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Updated: Aug 6, 2026
Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
Published on: May 24, 2018
Development of obesity and neurochemical backing in aurothioglucose-treated mice
E Kishi1, A Takahashi, H Ishimaru
1Department of Neuropsychopharmacology (Tsumura), Gunma University School of Medicine, Maebashi, Japan.
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.
Insights
Aurothioglucose (ATG) causes obesity by damaging hypothalamic and brainstem areas, increasing serotonin and activating the paraventricular nucleus (PVN) during recovery, suggesting PVN dysfunction is key to obesity development.
Area of Science:
- Neuroscience
- Endocrinology
- Neurochemistry
Background:
- Aurothioglucose (ATG) is known to induce obesity in rodent models.
- The precise neurochemical mechanisms underlying ATG-induced obesity require further elucidation.
Purpose of the Study:
- To investigate the neurochemical basis of ATG-induced obesity in mice.
- To identify specific brain regions and neurotransmitter systems affected by ATG.
Main Methods:
- Histological examination of lesion sites in the hypothalamus and nucleus of the solitary tract (NTS).
- Measurement of hypothalamic neurotransmitters, including serotonin (5-HT), acetylcholine, norepinephrine, and dopamine.
- Assessment of c-Fos-like immunoreactivity (Fos-IR) to identify neuronal activation patterns.
Main Results:
- ATG induced tissue loss in the ventromedial hypothalamic nucleus (VMH), arcuate nucleus, and NTS.
- Hypothalamic serotonin levels increased post-ATG, while other measured neurotransmitters remained unchanged.
- Early Fos-IR was observed around lesion sites, with later increases in the paraventricular nucleus (PVN) during recovery.
Conclusions:
- ATG-induced obesity is not solely due to VMH destruction.
- Neuronal dysfunction and restoration processes involving the PVN are critical for obesity development.
- NTS lesions and altered 5-HT systems may transiently affect food intake post-ATG.
