ArticlePloS one2012
Counteracting roles of AMP deaminase and AMP kinase in the development of fatty liver.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
108 citing papers in PubMed, 191 citations in OpenAlex.
- Nutrition, Cell Signalling, Mitochondrial Function, and Chronic Non-Communicable Disease.International journal of molecular sciences · 2026Review
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Fish oil rich in ω-3 fatty acid alleviates long-term high fructose consumption-induced fatty liver and kidney dysfunction in rats.Journal of food and drug analysis · 2025Article
- Article
- Article
- Observational
- Gender difference in the association between serum uric acid and metabolic dysfunction-associated steatotic liver disease in patients with newly diagnosed type 2 diabetes.BMC gastroenterology · 2025Article
- From Liver to Kidney: The Overlooked Burden of Nonalcoholic Fatty Liver Disease in Chronic Kidney Disease.Journal of clinical medicine · 2025Review
- Prediction of insulin resistance using multiple adaptive regression spline in Chinese women.Endocrine journal · 2025Article
- Do microglia metabolize fructose in Alzheimer's disease?Journal of neuroinflammation · 2025Review
- Aldose reductase, fructose and fat production in the liver.The Biochemical journal · 2025Review
- Transcriptomic Signature of Lipid Production in Australian Aurantiochytrium sp. TC20.Marine biotechnology (New York, N.Y.) · 2025Article
- Mindful Eating: A Deep Insight Into Fructose Metabolism and Its Effects on Appetite Regulation and Brain Function.Journal of nutrition and metabolism · 2025Review
- Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024Review
- The relationship between the systemic immune inflammation index and the nonalcoholic fatty liver disease in American adolescents.BMC gastroenterology · 2024Article
- Regulation of Fructose Metabolism in Nonalcoholic Fatty Liver Disease.Biomolecules · 2024Review
- Activation of AMPD2 drives metabolic dysregulation and liver disease in mice with hereditary fructose intolerance.Communications biology · 2024Article
- Quinoa (Food science & nutrition · 2023Article
- The fructose survival hypothesis for obesity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Sugar, salt, immunity and the cause of primary hypertension.Clinical kidney journal · 2023Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Fatty liver (hepatic steatosis) is associated with nucleotide turnover, loss of ATP and generation of adenosine monophosphate (AMP). It is well known that in fatty liver, activity of the AMP-activated kinase (AMPK) is reduced and that its stimulation can prevent hepatic steatosis by both enhancing fat oxidation and reducing lipogenesis. Here we show that another AMP dependent enzyme, AMPD2, has opposing effects on fatty acid oxidation when compared to AMPK. In human hepatocytres, AMPD2 activation -either by overexpression or by lowering intracellular phosphate levels with fructose- is associated with a significant reduction in AMPK activity. Likewise, silencing of AMPK spontaneously increases AMPD activity, demonstrating that these enzymes counter-regulate each other. Furthermore, we show that a downstream product of AMP metabolism through AMPD2, uric acid, can inhibit AMPK activity in human hepatocytes. Finally, we show that fructose-induced fat accumulation in hepatocytes is due to a dominant stimulation of AMPD2 despite stimulating AMPK. In this regard, AMPD2-deficient hepatocytes demonstrate a further activation of AMPK after fructose exposure in association with increased fatty acid oxidation, and conversely silencing AMPK enhances AMPD-dependent fat accumulation. In vivo, we show that sucrose fed rats also develop fatty liver that is blocked by metformin in association with both a reduction in AMPD activity and an increase in AMPK activity. In summary, AMPD and AMPK are both important in hepatic fat accumulation and counter-regulate each other. We present the novel finding that uric acid inhibits AMPK kinase activity in fructose-fed hepatocytes thus providing new insights into the pathogenesis of fatty liver.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.