Butyrate stimulates the secretion of apolipoprotein A-I and apolipoprotein B-100 in Hep G2 cells by different mechanisms

Kaptein, Allard; Roodenburg, L.; Princen, H.M.G.

doi:10.1016/0009-9120(92)80005-2

Cited by 4 publications

(4 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although butyrate was the most potent inducer, also propionate (28%) and valerate (73%) significantly increased ApoA-I secretion while acetate did not. In line with these studies by Kaptein et al, Malle et al confirmed in HUH-7 hepatoma cells that 2 mM butyrate increased the intracellular ApoA-I protein synthesis by three-fold after 48 h, whereas ApoA-I secretion was 2.5 times higher compared to the control [52][53][54]. More recently, Tayyeb et al showed that not only butyrate but also other SCFAs resulted in a dose-dependent stimulation of ApoA-I transcription after 48 h in HepG2 cells [16].…”

Section: Potential Effects Of Scfas On Apoa-i Metabolismsupporting

confidence: 59%

“…This indicates that butyrate specifically enhanced ApoA-I secretion. Interestingly, effects of butyrate exposure on hepatic ApoA-I secretion were time and dose-dependent [ 53 ]. Although butyrate was the most potent inducer, also propionate (28%) and valerate (73%) significantly increased ApoA-I secretion while acetate did not.…”

Section: Potential Effects Of Scfas On Apoa-i Metabolismmentioning

confidence: 99%

See 1 more Smart Citation

Potential Contribution of Short Chain Fatty Acids to Hepatic Apolipoprotein A-I Production

Popeijus

Zwaan

Tayyeb

2021

IJMS

View full text Add to dashboard Cite

Apolipoprotein A-I (ApoA-I) is the major protein of high density lipoprotein (HDL) particles and has a crucial role in reverse cholesterol transport (RCT). It has been postulated that elevating production of de novo ApoA-I might translate into the formation of new functional HDL particles that could lower cardiovascular disease (CVD) risk via RCT. During inflammation, serum ApoA-I concentrations are reduced, which contributes to the development of dysfunctional HDL particles as Serum Amyloid A (SAA) overtakes the position of ApoA-I within the HDL particles. Therefore, instead of elevating serum HDL cholesterol concentrations, rescuing lower serum ApoA-I concentrations could be beneficial in both normal and inflamed conditions. Several nutritional compounds, amongst others short chain fatty acids (SCFAs), have shown their capacity to modulate hepatic lipoprotein metabolism. In this review we provide an overview of HDL and more specific ApoA-I metabolism, SCFAs physiology and the current knowledge regarding the influence of SCFAs on ApoA-I expression and synthesis in human liver cells. We conclude that the current evidence regarding the effect of SCFAs on ApoA-I transcription and secretion is promising, however there is a need to investigate which dietary fibres could lead to increased SCFAs formation and consequent elevated ApoA-I concentrations.

show abstract

Section: Potential Effects Of Scfas On Apoa-i Metabolismsupporting

confidence: 59%

Section: Potential Effects Of Scfas On Apoa-i Metabolismmentioning

confidence: 99%

Potential Contribution of Short Chain Fatty Acids to Hepatic Apolipoprotein A-I Production

Popeijus

Zwaan

Tayyeb

2021

IJMS

View full text Add to dashboard Cite

show abstract

“…With regard to apolipoproteins, one should point out that divergent observations were recorded in HepG2 cells. When Kaptein et al (18,19) incubated this hepatoma cell line with butyrate, they noted an accelerated accumulation of apo A-I and apo B-100 in the medium. The discrepancy between their results and ours may be due to numerous factors, including cell origin, butyrate concentrations, and other experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…These effects on circulating cholesterol may be elicited by bile acid excretion, which is considered to be associated with the hypocholesterolemic action of dietary soluble fiber (33). Surprisingly, to our knowledge, there are no data on the ability of SCFAs to influence the synthesis and secretion of lipoproteins by the intestine, which is considered as one of the major players in lipid homeostasis (4,9,19,24,48). Only an indirect effect was suggested for butyrate in view of its conversion to ketone bodies and other metabolites in the gut, which are then capable of modifying lipid metabolism (17,38).…”

mentioning

confidence: 99%

Modulation of lipid synthesis, apolipoprotein biogenesis, and lipoprotein assembly by butyrate

Marcil¹,

Delvin²,

Seidman

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Short-chain fatty acids (SCFAs) are potent modulators of the growth, function, and differentiation of intestinal epithelia. In addition, high-fiber diets may protect against the development of atherosclerosis because of their cholesterol-lowering effects due, in large part, to SCFA production, liver sterol metabolism, and bile acid excretion. Although the small gut plays a major role in dietary fat transport and contributes substantially to plasma cholesterol and lipoprotein homeostasis, the impact of SCFAs on intestinal lipid handling remains unknown. In the present study, the modulation of lipid synthesis, apolipoprotein biogenesis, and lipoprotein secretion by butyrate was investigated in Caco-2 cells plated on permeable polycarbonate filters, which permit separate access to the upper and lower compartments of the monolayers. Highly differentiated and polarized cells (20 days of culture) were incubated for 20 h with 20 mM butyrate in the apical medium. In the presence of [14C]oleic acid, butyrate led to a significant reduction of secreted, labeled triglycerides (27%; P < 0.01) and phospholipids (25%; P < 0.05). Similarly, butyrate significantly decreased the incorporation of [14C]acetate into exported cholesteryl ester (49%; P < 0.005). As expected from these results, with [14C]oleic acid as a precursor, butyrate significantly (P < 0.05) diminished the delivery of radiolabeled chylomicrons and very low-density lipoproteins. In parallel, [35S]methionine pulse labeling of Caco-2 cells revealed the concomitant inhibitory effect of butyrate on the synthesis of apolipoproteins B-48 (28%; P < 0.05) and A-I (32%; P < 0.01). Collectively, our data indicate that butyrate may influence lipid metabolism in Caco-2 cells, thus suggesting a potential regulation of intestinal fat absorption and circulating lipoprotein concentrations.

show abstract

Butyrate generated by gut microbiota and its therapeutic role in metabolic syndrome

Bridgeman

Northrop

Melton

et al. 2020

Pharmacological Research

View full text Add to dashboard Cite

Butyrate stimulates the secretion of apolipoprotein A-I and apolipoprotein B-100 in Hep G2 cells by different mechanisms

Cited by 4 publications

References 9 publications

Potential Contribution of Short Chain Fatty Acids to Hepatic Apolipoprotein A-I Production

Potential Contribution of Short Chain Fatty Acids to Hepatic Apolipoprotein A-I Production

Modulation of lipid synthesis, apolipoprotein biogenesis, and lipoprotein assembly by butyrate

Butyrate generated by gut microbiota and its therapeutic role in metabolic syndrome

Contact Info

Product

Resources

About