FoxO1 integrates insulin signaling to VLDL production.

Kamagate, Adama; Dong, H. Henry

doi:10.4161/cc.7.20.6882

Cited by 127FOXO transcription factor regulationLipid metabolism and disordersDiabetes, Cardiovascular Risks, and Lipoproteins

FoxO1 integrates insulin signaling to VLDL production.

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Kamagate, Adama, Dong, H. Henry·2008·Cell Cycle

DOI 10.4161/cc.7.20.6882PMC PMC2664837

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Abstract

Very low-density lipoproteins (VLDL) are triglyceride-rich particles. VLDL is synthesized in hepatocytes and secreted from the liver in a pathway that is tightly regulated by insulin. Hepatic VLDL production is stimulated in response to reduced insulin action, resulting in increased release of VLDL into the blood under fasting conditions. Circulating VLDL serves as a vehicle for transporting lipids to peripheral tissues for energy homeostasis. Conversely, hepatic VLDL production is suppressed in response to increased insulin release after meals. This effect is critical for preventing prolonged excursion of postprandial plasma lipid profiles in normal individuals. In subjects with obesity and type 2 diabetes, the ability of insulin to regulate VLDL production becomes impaired due to insulin resistance in the liver, resulting in excessive VLDL secretion and accumulation of triglyceride-rich particles in the blood. Such abnormality in lipid metabolism characterizes the pathogenesis of hypertriglyceridemia and accounts for increased risk of coronary artery disease in obesity and type 2 diabetes. Nevertheless, the molecular basis that links insulin resistance to VLDL overproduction remains poorly understood. Our recent studies illustrate that the forkhead transcription factor FoxO1 acts in the liver to integrate hepatic insulin action to VLDL production. Augmented FoxO1 activity in insulin resistant livers promotes hepatic VLDL overproduction and predisposes to the development of hypertriglyceridemia. These new findings raise an important question: Is FoxO1 a therapeutic target for ameliorating hypertriglyceridemia? Here we discuss this question in the context of recent advances toward our understanding of the pathophysiology of hypertriglyceridemia.

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Hepatic insulin resistance may contribute to a high production rate of VLDL because insulin reduces apoB synthesis and VLDL secretion in the liver.
“Hepatic insulin resistance may contribute to a high production rate of VLDL because insulin reduces apoB synthesis and VLDL secretion in the liver (66, 67).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [67]
The sections “Insulin Regulation of VLDL Production” and “Hepatic Regulation of apoB Expression” say that insulin suppresses hepatic VLDL production and apoB expression, and that insulin resistance contributes to VLDL overproduction. The copy describes insulin’s effect on apoB chiefly through increased degradation and reduced secretion; it does not establish reduced apoB synthesis specifically. (LLM, conf=0.84)
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[68]Taghibiglou C Carpentier A Van Iderstine SC Chen B Rudy D Aiton A Lewis GF Adeli K Mechanisms of hepatic very low density lipoprotein overproduction in insulin resistance. Evidence for enhanced lipoprotein assembly, reduced intracellular ApoB degradation, and increased microsomal triglyceride transfer protein in a fructose-fed hamster model J Biol Chem 2000 275 8416 25 10722675

