Several humoral factors, such as
adiponectin and
urate, have been suggested to
affect metabolic syndromes. Previously, we reported a reduction in
blood adiponectin concentrations after a high-
fructose diet partially via the
vagus nerve in
rats. Although a lithogenic
diet (LD), i.e., supplementation of a normal control
diet (CT) with 0.6%
cholesterol and 0.2%
sodium cholate, reduced
blood adiponectin concentrations, the involvement of the
vagus nerve in this mechanism remains unclear. To estimate the involvement of the
vagus nerve in the
regulation of
blood adiponectin concentrations using an LD,
male imprinting control region
mice that had been vagotomized (HVx) or only laparotomized (Sham) were administered a CT or an LD for 10 weeks.
Serum adiponectin concentrations in the Sham-LD, HVx-CT, and HVx-LD groups were reduced by half compared with the Sham-CT group. The hepatic
mRNA levels of
fibroblast growth factor 21 (Fgf21), which reportedly stimulates
adiponectin secretion from
white adipose tissue, were lower in the LD groups compared with the CT groups. HepG2
hepatoma cells showed that various
bile acids reduced the
mRNA expression of FGF21. Moreover, the LD increased
serum urate concentrations and reduced hepatic expressions of the
acyl-CoA oxidase 1 (Acox1)
mRNA and
glucokinase, suggesting insufficient
regeneration of
ATP from AMP. In conclusion,
serum adiponectin concentration may be regulated via the
vagus nerve in normal
mice, whereas a reduction of hepatic Fgf21
mRNA by
bile acids may also lower
serum adiponectin levels. Moreover, the LD may promote hepatic AMP accumulation and subsequently increase the
serum urate concentration in
mice. (AU)