# From Childhood to Old Age: Current Knowledge and Practical Approaches to Metabolic Dysfunction-Associated Steatotic Liver Disease

**Authors:** Iwona Gorczyca-Głowacka, Michał Tarnowski, Anna Zmelonek-Znamirowska, Przemysław Wolak

PMC · DOI: 10.3390/jcm15041536 · Journal of Clinical Medicine · 2026-02-15

## TL;DR

This review explores how metabolic dysfunction-associated steatotic liver disease (MASLD) affects people from childhood to old age, emphasizing the importance of early detection and age-specific prevention strategies.

## Contribution

The paper provides a comprehensive, age-specific analysis of MASLD risk factors, diagnosis, and management across the lifespan.

## Key findings

- MASLD prevalence increases with age until middle adulthood but plateaus in the elderly.
- Obesity is the most significant risk factor for MASLD across all age groups.
- Lifestyle changes are the primary treatment, but are less effective in children and the elderly.

## Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the most common chronic liver diseases across all age groups. Methods: This review synthesizes the current evidence from landmark studies on the risk factors, diagnosis, and management of MASLD in pediatric, adult, and particularly elderly patients. Results: Based on the current data, we demonstrated that the prevalence of MASLD increases with age from childhood to middle adulthood, whereas, in elderly individuals, there is no further age-related increase observed. In the pathogenesis of the disease, familial and prenatal factors predominate in the youngest patients, while metabolic factors are the main contributors in adults. However, obesity remains the most significant risk factor for MASLD across all age groups. Therefore, systematic screening for MASLD should be strongly recommended in individuals with obesity. Laboratory parameters indicating an increased risk of MASLD are primarily recommended in screening regimens for children and adults; however, in elderly patients, these parameters may remain within normal ranges due to the long-standing disease course and progression toward fibrosis. On the basis of current studies and guidelines, we showed that lifestyle modification, including dietary changes and increased physical activity, is the cornerstone of treatment across all age groups. Nevertheless, non-pharmacological interventions have limitations in pediatric and elderly populations and are implemented less effectively in these groups than in middle-aged patients. Conclusions: The early identification of high-risk patients and implementation of multidisciplinary, age-targeted metabolic prevention strategies are essential to prevent MASLD progression and its non-liver complications.

## Linked entities

- **Diseases:** metabolic dysfunction-associated steatotic liver disease (MONDO:0013209), MASLD (MONDO:0013209)

## Full-text entities

- **Genes:** SHBG (sex hormone binding globulin) [NCBI Gene 6462] {aka ABP, SBP, TEBG}, GCKR (glucokinase regulator) [NCBI Gene 2646] {aka FGQTL5, GKRP}, LEP (leptin) [NCBI Gene 3952] {aka LEPD, OB, OBS}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, TM6SF2 (transmembrane 6 superfamily member 2) [NCBI Gene 53345], LOC102724197 (inactive glutathione hydrolase 2) [NCBI Gene 102724197] {aka GGT2}, FGF19 (fibroblast growth factor 19) [NCBI Gene 9965], GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, PNPLA3 (patatin like domain 3, 1-acylglycerol-3-phosphate O-acyltransferase) [NCBI Gene 80339] {aka ADPN, C22orf20, iPLA(2)epsilon}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}
- **Diseases:** metabolic dysregulation (MESH:D021081), abdominal obesity (MESH:D056128), lipodystrophy (MESH:D008060), Metabolic Dysfunction (MESH:D008659), hepatocellular carcinoma (MESH:D006528), endotoxic (MESH:D012772), Maternal (MESH:D000079262), lipid overload (MESH:D011017), celiac disease (MESH:D002446), cognitive/physical dysfunction (MESH:D003072), hypertriglyceridemia (MESH:D015228), frail (MESH:D000073496), vomiting (MESH:D014839), T2DM (MESH:D003924), inborn errors of metabolism (MESH:D008661), obstructive sleep apnea (MESH:D020181), MASH (MESH:D005234), weight gain (MESH:D015430), thyroid dysfunction (MESH:D013959), hepatic fat accumulation (MESH:D005218), gestational diabetes (MESH:D016640), thyroid hormone resistance (MESH:D018382), nausea (MESH:D009325), heart failure (MESH:D006333), Obesity (MESH:D009765), NASH (MESH:D005235), adipose (MESH:D018205), intestinal failure (MESH:D000090124), Drug-Induced Liver Injury (MESH:D056486), cryptogenic cirrhosis (MESH:C562577), overweight (MESH:D050177), liver impairment (MESH:D017093), cardiovascular (MESH:D002318), NAFLD (MESH:D065626), hypoglycemia (MESH:D007003), Gut dysbiosis (MESH:D064806), gastrointestinal (MESH:D005767), Diabetes (MESH:D003920), cancer (MESH:D009369), Gallstone (MESH:D042882), bone loss (MESH:D001847), loss of weight (MESH:D015431), hepatic fibrosis (MESH:D008103), Prediabetes (MESH:D011236), cytotoxic (MESH:D064420), chronic kidney disease (MESH:D051436), OSA (MESH:C535586), insulin resistance (MESH:D007333), hepatitis C (MESH:D019698), Disease (MESH:D004194), hepatocyte injury (MESH:D014947), hepatic inflammation (MESH:D007249), Liver Diseases (MESH:D008107), Fibrosis (MESH:D005355), hyperlipidemia (MESH:D006949), hyperandrogenism (MESH:D017588), cardiometabolic (MESH:D024821), physical disability (MESH:D059445), polycystic ovary syndrome (MESH:D011085), hypertension (MESH:D006973)
- **Chemicals:** diacylglycerol (MESH:D004075), alcohol (MESH:D000438), glucose (MESH:D005947), reactive oxygen species (MESH:D017382), ceramides (MESH:D002518), fructose (MESH:D005632), metformin (MESH:D008687), free fatty acids (MESH:D005230), testosterone (MESH:D013739), resmetirom (MESH:C588408), lipid (MESH:D008055), pioglitazone (MESH:D000077205), Butyrate (MESH:D002087), estradiol (MESH:D004958), choline (MESH:D002794), uric acid (MESH:D014527), vitamin E (MESH:D014810), valproate (MESH:D014635), triglyceride (MESH:D014280), fatty acids (MESH:D005227), carbohydrate (MESH:D002241), density lipoprotein (-), olive oil (MESH:D000069463), bile acid (MESH:D001647), sugars (MESH:D000073893)
- **Species:** gut metagenome (species) [taxon 749906], Ruminococcus (genus) [taxon 1263], Parabacteroides (genus) [taxon 375288], Prevotella (genus) [taxon 838], Coprococcus (genus) [taxon 33042], Bacteroides (genus) [taxon 816], Clostridium (genus) [taxon 1485], Bifidobacterium (genus) [taxon 1678], Lactobacillus (genus) [taxon 1578], Homo sapiens (human, species) [taxon 9606], Faecalibacterium (genus) [taxon 216851], Streptococcus (genus) [taxon 1301], Escherichia coli (E. coli, species) [taxon 562]
- **Mutations:** rs738409, rs1260326, rs58542926

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12942451/full.md

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942451/full.md

## References

97 references — full list in the complete paper: https://tomesphere.com/paper/PMC12942451/full.md

---
Source: https://tomesphere.com/paper/PMC12942451