title: Development of obesity and neurochemical backing in aurothioglucose-treated mice.
abstract: To clarify the neurochemical backing of aurothioglucose (ATG)-induced obesity in mice, we investigated lesion sites, hypothalamic neurotransmitters and c-Fos-like immunoreactivity (Fos-IR). At day 2 after ATG, tissue loss or cells death was observed in several parts of the ventral area of the ventromedial hypothalamic nucleus (VMH), and the dorsal area of arcuate nucleus and in the nucleus of the solitary tract (NTS). However, the greater part of the VMH was retained. Body weight began to increase in week 1. Hypothalamic serotonin (5-HT) and the metabolites were increased at day 2. The contents of acetylcholine, norepinephrine and dopamine in the hypothalamus showed no significant change. In week 1, the area shown tissue loss was compacted and plugged up. In the control group, most obvious c-Fos-like immunoreactive region was paraventricular nucleus (PVN). At day 2, Fos-IR was observed around destroyed regions in the hypothalamus and NTS, but few Fos-IR was found in the other regions including PVN. The Fos-IR around destroyed regions diminished after week 1. In week 3, Fos-IR in the PVN increased. These results suggest that the development of ATG-induced obesity cannot be attributed to solely VMH destruction. The restoration processes of the neuronal dysfunction involving PVN seem to play an important role in the development of obesity. NTS lesion and 5-HT system might contribute to decrease in food intake for several days after ATG.
authors.affiliation: Department of Neuropsychopharmacology (Tsumura), Gunma University School of Medicine, Maebashi, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Kishi
authors.forename: A
authors.initials: A
authors.lastname: Takahashi
authors.forename: H
authors.initials: H
authors.lastname: Ishimaru
authors.forename: Y
authors.initials: Y
authors.lastname: Ikarashi
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000032:analysis; D000109:Acetylcholine / Q000032:analysis; D000818:Animals; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000032:analysis; D018501:Antirheumatic Agents; D006051:Aurothioglucose; D001923:Brain Chemistry / Q000502:physiology*; D003561:Cytarabine / Q000032:analysis; D003630:Daunorubicin / Q000032:analysis; D006719:Homovanillic Acid / Q000032:analysis; D006897:Hydroxyindoleacetic Acid / Q000032:analysis; D008297:Male; D015122:Mercaptopurine / Q000032:analysis; D051379:Mice; D009638:Norepinephrine / Q000032:analysis; D009765:Obesity / Q000139:chemically induced / Q000503:physiopathology*; D010286:Paraventricular Hypothalamic Nucleus / Q000737:chemistry; D011239:Prednisolone / Q000032:analysis; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis; D012701:Serotonin / Q000032:analysis; D017552:Solitary Nucleus / Q000737:chemistry; D014697:Ventromedial Hypothalamic Nucleus / Q000737:chemistry; D014750:Vincristine / Q000032:analysis
chemical_list: D018501:Antirheumatic Agents; D016760:Proto-Oncogene Proteins c-fos; D003561:Cytarabine; D015102:3,4-Dihydroxyphenylacetic Acid; D006051:Aurothioglucose; D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014750:Vincristine; D011239:Prednisolone; D015122:Mercaptopurine; D000109:Acetylcholine; D009638:Norepinephrine; D006719:Homovanillic Acid; D003630:Daunorubicin