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Moreover, de novo lipogenesis is not induced upon a short-term dietary fat challenge in human subjects [24], [25].
Absence of TLR4 also modestly improved systemic insulin sensitivity in female mice upon high fat challenge, presumably through reduced production of proinflammatory cytokines in liver and adipose tissue.
Wood and colleagues determined dietary modification modulates airway inflammation in an acute high fat challenge, but no studies have reported chronic diet and the airway inflammatory response.
Among other studies, one in which healthy men were subjected to a water test and a 6-h fat challenge showed that after the fat challenge, neutrophil counts and activation of monocytes and neutrophils were increased compared with values after the water test (23).
Moreover, increases in postprandial CRP have been reported after OGTT [ 30] and OLTT [ 15] challenges, whereas other studies did not observe significant differences in CRP after a high fat challenge [ 17, 27, 31].
Although there have been numerous studies of the effects of combination therapy with fibrates and statins on fasting plasma lipids (13– 17, 28) and the effects of fibrate monotherapy on PP TG levels after a standardized fat challenge (29, 30), there have been no studies comparing PP TG levels with fibrate plus statin to statin alone.
Recent animal studies have found that high-fat challenges recruit inflammatory cells [ 38], but only one human study has found increased neutrophils in the postprandial period in healthy control subjects [ 17].
As assessed by the structure model index, bone microarchitecture changed from plate- to rod-like appearance upon high-fat challenge.
These unique data highlight that a chronic high-fat challenge has crucial effects on the severity of the Enpp1−/− bone phenotype.
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