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Title[redir]:
Current Opinion in Lipidology
Description:
s in insulin signaling have allowed us, for the first time, to dissect which features of the metabolic syndrome can be caused by insulin resistance. Recent findings Liver insulin receptor knockout mice show that hepatic insulin resistance can produce hyperglycemia, increased apolipoprotein B secretion and atherosclerosis, and increased biliary cholesterol secretion and cholesterol gallstones. Many of these changes may be due to disinhibition of the transcription factor, forkhead box O1. Yet, neither liver insulin receptor knockout mice nor humans with insulin receptor mutations develop the hypertriglyceridemia or hepatic steatosis associated with the metabolic syndrome. Summary These data point to a central role for insulin resistance in the pathogenesis of the metabolic syndrome, as hyperglycemia, atherosclerosis, and cholesterol gallstones can all be caused by insulin resistance. However, hypertriglyceridemia and hepatic steatosis are not due directly to insulin resistance and should be considered pathogenically distinct features of the metabolic syndrome....
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Keywords {🔍}
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journal authors submit full text access forkhead box o1 artificial intelligence training etoc alerts hepatic insulin resistance service request 800-638-3030 register subscribe recent studies individual subscribers log journal tables issue insulin resistance insulin signaling increased apolipoprotein website subscribe journal mice cholesterol gallstones center submit hepatic steatosis metabolic syndrome cohn dissecting joel ta sudha ba 20 years ago great deal genetic defects transcription factor data point email inbox rights reserved data mining central role produce hyperglycemia due directly authors content features secretion log subscribers text role due hyperglycemia edited jeffrey biddinger lipidology 20
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