Impairment of sympathoadrenomedullar system has been suggested to have a role in obesity. The activity of adrenal medullae (AM) isolated from 90-day-old obese-induced L-monosodium glutamate (MSG) male mice was studied. MSG treatment induced obesity without hyperphagia, while MSG-animals were shorter and lighter than the controls. Catecholamines (CA) gland content decreased in MSG-mice, while secretory response to carbachol was similar in isolated AM of both groups. However, high extracellular potassium did not stimulate CA secretion on AM isolated from obese animals as occurred in controls. Cholinesterase activity of adrenal glands homogenate was impaired in MSG-mice. Results suggest that MSG-hypothalamus lesions could cause impairment of sympathetic transmission in AM, which impose less CA accumulation and alter secretion response in AM. These defects might be involved at the onset of MSG obesity.
No takes yet. Share an insight, caveat, or question.
Borges et al. (2001) studied this question.