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Oleate oxidation by muscle homogenates was increased by high fat feeding and decreased by iron deficiency despite high fat feeding.
We examined the effect of high fat feeding on the expression of Fto in hypothalamic nuclei.
High fat feeding resulted in defects in both whole body and hepatic glucose metabolism.
High fat feeding did not affect the PGC1α content in TA muscle.
Over the duration of high fat feeding, glucose tolerance became increasingly impaired (Figure 2E-H).
These results indicate that Genz-112638 largely prevented the development of hepatic steatosis caused by high fat feeding.
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LPL mRNA expression was unchanged by high fat-feeding, confirming previous observations [31].
Interestingly, short-term high-fat chow caused similar bone loss as extended high-fat feeding.
To assess whether high-fat feeding modulated hepatic lipid secretion, we determined VLDL-TG production rates.
During high-fat feeding depot-dependent differences in hyperplasia and hypertrophy are observed [13].
Hepatic lipids are generally considered to be supplied from extra-hepatic lipids under high-fat feeding.
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