Energy Balances in Obese Mice

Abstract

According to most existing theories, the regulation of energy balance is achieved by control of energy intake. This study was undertaken to find out whether there was control of energy output as well. Food intake, energy balance and the feed efficiency of weanling female mice made obese with injections of gold-thioglucose and monosodium glutamate indicate that the obesity is primarily due to an increased energetic efficiency, and suggest that the hypothalamus plays a role in controlling energy output. In the case of treatment with MSG, a relative obesity was observed, i.e. an increase in body fat without any change in body weight. This indicates that the CNS centres for the regulation of body weight and body fat are probably not the same. It is suggested that MSG obesity will be a suitable model for comparative studies of body weight and the regulation of fat content. It is concluded that chemically induced obesity is due more to a lower metabolic rate than to an elevated food intake.

Effects of the neonatal treatment with monosodium glutamate on myenteric neurons and the intestine wall in the ileum of rats

“…Obesity from the neonatal administration of MSG may result from a general slowing down of the metabolism rather than from a higher food intake. 50 …”

Decreased lipolysis and enhanced glycerol and glucose utilization by adipose tissue prior to development of obesity in monosodium glutamate (MSG) treated-rats

“…3,4 Unlike obesity induced by gold thioglucose or bipiperidyl mustard which are associated with hyperphagia, obesity in neonatal MSG-treated rodents, is not a result of overeating. In mice, MSG obesity is associated with a doubling of metabolic ef®ciency, 5 secondary to the high level of corticosterone. 6 In MSG-treated rats high levels of corticosterone have also been described 7,8 and this is probably related to the central (via sympathetic nervous system) or directly suppresive effect of glucocorticoids on brown adipose tissue (BAT) activity.…”

Effect of Food Restriction on Energy Expenditure of Monosodium Glutamate-Induced Obese Rats

“…Different authors have suggested that MSG obesity could be the result of a lower metabolic rate rather than of elevated food intake [7][8][9][10] . In fact, we have found an increase in fat storages in MSG animals (around 140%), despite the reduction in food intake, which can be justified by the significant reduction in energy expenditure presented by these animals.…”

“…Different authors have shown that MSG obesity can be the consequence of low energy expenditure of the animals injected neonatally with MSG [7][8][9][10] . Decreases in interscapular brown adipose tissue (BAT) mitochondrial guanosine-5 -diphosphate binding and oxygen consumption in MSG-treated mice were described by Yoshioka et al [7,10] .…”