mitochondrial alterations play an important role in the mutual interaction of metabolic disorders with some drugs and alcohol abuse.**

## Emerging Treatments That Target Mitochondria

Several existing and investigational treatments for fatty liver disease work — directly or indirectly — by affecting liver mitochondria. The authors highlight that recent clinical studies have assessed the effects of diets and bariatric surgery on hepatic mitochondria, which are **evolving as an interesting therapeutic target in NAFLD**.

The interventions discussed in the review include:

-
**Hypocaloric diet and weight loss**: Indirectly affects mitochondria by reducing fat supply and improving insulin sensitivity
-
**Bariatric surgery**: Produces dramatic weight loss and improves metabolic health, with beneficial effects on hepatic mitochondria
-
**GLP-1 receptor agonists** (like semaglutide): Used for diabetes and obesity, these affect hepatic mitochondria indirectly through weight loss and improved metabolism
-
**Thyroid hormone receptor (THRβ) agonists**: Directly target liver mitochondria and have shown beneficial effects on fatty liver disease
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**PPARα and PPARδ agonists**: Regulate genes involved in mitochondrial fatty acid oxidation
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**Metformin**: At low doses, inhibits mitochondrial GPD2 (a key enzyme in the glycerol phosphate shuttle); at higher doses, inhibits ETC complex I and subsequently activates AMPK, a master regulator of mitochondrial biogenesis
-
**FXR agonists** and **ACC1/2 inhibitors**: Target metabolic pathways that interact with mitochondrial function
-
**SGLT2 inhibitors**: May affect mitochondrial function indirectly through metabolic improvements

The authors note that several interventions directly (e.g., thyroid hormone receptor agonists) or indirectly (e.g., weight loss) affect hepatic mitochondria and have beneficial effects on fatty liver diseases. This suggests that **mitochondrial targets should be further evaluated for the treatment of NAFLD**.

## What This Means for Patients

These findings carry several important messages for patients with fatty liver disease or at risk for it:

-
**Early liver fat accumulation is not inevitable**: The liver's mitochondria can adapt in early obesity, increasing their fat-burning capacity by 85% or more. This natural defense mechanism can protect the liver — for a time.
-
**There is a tipping point**: With higher-grade obesity and type 2 diabetes, mitochondrial capacity can decline, and oxidative stress takes over, favoring progression from steatosis to steatohepatitis and fibrosis.
-
**Medications matter**: Certain drugs (amiodarone, valproic acid, and others) can severely impair mitochondrial function. If you take these medications, discuss liver monitoring with your doctor — especially if you also have obesity or diabetes.
-
**Alcohol is riskier than you might think**: Even moderate alcohol use may accelerate liver damage when combined with metabolic disease, because alcohol and metabolic stress damage mitochondria through overlapping and additive pathways.
-
**Weight loss is powerful medicine**: Both lifestyle changes (hypocaloric diet) and bariatric surgery improve fatty liver disease at least partly by restoring healthier mitochondrial function.
-
**New treatments are on the horizon**: Medications that directly target mitochondrial pathways (like THRβ agonists) are being developed and tested, offering hope for treatments that address the root cause of the disease rather than just its symptoms.

## What This Review Could Not Prove

The authors are clear about the limitations of the current evidence. Studying mitochondria in human livers is technically challenging and often requires invasive procedures like liver biopsy, which limits the size and scope of studies. Many of the techniques used — high-resolution respirometry, MRS, PET — require specialized equipment and expertise available only at certain centers.

Some findings are inconsistent across studies. For example, studies in obese people with steatosis have produced heterogeneous results regarding hepatic energy metabolism, likely due to differences in obesity grade and duration, age, liver fat content, and whether liver histology was available. The fact that some studies show no change in ATP content while others show increased TCA cycle flux highlights the complexity of mitochondrial adaptations.

The review also acknowledges that much of what we know about mitochondrial quality control (dynamics, mitophagy, the unfolded protein response) comes from preclinical studies, with limited validation in human liver tissue. No single accepted marker for mitochondrial content exists for the liver, and many techniques lack validation.

Additionally, the review notes that rare diseases (lipodystrophies, inborn errors of metabolism) that also cause fatty liver were beyond the scope of this review, meaning the findings primarily apply to obesity- and T2DM-related NAFLD.

