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The mechanisms underlying these alterations include a twofold increase compared with wild-type mice in tissue glycogen storage during the fed state, a 40% reduction in hepatic glucose production in the fasted state, and a 27-fold increase in de novo fatty acid synthesis in liver during the fed state. Thus, the inability to store energy in adipose tissue in the fld mouse leads to a compensatory increase in glycogen storage for use during the fasting period and reliance upon hepatic fatty acid synthesis to provide fuel for peripheral tissues during the fed state. The increase in hepatic fatty acid synthesis and peripheral utilization provides a potential mechanism to ameliorate fatty liver in the fld that would otherwise occur as a consequence of adipose tissue dysfunction.<\/jats:p>","DOI":"10.2337\/db06-0260","type":"journal-article","created":{"date-parts":[[2006,11,28]],"date-time":"2006-11-28T02:41:20Z","timestamp":1164681680000},"page":"3429-3438","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":41,"title":["Lipin Deficiency Impairs Diurnal Metabolic Fuel Switching"],"prefix":"10.2337","volume":"55","author":[{"given":"Jun","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Medicine, State University of New York at Stony Brook, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.N. 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