FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2058555764> ?p ?o ?g. }

• W2058555764 endingPage "19" @default.
• W2058555764 startingPage "1" @default.
• W2058555764 abstract "Insulin resistant states are commonly associated with an atherogenic dyslipidemia that contributes to significantly higher risk of atherosclerosis and cardiovascular disease. Indeed, disorders of carbohydrate and lipid metabolism co-exist in the majority of subjects with the “metabolic syndrome” and form the basis for the definition and diagnosis of this complex syndrome. The most fundamental defect in these patients is resistance to cellular actions of insulin, particularly resistance to insulin-stimulated glucose uptake. Insulin insensitivity appears to cause hyperinsulinemia, enhanced hepatic gluconeogenesis and glucose output, reduced suppression of lipolysis in adipose tissue leading to a high free fatty acid flux, and increased hepatic very low density lipoprotein (VLDL) secretion causing hypertriglyceridemia and reduced plasma levels of high density lipoprotein (HDL) cholesterol. Although the link between insulin resistance and dysregulation of lipoprotein metabolism is well established, a significant gap of knowledge exists regarding the underlying cellular and molecular mechanisms. Emerging evidence suggests that insulin resistance and its associated metabolic dyslipidemia result from perturbations in key molecules of the insulin signaling pathway, including overexpression of key phosphatases, downregulation and/or activation of key protein kinase cascades, leading to a state of mixed hepatic insulin resistance and sensitivity. These signaling changes in turn cause an increased expression of sterol regulatory element binding protein (SREBP) 1c, induction of de novo lipogensis and higher activity of microsomal triglyceride transfer protein (MTP), which together with high exogenous free fatty acid (FFA) flux collectively stimulate the hepatic production of apolipoprotein B (apoB)-containing VLDL particles. VLDL overproduction underlies the high triglyceride/low HDL-cholesterol lipid profile commonly observed in insulin resistant subjects." @default.
• W2058555764 created "2016-06-24" @default.
• W2058555764 creator A5030295153 @default.
• W2058555764 creator A5051320270 @default.
• W2058555764 creator A5058472174 @default.
• W2058555764 date "2006-06-01" @default.
• W2058555764 modified "2023-10-01" @default.
• W2058555764 title "Lipid and lipoprotein dysregulation in insulin resistant states" @default.
• W2058555764 cites W1480986665 @default.
• W2058555764 cites W1493788388 @default.
• W2058555764 cites W1498897377 @default.
• W2058555764 cites W1499420960 @default.
• W2058555764 cites W1501152217 @default.
• W2058555764 cites W1512072195 @default.
• W2058555764 cites W1525497997 @default.
• W2058555764 cites W1539281575 @default.
• W2058555764 cites W1547466369 @default.
• W2058555764 cites W1561809228 @default.
• W2058555764 cites W1564372585 @default.
• W2058555764 cites W1568792804 @default.
• W2058555764 cites W1577300587 @default.
• W2058555764 cites W1591823948 @default.
• W2058555764 cites W1599366995 @default.
• W2058555764 cites W1697523131 @default.
• W2058555764 cites W179857658 @default.
• W2058555764 cites W1820484722 @default.
• W2058555764 cites W1836112660 @default.
• W2058555764 cites W1887621239 @default.
• W2058555764 cites W1921601722 @default.
• W2058555764 cites W1936800019 @default.
• W2058555764 cites W1956183677 @default.
• W2058555764 cites W1964240864 @default.
• W2058555764 cites W1964558072 @default.
• W2058555764 cites W1965371391 @default.
• W2058555764 cites W1966499699 @default.
• W2058555764 cites W1968284284 @default.
• W2058555764 cites W1968304085 @default.
• W2058555764 cites W1969292983 @default.
• W2058555764 cites W1973024955 @default.
• W2058555764 cites W1973630137 @default.
• W2058555764 cites W1975276753 @default.
• W2058555764 cites W1975388439 @default.
• W2058555764 cites W1975459913 @default.
• W2058555764 cites W1977128714 @default.
• W2058555764 cites W1978667085 @default.
• W2058555764 cites W1980828966 @default.
• W2058555764 cites W1983526815 @default.
• W2058555764 cites W1986310189 @default.
• W2058555764 cites W1986503794 @default.
• W2058555764 cites W1986917180 @default.
• W2058555764 cites W1989324173 @default.
• W2058555764 cites W1989719065 @default.
• W2058555764 cites W1990953214 @default.
• W2058555764 cites W1991735443 @default.
• W2058555764 cites W1993501237 @default.
• W2058555764 cites W1993702135 @default.
• W2058555764 cites W1994597386 @default.
• W2058555764 cites W1995283486 @default.
• W2058555764 cites W1995370334 @default.
• W2058555764 cites W1995588427 @default.
• W2058555764 cites W2000623239 @default.
• W2058555764 cites W2000973674 @default.
• W2058555764 cites W2001112180 @default.
• W2058555764 cites W2003659422 @default.
• W2058555764 cites W2004462369 @default.
• W2058555764 cites W2010291284 @default.
• W2058555764 cites W2012079492 @default.
• W2058555764 cites W2012514869 @default.
• W2058555764 cites W2012663527 @default.
• W2058555764 cites W2012741873 @default.
• W2058555764 cites W2013408977 @default.
• W2058555764 cites W2014318859 @default.
• W2058555764 cites W2017058300 @default.
• W2058555764 cites W2018715171 @default.
• W2058555764 cites W2018950721 @default.
• W2058555764 cites W2019066384 @default.
• W2058555764 cites W2020659754 @default.
• W2058555764 cites W2022005733 @default.
• W2058555764 cites W2022232240 @default.
• W2058555764 cites W2022567777 @default.
• W2058555764 cites W2023612431 @default.
• W2058555764 cites W2025577409 @default.
• W2058555764 cites W2026784736 @default.
• W2058555764 cites W2028782957 @default.
• W2058555764 cites W2030510579 @default.
• W2058555764 cites W2030612875 @default.
• W2058555764 cites W2030905678 @default.
• W2058555764 cites W2031026183 @default.
• W2058555764 cites W2031484324 @default.
• W2058555764 cites W2033167203 @default.
• W2058555764 cites W2033429522 @default.
• W2058555764 cites W2033531132 @default.
• W2058555764 cites W2034299473 @default.
• W2058555764 cites W2034476706 @default.
• W2058555764 cites W2034767967 @default.
• W2058555764 cites W2035226271 @default.
• W2058555764 cites W2037379679 @default.
• W2058555764 cites W2039592725 @default.

• next