## Practical Recommendations for Patients

Based on this research, here are actionable steps patients can discuss with their healthcare providers:

1.
**Know your risk**: If you have obesity, type 2 diabetes, or insulin resistance, you are at elevated risk for fatty liver disease. Ask your doctor about liver enzyme tests and, if indicated, imaging studies to assess liver fat.
1.
**Prioritize weight management**: Given the strong evidence that weight loss (through diet, exercise, medication, or bariatric surgery) improves mitochondrial function and fatty liver, aim for gradual, sustainable weight loss. Even modest weight loss (5–10%) has been shown to improve liver fat and inflammation.
1.
**Be cautious with alcohol**: If you have metabolic disease or NAFLD, discuss alcohol use with your doctor. The evidence that alcohol and metabolic stress synergistically damage mitochondria suggests that even moderate drinking may carry greater risk than previously recognized.
1.
**Review your medications**: If you take medications known to affect mitochondria (like amiodarone or valproic acid), ask your doctor about liver monitoring. Never stop prescribed medications without medical supervision.
1.
**Watch for drug interactions**: Be cautious about combining medications that stress the liver — including over-the-counter products. Acetaminophen (paracetamol) is metabolized by mitochondrial CYP2E1, and excessive use can stress mitochondrial function.
1.
**Stay informed about new treatments**: Clinical trials of medications targeting mitochondrial pathways are ongoing. Ask your hepatologist about emerging therapies and whether you might be a candidate for clinical trials.
1.
**Manage diabetes aggressively**: Since type 2 diabetes worsens mitochondrial decline, good glycemic control may help protect your liver's mitochondria.

## Frequently Asked Questions

### What are mitochondria and why do they matter for fatty liver disease?

Mitochondria are tiny energy-producing structures inside liver cells. They burn fats and other fuels to make ATP, the body's energy currency. In fatty liver disease, mitochondria can initially adapt to burn extra fat, but under constant stress they fail, driving inflammation and scarring. This process is central to the progression from simple fatty liver to more serious liver damage.

### How does fatty liver disease progress from simple fat accumulation to NASH?

At first, in early obesity, mitochondria work harder to burn excess fat, protecting the liver. But as fat keeps accumulating, this adaptation fails. Mitochondria become less efficient, producing harmful reactive oxygen species and toxic fat byproducts. This triggers inflammation and activates liver scarring cells, leading to NASH, fibrosis, and eventually cirrhosis if untreated.

### Which medications can damage liver mitochondria and worsen fatty liver?

Several common medications can harm mitochondria, including amiodarone for heart rhythm, valproic acid for seizures, ibuprofen, clozapine, stavudine, linezolid, and troglitazone. These drugs impair fat burning or energy production in mitochondria. If you take these and have obesity or diabetes, your doctor should monitor your liver function regularly to prevent injury.

### Is alcohol more dangerous if I already have metabolic fatty liver disease?

Yes. Alcohol and metabolic stress such as obesity or diabetes damage mitochondria through overlapping pathways. Alcohol affects nearly every part of mitochondrial function, and when combined with metabolic disease, it creates a 'double hit' that can speed up progression to steatohepatitis and fibrosis. Even moderate drinking may carry greater risk in people with underlying metabolic disease.

### What treatments are available that target mitochondria for fatty liver?

Several existing and new treatments affect mitochondria. Weight loss through diet or bariatric surgery improves mitochondrial function. GLP-1 receptor agonists like semaglutide, thyroid hormone receptor agonists, PPAR agonists, metformin, and other drugs directly or indirectly support mitochondrial health. Clinical trials are testing new mitochondrial-targeting therapies, so ask your hepatologist about emerging options.

### How can I protect my liver mitochondria and prevent fatty liver progression?

The most powerful step is gradual weight loss of 5–10%, which improves mitochondrial function and liver fat. Manage type 2 diabetes aggressively to control blood sugar. Limit alcohol, especially if you have metabolic disease. Review medications with your doctor, and avoid excess acetaminophen. Ask about liver enzyme tests if you are at risk due to obesity or diabetes.

### What are the limitations of current research on liver mitochondria?

Studying liver mitochondria is difficult because it often requires invasive biopsy. Techniques like high-resolution respirometry or MRI spectroscopy are complex and not widely available. Findings vary between studies due to differences in patient age, obesity grade, and liver fat. No single accepted marker for mitochondrial content exists, and much knowledge about quality control comes from animal studies, not humans.

## Source Information

**Original article title:** Dusseldorf Mitochondrial alterations in fatty liver diseases

**Authors:** Bernard Fromenty and Michael Roden

**Journal:** Journal of Hepatology, February 2023, vol. 78, pp. 415–429

**DOI:** https://doi.org/10.1016/j.jhep.2022.09.020

**Publication date:** Available online October 7, 2022; received June 10, 2022; accepted September 17, 2022

**Publisher:** Elsevier B.V. on behalf of the European Association for the Study of the Liver (open access under CC BY-NC-ND license)

This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and does not replace professional medical advice. Always consult your healthcare provider about your specific condition and treatment options.


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