Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease

Mota, Manoela; Banini, Bubu A.; Cazanave, Sophie C.; Sanyal, Arun J.

doi:10.1016/j.metabol.2016.02.014

Cited by 570Liver Disease Diagnosis and TreatmentEndoplasmic Reticulum Stress and DiseaseDiet, Metabolism, and Disease

Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease

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Mota, Manoela, Banini, Bubu A., Cazanave, Sophie C., Sanyal, Arun J.·2016·Metabolism

DOI 10.1016/j.metabol.2016.02.014PMC PMC4931958

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Abstract

The exposure of hepatocytes to high concentrations of lipids and carbohydrates and the ensuing hepatocellular injury are termed lipotoxicity and glucotoxicity, respectively. A common denominator is metabolic derangement, especially in regards to intracellular energy homeostasis, which is brought on by glucose intolerance and insulin resistance in tissues. In this review, we highlight the lipids and carbohydrates that provoke hepatocyte injury and the mechanisms involved in lipotoxicity and glucotoxicity, including endoplasmic reticulum stress, oxidative stress and mitochondrial impairment. Through upregulation of proteins involved in various pathways including PKR-like ER kinase (PERK), CCAAT/enhancer-binding homologous protein (CHOP), c-Jun NH2-terminal kinase-1 (JNK), Bcl-2 interacting mediator (BIM), p53 upregulated modulator of apoptosis (PUMA), and eventually caspases, hepatocytes in lipotoxic states ultimately undergo apoptosis. The protective role of certain lipids and possible targets for pharmacological therapy are explored. Finally, we discuss the role of high fructose and glucose diets in contributing to organelle impairment and poor glucose transport mechanisms, which perpetuate hyperglycemia and hyperlipidemia by shunting of excess carbohydrates into lipogenesis.

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Persistent elevated levels of glucose can swamp the glycolytic process and inhibit glyceraldehyde catabolism, which promotes reactive oxygen species (ROS) production and oxidative damage, inducing β cells apoptosis and inhibiting β cells secretion.
“Persistent elevated levels of glucose can swamp the glycolytic process and inhibit glyceraldehyde catabolism, which promotes reactive oxygen species (ROS) production and oxidative damage, inducing β cells apoptosis and inhibiting β cells secretion (73, 74).”
From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [73]

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Authors: Mota, M., Banini, B. A., Cazanave, S. C., & Sanyal, A. J.
Affiliations: Virginia Commonwealth University (US)
Corresponding author: Mota, Manoela
Sanyal, Arun J.
ORCID: Mota, Manoela
Banini, Bubu A.
Cazanave, Sophie C.
Sanyal, Arun J.
Venue: Metabolism
Publisher: Elsevier BV
Published: 2016-08
Volume: 65
Issue: 8
Pages: 1049-1061
ISSN: 0026-0495 (ISSN-L)
DOI: 10.1016/j.metabol.2016.02.014
PMC: PMC4931958
OpenAlex: W2289624028
Cited by: 570
References: 121
Citations by year: 2026: 38 · 2025: 61 · 2024: 85 · 2023: 67 · 2022: 90 · 2021: 71 · 2020: 55 · 2019: 34 · 2018: 43 · 2017: 20 · 2016: 5 · 2012: 1
FWCI: 4.60
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Metabolism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Diabetes and Digestive and Kidney Diseases (R03DK081450, T32DK007150, R01DK081410)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords: lipotoxicity, glucotoxicity, non-alcoholic fatty liver disease, hepatocyte injury, insulin resistance, impaired glucose tolerance, endoplasmic reticulum stress, oxidative stress, mitochondrial dysfunction, apoptosis, PERK/CHOP pathway, PUMA, caspases, high-fructose diet, glucose transport, lipogenesis, hyperglycemia, hyperlipidemia, energy homeostasis
MeSH terms: Humans, Insulin Resistance, Mitochondria, Signal Transduction, Glucose Intolerance, Oxidative Stress, JNK Mitogen-Activated Protein Kinases, Transcription Factor CHOP, Endoplasmic Reticulum Stress, Non-alcoholic Fatty Liver Disease

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Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease

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