Abstract
Patients with adult growth hormone deficiency exhibit visceral fat accumulation, which
gives rise to a cluster of metabolic disorders such as impaired glucose tolerance
and dyslipidemia. Plasma growth hormone levels are lower in obese patients with metabolic
syndrome than in healthy subjects. Here we examined the hypothesis that exogenous
growth hormone administration regulates function of adipose tissue to improve glucose
tolerance in diet-induced obese mice. Twelve-week-old obese male C57BL/6 J mice received
bovine growth hormone daily for 6 weeks. In epididymal fat, growth hormone treatment
antagonized diet-induced changes in the gene expression of adiponectin, leptin, and
monocyte chemoattractant protein-1, and significantly increased the gene expression
of interleukin-10 and CD206. Growth hormone also suppressed the accumulation of oxidative
stress marker, thiobarbituric acid-reactive substances, in the epididymal fat and
enhanced the gene expression of anti-oxidant enzymes. Moreover, growth hormone significantly
restored glucose tolerance in obese mice. In cultured 3T3-L1 adipocytes, growth hormone
prevented the decline in adiponectin gene expression in the presence of hydrogen peroxide.
These results suggest that growth hormone administration ameliorates glucose intolerance
in obese mice presumably by decreasing adipose mass, oxidative stress, and chronic
inflammation in the visceral fat.
Key words
growth hormone - adipose tissue - oxidative stress - inflammation - adiponectin -
glucose tolerance
