Insulin decreases chylomicron production in human fetal small intestine

Loirdighi, N.; Ménard, Daniel; Lévy, Émile

doi:10.1016/0167-4889(92)90015-4

Cited by 35 publications

(28 citation statements)

References 25 publications

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“…26 Lipid transport in the enterocyte is also regulated by insulin. 9,27,28 The importance of insulin action on the gut has been illustrated by functional alterations present in animals with drug-induced T2D, [29][30][31] which also display enhanced intestinal absorption of several nutrients, including glucose and amino acids, 29,30 as well as increased mucosal mass. 31,32 Many of these alterations can be restored to control levels by the administration of insulin.…”

Section: Discussionmentioning

confidence: 99%

Intestinal Lipid Handling

Veilleux

Grenier

Marceau

et al. 2014

ATVB

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Insulin resistance (IR) is the central feature of type 2 diabetes mellitus (T2D) and represents a major complication, commonly associated with atherogenic dyslipidemia. The latter is characterized by hypertriglyceridemia, elevated plasma very-low-density lipoprotein, reduced high-density lipoprotein (HDL), and presence of small, dense low-density lipoprotein (LDL).1 This atherogenic dyslipidemia is increasingly recognized as a postprandial phenomenon, 2 because postprandial triglyceride-rich lipoproteins (TRLs) and chylomicron remnants have been implicated as significant risk factors for atherosclerosis.3-5 Exaggerated hepatic very-low-density lipoprotein production and impaired plasma triglyceride clearance are thought to play a key role in this disorder. However, mounting evidence underlines the active implication of the small intestine in postprandial lipid alterations.It currently becomes clear that the small intestine is far from being a simple absorptive organ as it was previously thought. Indeed, recent studies have demonstrated that the small intestine regulates lipid metabolism in fed and fasting states and may, therefore, be central in lipid homeostasis in both normal physiology and pathophysiological conditions. 6-8 Lipid synthesis as well as lipoprotein assembly and secretion occur in this tissue, and these metabolic pathways are sensitive to several hormones such as insulin.9 Maintaining normal lipid homeostasis seems to require an interaction between intestinal and hepatic metabolism to adequately manage dietary intake. Otherwise, an imbalance in the lipid metabolism may lead to dyslipidemia and to increased risks of cardiovascular diseases (CVDs).Studies primarily on animal models (fructose-fed hamster; Psammomys obesus, JCR:LA-cp rat) have pointed out the © 2014 American Heart Association, Inc. Objective-Animal models have evidenced the role of intestinal triglyceride-rich lipoprotein overproduction in dyslipidemia. However, few studies have confronted this issue in humans and disclosed the intrinsic mechanisms. This work aimed to establish whether intestinal insulin resistance modifies lipid and lipoprotein homeostasis in the intestine of obese subjects. Approach and Results-Duodenal specimens obtained from 20 obese subjects undergoing bariatric surgery were paired for age, sex, and body mass index with or without insulin resistance, as defined by the homeostasis model assessment of insulin resistance. Insulin signaling, biomarkers of inflammation and oxidative stress, and lipoprotein assembly were assessed. The intestine of insulin-resistant subjects showed defects in insulin signaling as demonstrated by reduced protein kinase B phosphorylation and increased p38 mitogen-activated protein kinase phosphorylation, likely as the result of high oxidative stress (evidenced by malondialdehyde and conjugated dienes) and inflammation (highlighted by nuclear factor-κB, tumor necrosis factor-α, interleukin-6, intercellular adhesion molecule-1, and cyclooxygenase-2). Enhanced de novo lipogenesis rate and a...

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Section: Discussionmentioning

confidence: 99%

Intestinal Lipid Handling

Veilleux

Grenier

Marceau

et al. 2014

ATVB

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“…14 C]oleic acid were next separated by thin layer chromatography using the solvent mixture hexane/ether/acetic acid (80:20:3 (v/v)) as described previously (37,38). The area corresponding to each lipid was scratched off of the thin layer chromatography plates, and the silica powder was placed in a scintillation vial with Ready Safe counting fluid (Beckman, Fullerton, CA).…”

Section: Measurement Of Lipid Synthesis and Secretionmentioning

confidence: 99%

Modification in Oxidative Stress, Inflammation, and Lipoprotein Assembly in Response to Hepatocyte Nuclear Factor 4α Knockdown in Intestinal Epithelial Cells

Marcil

Seidman

Sinnett

et al. 2010

Journal of Biological Chemistry

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“…After a 3 h stabilization period, the medium was changed with a fresh one containing a final amount of 0.13 ~tmol/ml of unlabeled oleic acid attached to albumin. The preparation of oleate/albumin complex was prepared as detailed previously [5][6][7][8]. Insulin was added at concentrations of 3 mU/ml and intestinal explants were cultured for 42 h.…”

Section: Intestinal Specimens and Culture Conditionsmentioning

confidence: 99%

“…This efficient lipoprotein-lipid transport proved to be influenced by the developmental process and a certain number of hormones [5 7]. In particular, the addition of insulin to the culture medium significantly decreased the output of chylomicrons [8]. In this *Corresponding author.…”

Section: Introductionmentioning

confidence: 99%

Insulin modulation of newly synthesized apolipoproteins B‐100 and B‐48 in human fetal intestine: Gene expression and mRNA editing are not involved

et al. 1996

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We investigated insulin's effect on intestinal lipid transport and, particularly, the biogenesis of apolipoproteins crucial to lipoprotein secretion. Adding insulin (3 mU) to the serum-free medium of cultured jejunal explants from human fetuses (17-20 weeks) reduced triglyceride and chylomicron production and inhibited apo B-48 and apo B-100 secretion. When apo B mRNA was assayed by RT-PCR and its editing by primer extension, no change was detectable following the addition of insulin. HDL lipid content, apo A-1 synthesis and RNA level were unaffected by insulin. Collectively, these results suggest that the insulin-stimulated decline in intestinal chylomicron output may involve apo B co-or post-translational modifications.

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Insulin decreases chylomicron production in human fetal small intestine

Cited by 35 publications

References 25 publications

Intestinal Lipid Handling

Intestinal Lipid Handling

Modification in Oxidative Stress, Inflammation, and Lipoprotein Assembly in Response to Hepatocyte Nuclear Factor 4α Knockdown in Intestinal Epithelial Cells

Insulin modulation of newly synthesized apolipoproteins B‐100 and B‐48 in human fetal intestine: Gene expression and mRNA editing are not involved

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