title: Growth hormone ameliorates adipose dysfunction during oxidative stress and inflammation and improves glucose tolerance in obese mice.
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.
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fukushima
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Okamoto
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Katsumata
authors.affiliation: Division of Endocrinology, Diabetology and Atherosclerosis Medicine, Nippon Medical School Musashi-kosugi Hospital, Kawasaki, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ishikawa
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ishii
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Okamoto
authors.affiliation: Department of Bioregulation, Nippon Medical School, Kawasaki, Kanagawa, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Minami
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D002417:Cattle; D018149:Glucose Intolerance / Q000188:drug therapy / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D013006:Growth Hormone / Q000008:administration & dosage*; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D037181:Lectins, C-Type / Q000235:genetics / Q000276:immunology; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000235:genetics / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D009765:Obesity / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D011956:Receptors, Cell Surface / Q000235:genetics / Q000276:immunology
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D037181:Lectins, C-Type; D020738:Leptin; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D011956:Receptors, Cell Surface; D016753:Interleukin-10; C073294:growth hormone, bovine; D013006:Growth Hormone