Insulin Acutely Inhibits Intestinal Lipoprotein Secretion in Humans in Part by Suppressing Plasma Free Fatty Acids

Pavlic, Mirjana; Xiao, Changting; Szeto, Linda; Patterson, Bruce W.; Lewis, Gary F.

doi:10.2337/db09-1297

Cited by 87 publications

(84 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The mechanism underlying this effect remains unclear, but it is compatible with the idea that prolonged exposure to high levels of circulating FFAs increases enterocyte TG content, leading to the inhibition of SREBP expression and the adaptive repression of intestinal de novo lipogenesis and lipid absorption. transition and postprandial hyperglycemia coupled with GLP-1 has been shown to stimulate ␤ -cell insulin secretion, which in turn may acutely suppress lipoprotein assembly and secretion in the liver and the intestine ( 40 ). Therefore, the discrepancies between our fi ndings in nondiabetic insulin-resistant subjects and the fi ndings of the studies performed in diabetics could be related to the presence of relative insulin insuffi ciency along with resistance in diabetic subjects that could stimulate MTP expression.…”

Section: Intestinal Protein Levels Assessed By Lc-ms/mscontrasting

confidence: 54%

Key intestinal genes involved in lipoprotein metabolism are downregulated in dyslipidemic men with insulin resistance

Couture

Tremblay

Kelly

et al. 2014

Journal of Lipid Research

View full text Add to dashboard Cite

Dyslipidemia is an important feature of insulin resistance (IR) that contributes to the pathogenesis of atherosclerosis and increases the risk of cardiovascular disease ( 1 ). Dyslipidemia associated with IR is typically characterized by elevated concentrations of triglyceride-rich lipoproteins (TRLs), reduced plasma levels of HDL-cholesterol (HDL-C), an increased number of small dense LDL particles, and greater levels of free fatty acid (FFA) ( 1 ). Metabolic kinetic studies have indicated that the increased plasma levels of TRLs in individuals with IR are caused by the elevated secretion of both hepatic (apoB-100-containing) and intestinal (apoB-48-containing) lipoproteins in fasting and postprandial states ( 2-5 ). We have already shown that the intestinal lipoprotein production rate (PR) is markedly greater in dyslipidemic patients with type 2 diabetes ( 6 ). This relationship is of signifi cant interest because there is now convincing evidence indicating that elevated levels of intestine-derived lipoproteins are proatherogenic and associated with an increased risk of cardiovascular disease ( 7-9 ). Hence, a better understanding of the factors regulating intestinal lipoprotein secretion could potentially lead to rational therapeutic strategies to reduce cardiovascular risk in this vulnerable group of patients. Abstract Insulin resistance (IR) is

show abstract

Section: Intestinal Protein Levels Assessed By Lc-ms/mscontrasting

confidence: 54%

Key intestinal genes involved in lipoprotein metabolism are downregulated in dyslipidemic men with insulin resistance

Couture

Tremblay

Kelly

et al. 2014

Journal of Lipid Research

View full text Add to dashboard Cite

show abstract

“…The postprandial exercise also transiently mitigated the suppression of FFA after the ingestion of the cookie. It is known that insulin acutely suppresses the lipoprotein production from both endogenous and exogenous sources, which may be caused by an insulinmediated suppression of circulating FFAs and also the direct effects of insulin (16,17).…”

Section: Discussionmentioning

confidence: 99%

Effects of Aerobic Exercise on Postprandial Carbohydrate and Lipoprotein Metabolism Following Cookie Ingestion in Healthy Young Women

Hashimoto

Mizutani

Suzuki

et al. 2015

J Nutr Sci Vitaminol

View full text Add to dashboard Cite

SummaryWe examined the acute effects of postprandial aerobic exercise on glucose and lipid metabolism following cookie ingestion. Fifteen healthy young women with a sedentary lifestyle, normal weight and apolipoprotein E3/3 participated. After a 12-h overnight fast, each subject ingested a cookie (1.53 g/kg, Meal Test C) and then performed two trials, one with postprandial exercise (E trial) and one without exercise (C trial), in a randomized crossover design. A single 30-min bout of walking exercise was performed 20 min after the cookie intake. Venous blood samples were drawn before (0 h) and 20 min and 1, 2, 4, and 6 h after cookie ingestion. The Dglucose concentration was not significantly different between the two trials, but the Dinsulin concentration at 1 h and the incremental area under the curve (IAUC) (0-2 h)-insulin in the E trial were significantly lower than in the C trial. The ratio of glucose/insulin at 1 h was significantly higher in the E trial than in the C trial. The DTG, DRLP-TG, DapoB48 and DRemL-C concentrations at 1 h in the E trial were significantly higher than in the C trial. The IAUC (0-2 h)-apoB48 in the E trial was significantly larger than in the C trial. Postprandial exercise showed an insulin-sparing effect following the cookie ingestion by increasing insulin sensitivity. However, postprandial exercise transiently stimulated the secretion of exogenous apoB48-containing lipoprotein during the early period, and no further effects were observed. These results suggest that postprandial aerobic exercise is effective for the promotion of postprandial carbohydrate metabolism, but not lipidemia.

