This study was designed to examine the impact of AMPK deficiency on cardiac dysfunction following high fat feeding.
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.
Clearly, more work is required to understand the mechanism for lowering serum TG during high fat feeding.
The high fat diet had a lower FQ = 0.80 and RQ immediately dropped at the onset of high fat feeding to a value slightly higher than FQ.
Hence, these observations suggest that only after prolonged high fat feeding excess fat in the diet is stored in the form of adipose tissue.
