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November 15, 2016Scientific ReportsOpen Access

Fasting and Feeding Signals Control the Oscillatory Expression of Angptl8 to Modulate Lipid Metabolism

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Key result

Hepatic Angptl8 expression is rhythmically regulated by LXRα during feeding and glucocorticoid receptor signaling during fasting, and its overexpression dramatically elevates plasma triglyceride and non-esterified fatty acid levels in dexamethasone-treated mice.

Population

Eight- to twelve-week-old C57BL/6J male mice, liver-specific Bmal1-knockout mice, cultured mouse primary…

Comparison

Fasting/refeeding protocols, dexamethasone… vs Ad libitum feeding, vehicle/PBS injection, or…

Design

Preclinical, Mice were randomly separated into groups

Authors

FDFabin DangCase Western Reserve UniversityRWRong WuJohns Hopkins UniversityPWPengfei WangHebei University of Engineering

Discussion

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Overview

Should not yet change lipid management with glucocorticoids; leaves open Angptl8 targeting for dyslipidemia in humans.

Structured PICO

P
Population
Preclinical study using 8- to 12-week-old male C57BL/6 mice and primary hepatocytes to investigate the regulation of Angptl8 expression and its role in lipid metabolism.
I
Intervention
Fasting/refeeding protocols, dexamethasone, mifepristone (RU486), T0901317, GSK2033, and adenoviral overexpression/knockout of Angptl8, LXRα, or GR
C
Comparator
Ad libitum feeding, vehicle/PBS injection, or control adenoviruses (Ad-GFP)
O
Outcome
Angptl8 mRNA and protein expression, and plasma triglyceride (TG) and non-esterified fatty acid (NEFA) levelssurrogate

Angptl8 expression is diurnally regulated by fasting/feeding signals via LXRα and GR, and its overexpression exacerbates hypertriglyceridemia in glucocorticoid-treated mice, highlighting its role in lipid homeostasis.

Limitations

  • The study is preclinical and conducted in mice and cell cultures, which may not fully translate to human physiology.
  • The exact mechanism by which Angptl8 overexpression upregulates lipid metabolism genes in the liver remains to be fully elucidated.

Cite This Study

Dang et al. (2016) studied Hypertriglyceridemia and Lipid Metabolism. Fasting/feeding signals and Glucocorticoids (Dexamethasone) vs. Vehicle/PBS or ad libitum feeding was evaluated on Hepatic Angptl8 expression and plasma triglyceride/NEFA levels. Hepatic Angptl8 expression is rhythmically regulated by LXRα during feeding and glucocorticoid receptor signaling during fasting, and its overexpression dramatically elevates plasma triglyceride and non-esterified fatty acid levels in dexamethasone-treated mice.

synapsesocial.com/papers/6a20e95a920f77b2c049e1eahttps://doi.org/10.1038/srep36926
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Angiopoietin-like 4 (ANGPTL4, Fasting-induced Adipose Factor) Is a Direct Glucocorticoid Receptor Target and Participates in Glucocorticoid-regulated Triglyceride Metabolism2009 · 165 citations
  2. 2Remnant Lipoproteins: A Subfraction of Plasma Triglyceride-Rich Lipoproteins Associated with Postprandial Hyperlipidemia2014 · 3 citations
  3. 3A lipasin/Angptl8 monoclonal antibody lowers mouse serum triglycerides involving increased postprandial activity of the cardiac lipoprotein lipase2015 · 85 citations
  4. 4Angiopoietin-like Protein 3 Mediates Hypertriglyceridemia Induced by the Liver X Receptor2003 · 145 citations
  5. 5ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure2015 · 134 citations