The Liver as an Endocrine Organ—Linking NAFLD and Insulin Resistance

Watt, Matthew J; Miotto, Paula M; De Nardo, William; Montgomery, Magdalene K

doi:10.1210/er.2019-00034

Cited by 620Liver Disease Diagnosis and TreatmentAdipokines, Inflammation, and Metabolic DiseasesLiver physiology and pathology

The Liver as an Endocrine Organ—Linking NAFLD and Insulin Resistance

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Watt, Matthew J, Miotto, Paula M, De Nardo, William, Montgomery, Magdalene K·2019·Endocrine Reviews

DOI 10.1210/er.2019-00034

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Abstract

The liver is a dynamic organ that plays critical roles in many physiological processes, including the regulation of systemic glucose and lipid metabolism. Dysfunctional hepatic lipid metabolism is a cause of nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disorder worldwide, and is closely associated with insulin resistance and type 2 diabetes. Through the use of advanced mass spectrometry “omics” approaches and detailed experimentation in cells, mice, and humans, we now understand that the liver secretes a wide array of proteins, metabolites, and noncoding RNAs (miRNAs) and that many of these secreted factors exert powerful effects on metabolic processes both in the liver and in peripheral tissues. In this review, we summarize the rapidly evolving field of “hepatokine” biology with a particular focus on delineating previously unappreciated communication between the liver and other tissues in the body. We describe the NAFLD-induced changes in secretion of liver proteins, lipids, other metabolites, and miRNAs, and how these molecules alter metabolism in liver, muscle, adipose tissue, and pancreas to induce insulin resistance. We also synthesize the limited information that indicates that extracellular vesicles, and in particular exosomes, may be an important mechanism for intertissue communication in normal physiology and in promoting metabolic dysregulation in NAFLD.

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The liver secretes about 2,500 proteins identified by liquid chromatography and mass spectrometry.
“with ~2,500 liver-secreted proteins identified using modern liquid chromatography and mass spectroscopy technologies39.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [39]
Liver-derived exerkines affect glucose and/or lipid metabolism, WAT browning, lipolysis and cellular homeostasis.
“These exerkines affect glucose and/or lipid metabolism (for example, angiopoietin-like protein 4 in humans and animal models39,79), browning of WAT (FGF21 in a mouse model106), lipolysis (FGF21 in humans and a mouse model77) and the maintenance of cellular homeostasis (heat shock protein 72 in humans107).”
From Exerkines in health, resilience and disease (2022) · cites this paper as [39]
Fetuin-A worsens peripheral insulin resistance by reducing insulin signalling and GLUT4 trafficking.
“fetuin-A worsens peripheral insulin resistance by reducing insulin signalling and glucose transporter type 4 trafficking39.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [39]
Activin-E is elevated in the livers and serum of humans with obesity and NAFLD.
“Activin-E is elevated in the livers and serum of humans with obesity and NAFLD (Table 1) [29]”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [29]
Knockdown of FST in mice improves insulin sensitivity.
“Furthermore, knockdown of FST in mice improved insulin sensitivity [29,196].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [29]

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Loomba R, Sanyal AJ. The global NAFLD epi- demic.Nat Rev Gastroenterol Hepatol. 2013;10(11): 686-690.
Stefan N, Fritsche A, Schick F, Häring HU. Pheno- types of prediabetes and stratification of car- diometabolic risk. Lancet Diabetes Endocrinol. 2016; 4(9):789-798.

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Authors: Watt, M. J., Miotto, P. M., De Nardo, W., & Montgomery, M. K.
Affiliations: The University of Melbourne (AU)
Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia
Corresponding author: Watt, Matthew J
ORCID: Watt, Matthew J
Miotto, Paula M
Montgomery, Magdalene K
Venue: Endocrine Reviews
Publisher: The Endocrine Society
Published: 2019-04-25
Volume: 40
Issue: 5
Pages: 1367-1393
ISSN: 0163-769X (ISSN-L)
1945-7189
DOI: 10.1210/er.2019-00034
OpenAlex: W2942227779
Cited by: 615
References: 385
Citations by year: 2026: 61 · 2025: 98 · 2024: 109 · 2023: 98 · 2022: 128 · 2021: 83 · 2020: 31 · 2019: 7
FWCI: 9.07
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Endocrine Reviews (publishedVersion)
PubMed (publishedVersion)
Funders: National Health and Medical Research Council (APP1077703, APP1143224, APP1162511, APP1156508)
Natural Sciences and Engineering Research Council of Canada
Melbourne Research Scholarship, University of Melbourne (AU)
Topics: Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords: non-alcoholic fatty liver disease, insulin resistance, hepatokines, hepatic lipid metabolism, microRNA, extracellular vesicles, exosomes, type 2 diabetes, muscle metabolism, adipose tissue, pancreas
MeSH terms: Animals, Diabetes Mellitus, Type 2, Endocrine Glands, Humans, Insulin Resistance, Liver, Dyslipidemias, Lipid Metabolism, Non-alcoholic Fatty Liver Disease

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The Liver as an Endocrine Organ—Linking NAFLD and Insulin Resistance

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