Intestinal lipoprotein overproduction in insulin-resistant states
Current Opinion in Lipidology, ISSN: 0957-9672, Vol: 19, Issue: 3, Page: 221-228
2008
- 112Citations
- 57Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations112
- Citation Indexes112
- 112
- CrossRef95
- Captures57
- Readers57
- 57
Review Description
PURPOSE OF REVIEW: Excessive postprandial lipemia is highly prevalent in obese and insulin-resistant/type 2 diabetic individuals and substantially increases the risk of atherosclerosis and cardiovascular disease. This article will review our current understanding of the link between insulin resistance and intestinal lipoprotein overproduction and highlight some of the key recent findings in the field. RECENT FINDINGS: Emerging evidence from several animal models of insulin resistance as well as insulin-resistant humans clearly supports the link between insulin resistance and aberrant intestinal lipoprotein metabolism. In insulin-resistant states, elevated free fatty acid flux into the intestine, downregulation of intestinal insulin signaling and upregulation of microsomal triglyceride transfer protein all appear to stimulate intestinal lipoprotein production. Gut peptides, GLP-1 and GLP-2, may be important regulators of intestinal lipid absorption and lipoprotein production. SUMMARY: Available evidence in humans and animal models strongly favors the concept that the small intestine is not merely an absorptive organ but rather plays an active role in regulating the rate of production of triglyceride-rich lipoproteins. Metabolic signals in insulin resistance and type 2 diabetes and in some cases an aberrant intestinal response to these factors all contribute to the enhanced formation and secretion of triglyceride-rich lipoproteins. © 2008 Lippincott Williams & Wilkins, Inc.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=43249119219&origin=inward; http://dx.doi.org/10.1097/mol.0b013e3282ffaf82; http://www.ncbi.nlm.nih.gov/pubmed/18460911; https://journals.lww.com/00041433-200806000-00002; http://content.wkhealth.com/linkback/openurl?sid=WKPTLP:landingpage&an=00041433-200806000-00002; https://dx.doi.org/10.1097/mol.0b013e3282ffaf82; https://insights.ovid.com/crossref?an=00041433-200806000-00002
Ovid Technologies (Wolters Kluwer Health)
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