show abstract

“…Insulin-mediated suppression involves the activation of phosphatidylinositide-3-kinase by the insulin receptor transduced through insulin receptor substrates; a process that correlates with the translocation of activated phosphatidylinositide-3-kinase to intracellular membranes [311]. Insulin-induced suppression of intestinal lipoprotein secretion is both direct and indirect through suppression of circulating free fatty acids [312].…”

Section: Hormones and Lipid Metabolismmentioning

confidence: 99%

Recent advances in physiological lipoprotein metabolism

Ramasamy

2014

Clinical Chemistry and Laboratory Medicine (CCLM)

188

159

View full text Add to dashboard Cite

Abstract:Research into lipoprotein metabolism has developed because understanding lipoprotein metabolism has important clinical indications. Lipoproteins are risk factors for cardiovascular disease. Recent advances include the identification of factors in the synthesis and secretion of triglyceride rich lipoproteins, chylomicrons (CM) and very low density lipoproteins (VLDL). These included the identification of microsomal transfer protein, the cotranslational targeting of apoproteinB (apoB) for degradation regulated by the availability of lipids, and the characterization of transport vesicles transporting primordial apoB containing particles to the Golgi. The lipase maturation factor 1, glycosylphosphatidylinositol-anchored high density lipoprotein binding protein 1 and an angiopoietin-like protein play a role in lipoprotein lipase (LPL)-mediated hydrolysis of secreted CMs and VLDL so that the right amount of fatty acid is delivered to the right tissue at the right time. Expression of the low density lipoprotein (LDL) receptor is regulated at both transcriptional and posttranscriptional level. Proprotein convertase subtilisin/ kexin type 9 (PCSK9) has a pivotal role in the degradation of LDL receptor. Plasma remnant lipoproteins bind to specific receptors in the liver, the LDL receptor, VLDL receptor and LDL receptor-like proteins prior to removal from the plasma. Reverse cholesterol transport occurs when lipid free apoAI recruits cholesterol and phospholipid to assemble high density lipoprotein (HDL) particles. The discovery of ABC transporters (ABCA1 and ABCG1) and scavenger receptor class B type I (SR-BI) provided further information on the biogenesis of HDL. In humans HDLcholesterol can be returned to the liver either by direct uptake by SR-BI or through cholesteryl ester transfer protein exchange of cholesteryl ester for triglycerides in apoB lipoproteins, followed by hepatic uptake of apoB containing particles. Cholesterol content in cells is regulated by several transcription factors, including the liver X receptor and sterol regulatory element binding protein. This review summarizes recent advances in knowledge of the molecular mechanisms regulating lipoprotein metabolism.Keywords: ABCA1; angiopoietin-like proteins; apoC; apoAI; apolipoprotein E (apoE); cholesterol ester transfer protein; chylomicron; LDL receptor; lecithin cholesterol acyl transferase; lipoprotein(a); lipoprotein lipase; microsomal transfer protein; propertin convertase subtilisin/ kexin type 9; SR-BI; phospholipid transfer protein; very low density lipoproteins (VLDL). Abstract 1695

show abstract

Insulin Acutely Inhibits Intestinal Lipoprotein Secretion in Humans in Part by Suppressing Plasma Free Fatty Acids

Cited by 87 publications

References 58 publications

Key intestinal genes involved in lipoprotein metabolism are downregulated in dyslipidemic men with insulin resistance

Key intestinal genes involved in lipoprotein metabolism are downregulated in dyslipidemic men with insulin resistance

Effects of Aerobic Exercise on Postprandial Carbohydrate and Lipoprotein Metabolism Following Cookie Ingestion in Healthy Young Women

Recent advances in physiological lipoprotein metabolism

Contact Info

Product

Resources

About