The role of apolipoprotein A-IV in regulating glucagon-like peptide-1 secretion

Wang, Fei; Yang, Qing; Huesman, Sarah; Xu, Min; Li, Xiaoming; Lou, Dan; Woods, Stephen C.; Marziano, Corina; Tso, Patrick

doi:10.1152/ajpgi.00075.2015

Cited by 8 publications

(3 citation statements)

References 42 publications

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“…16,40 This model offers several advantages for our study at hand. First, the model allows collection of mesenteric lymph directly after a stimuli—in this case a dietary lipid challenge—and therefore allows measurements of substances before they enter the blood and become metabolized.…”

Section: Discussionmentioning

confidence: 99%

Antibiotics Suppress Activation of Intestinal Mucosal Mast Cells and Reduce Dietary Lipid Absorption in Sprague-Dawley Rats

et al. 2016

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BACKGROUND & AIMS The gut microbiota affects intestinal permeability and mucosal mast cells (MMCs) responses. Activation of MMCs has been associated with absorption of dietary fat. We investigated whether the gut microbiota contributes to the fat-induced activation of MMCs in rats, and how antibiotics might affect this process. METHODS Adult male Sprague-Dawley rats were given streptomycin and penicillin for 4 days (n = 6–8) to reduce the abundance of their gut flora, or normal drinking water (controls, n = 6–8). They underwent lymph fistula surgery and after an overnight recovery were given an intraduodenal bolus of intralipid. We collected intestinal tissues and lymph fluid and assessed activation of MMCs, intestinal permeability, and fat transport parameters. RESULTS Compared with controls, intestinal lymph from rats given antibiotics had reduced levels of mucosal mast cell protease II (produced by MMCs) and decreased activity of diamine oxidase (produced by enterocytes) (P < .05). Rats given antibiotics had reduced intestinal permeability in response to dietary lipid compared with controls (P < .01). Unexpectedly, antibiotics also reduced lymphatic transport of triacylglycerol and phospholipid (P < .01), concomitant with decreased levels of mucosal apolipoproteins B, A-I, and A-IV (P < .01). No differences were found in intestinal motility or luminal pancreatic lipase activity between rats given antibiotics and controls. These effects were not seen with an acute dose of antibiotics or 4 weeks after the antibiotic regimen ended. CONCLUSIONS The intestinal microbiota appears to activate MMCs after the ingestion of fat in rats; this contributes to fat-induced intestinal permeability. We found that the gut microbiome promotes absorption of lipid, probably by intestinal production of apolipoproteins and secretion of chylomicrons.

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Section: Discussionmentioning

confidence: 99%

Antibiotics Suppress Activation of Intestinal Mucosal Mast Cells and Reduce Dietary Lipid Absorption in Sprague-Dawley Rats

et al. 2016

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“…Interestingly, in another experiment conducted by the same group, acute administration of ApoA-IV prior to intraduodenal Ensure infusion did not alter GLP-1 levels in wildtype mice or the ApoA-IV-/- mice. They attributed the increased GLP-1 levels in the ApoA-IV knockout mice to increased expression of Gpr119 in the ileum [Wang et al 2015].…”

Section: Nutrient Regulationmentioning

confidence: 99%

Stimulation of incretin secreting cells

Pais

Gribble

Reimann

2015

Therapeutic Advances in Endocrinology

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The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon like peptide-1 (GLP-1) are secreted from enteroendocrine cells in the gut and regulate physiological and homeostatic functions related to glucose control, metabolism and food intake. This review provides a systematic summary of the molecular mechanisms underlying secretion from incretin cells, and an understanding of how they sense and interact with lumen and vascular factors and the enteric nervous system through transporters and G-protein coupled receptors (GPCRs) present on their surface to ultimately culminate in hormone release. Some of the molecules described below such as sodium coupled glucose transporter 1 (SGLT1), G-protein coupled receptor (GPR) 119 and GPR40 are targets of novel therapeutics designed to enhance endogenous gut hormone release. Synthetic ligands at these receptors aimed at treating obesity and type 2 diabetes are currently under investigation.

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“…ApoA-IV is a satiety factor and promotes thermogenesis in brown adipose tissue (12)(13)(14). It has anti-diabetic (15)(16)(17), antioxidant (18), anti-atherosclerotic (19,20), anti-apoptotic (21) and anti-thrombotic properties (22) and inhibits intestinal inflammation and pro-inflammatory cytokine expression in animal models, as well as allergy-driven inflammation in humans and mice (20,23,24). The anti-inflammatory properties of apoA-IV are potentially clinically relevant and they have recently been identified as an independent risk marker of reduced inflammation in chronic kidney disease (25).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Vascular Inflammation by Apolipoprotein A-IV

Shearston

Tan

Cochran

et al. 2022

Front. Cardiovasc. Med.

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BackgroundApolipoprotein (apo) A-IV, the third most abundant apolipoprotein in human high density lipoproteins (HDLs), inhibits intestinal and systemic inflammation. This study asks if apoA-IV also inhibits acute vascular inflammation.MethodsInflammation was induced in New Zealand White rabbits by placing a non-occlusive silastic collar around the common carotid artery. A single 1 mg/kg intravenous infusion of lipid-free apoA-IV or saline (control) was administered to the animals 24 h before collar insertion. The animals were euthanised 24 h post-collar insertion. Human coronary artery cells (HCAECs) were pre-incubated with reconstituted HDLs containing apoA-IV complexed with phosphatidylcholine, (A-IV)rHDLs, then activated by incubation with tumour necrosis factor (TNF)-α. Cell surface vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in the TNF-α-activated HCAECs was quantified by flow cytometry. VCAM-1, ICAM-1 and 3β-hydroxysteroid-Δ24 reductase (DHCR24) mRNA levels were quantified by real time PCR.ResultsApolipoprotein ApoA-IV treatment significantly decreased collar-induced endothelial expression of VCAM-1, ICAM-1 and neutrophil infiltration into the arterial intima by 67.6 ± 9.9% (p < 0.01), 75.4 ± 6.9% (p < 0.01) and 74.4 ± 8.5% (p < 0.05), respectively. It also increased endothelial expression of DHCR24 by 2.6-fold (p < 0.05). Pre-incubation of HCAECs with (A-IV)rHDLs prior to stimulation with TNF-α inhibited VCAM-1 and ICAM-1 protein levels by 62.2 ± 12.1% and 33.7 ± 5.7%, respectively. VCAM-1 and ICAM-1 mRNA levels were decreased by 55.8 ± 7.2% and 49.6 ± 7.9%, respectively, while DHCR24 mRNA expression increased by threefold. Transfection of HCAECs with DHCR24 siRNA attenuated the anti-inflammatory effects of (A-IV)rHDLs. Pre-incubation of TNF-α-activated HCAECs with (A-IV)rHDLs also inhibited nuclear translocation of the p65 subunit of nuclear factor-κB (NF-κB), and decreased IκBα phosphorylation.ConclusionThese results indicate that apoA-IV inhibits vascular inflammation in vitro and in vivo by inhibiting NF-κB activation in a DHCR24-dependent manner.

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The role of apolipoprotein A-IV in regulating glucagon-like peptide-1 secretion

Cited by 8 publications

References 42 publications

Antibiotics Suppress Activation of Intestinal Mucosal Mast Cells and Reduce Dietary Lipid Absorption in Sprague-Dawley Rats

Antibiotics Suppress Activation of Intestinal Mucosal Mast Cells and Reduce Dietary Lipid Absorption in Sprague-Dawley Rats

Stimulation of incretin secreting cells

Inhibition of Vascular Inflammation by Apolipoprotein A-IV

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