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ATF4 Protein Deficiency Protects against High Fructose-induced Hypertriglyceridemia in Mice
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NAFLD and Diabetes: Two Sides of the Same Coin? Rationale for Gene-Based Personalized NAFLD Treatment
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Clever cancer strategies with FoxO transcription factors
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New Strategies for Alzheimer Disease and Cognitive Impairment
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Metabolic Syndrome in Pediatrics: Old Concepts Revised, New Concepts Discussed
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Involvement of Essential Signaling Cascades and Analysis of Gene Networks in Diabesity
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Novel Avenues of Drug Discovery and Biomarkers for Diabetes Mellitus
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FoxO1 Links Hepatic Insulin Action to Endoplasmic Reticulum Stress
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Components of the metabolic syndrome in early childhood in very-low-birth-weight infants and term small and appropriate for gestational age infants
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Erythropoietin, Forkhead Proteins, and Oxidative Injury: Biomarkers and Biology
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Long-term high-protein diet intake reverts weight gain and attenuates metabolic dysfunction on high-sucrose-fed adult rats
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Exercise and Metformin Intervention Prevents Lipotoxicity‐Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK/Nrf2/HO‐1 Signaling Pathway in db/db Mice
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Involvement of Transcription Factor FoxO1 in the Pathogenesis of Polycystic Ovary Syndrome
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Expression profile for metabolic and growth-related genes in domesticated and transgenic coho salmon (Oncorhynchus kisutch) modified for increased growth hormone production
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FOXO1 Mediates the Autocrine Effect of Endothelin-1 on Endothelial Cell Survival
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Modulation of lipid metabolism with the overexpression of NPC1L1 in mouse liver
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Differential impact of selective GH deficiency and endogenous GH excess on insulin-mediated actions in muscle and liver of male mice
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Screening for nonalcoholic fatty liver disease in patients with type 2 diabetes mellitus using transient elastography - a prospective, cross sectional study
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The mechanistic basis for the induction of hepatic steatosis by xenobiotics
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Tumor necrosis factor-α increases angiopoietin-like protein 2 gene expression by activating Foxo1 in 3T3-L1 adipocytes
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Components of the Metabolic Syndrome in Early Childhood in Very-Low-Birth-Weight Infants
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Gymnema Sylvestre Supplementation Restores Normoglycemia, Corrects Dyslipidemia, and Transcriptionally Modulates Pancreatic and Hepatic Gene Expression in Alloxan-Induced Hyperglycemic Rats
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Is nuclear deficiency of FoxO1 due to increased growth factor/PI3K/Akt-signalling in acne vulgaris reversed by isotretinoin treatment?
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Functional Analysis of Promoters from Three Subtypes of the PI3K Family and Their Roles in the Regulation of Lipid Metabolism by Insulin in Yellow Catfish Pelteobagrus fulvidraco
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Single-Gene Congenic Strain Reveals the Effect of Zbtb16 on Dexamethasone-Induced Insulin Resistance
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Comprehensive Transcriptome Analyses of the Fructose-Fed Syrian Golden Hamster Liver Provides Novel Insights into Lipid Metabolism
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Commensal lactic acid-producing bacteria affect host cellular lipid metabolism through various cellular metabolic pathways: Role of mTOR, FOXO1, and autophagy machinery system
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FoxO1 inhibits transcription and membrane trafficking of epithelial sodium channel (ENaC)
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FoxO6-Mediated TXNIP Induces Lipid Accumulation in the Liver through NLRP3 Inflammasome Activation
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LncRNA MEG3 Restrains Hepatic Lipogenesis via the FOXO1 Signaling Pathway in HepG2 Cells
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Metabolic syndrome is a real disease and premalignant state induced by oncogenic stresses to block malignant transformation
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Team players in the pathogenesis of metabolic dysfunctions-associated steatotic liver disease: The basis of development of pharmacotherapy
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Viscosol Treatment Ameliorates Insulin‐Mediated Regulation of Dyslipidemia, Hepatic Steatosis, and Lipid Metabolism by Targeting PTP1B in Type‐2 Diabetic Mice Model
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The hypothetical role of FoxO1 in acne is interesting, but more study is needed before any conclusions can be drawn
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The association of non-HDL-C, NHHR, RC, and RCII with coronary artery stenosis severity in patients with acute coronary syndrome combined with cardiometabolic multimorbidity
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Authors: Kamagate, A., & Dong, H. H.
Affiliations: University of Pittsburgh (US)
ORCID: Dong, H. Henry
Venue: Cell Cycle
Publisher: Informa UK Limited
Published: 2008-10-15
Volume: 7
Issue: 20
Pages: 3162-3170
ISSN: 1538-4101 (ISSN-L)
1551-4005
DOI: 10.4161/cc.7.20.6882
PMC: PMC2664837
OpenAlex: W2051781840
Cited by: 127
References: 158
Citations by year: 2026: 2 · 2025: 4 · 2024: 8 · 2023: 8 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 1 · 2018: 7 · 2017: 3 · 2016: 2 · 2015: 7 · 2014: 6 · 2013: 12 · 2012: 8
FWCI: 1.08
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Cell Cycle (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: American Diabetes Association
National Institute of Diabetes and Digestive and Kidney Diseases (DK066301, R01DK066301)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords: FOXO1, insulin signaling, VLDL production, hepatic insulin resistance, hypertriglyceridemia, triglyceride-rich lipoproteins, hepatic lipid metabolism, type 2 diabetes, obesity, forkhead transcription factor, therapeutic target
MeSH terms: Forkhead Box Protein O1, Animals, Apolipoproteins B, Cell Line, Humans, Insulin, Lipoproteins, VLDL, Liver, Hypertriglyceridemia, Signal Transduction, Forkhead Transcription Factors

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FoxO1 integrates insulin signaling to VLDL production.

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