Investigations into the induction and effects of obesity in various murine models

There is at present much concern over the increased
incidence of obesity in modern society. An increased
energy intake and/or a decreased energy expenditure will
lead to obesity. Murine models have been used to study the
normal fat deposition during growth and excess fat
deposition of obesity.
Investigation of adipose depots during growth suggested
that for the two strains of mice and the C57B1/6 ob/ob mice
studied, the subcutaneous depot was the prominent fat store
at weaning and that the proportion of fat in this depot
decreased whilst that in the gonadal depot increased with
age. Adult ob/ob mice had a large proportion of their fat
stored subcutaneously although weight-reduction of male
ob/ob mice resulted in a decrease in this depot size.
Goldthioglucose and Bipiperidyl mustard have been used to
induce obesity in mice. The results suggest this syndrome
to be due to a metabolic defect since hyperphagia,
hyperinsulinaemia and weight gains, the characteristic
features of a regulatory defect were found to be
diet-dependent and not essential for obesity-induction. It
was demonstrated that the ventromedial hypothalamus
regulated the total fat stores but not the fat content of
each depot.
The genetically-obese(ob/ob) syndrome was confirmed to be
due to both hyperphagia and a reduced energy expenditure.
These mice had a reduced feeding drive on fasting and they
protected their excess fat stores(on fasting) by
proteinolysis. Weight-reduction by meal-feeding did not
decrease the proportion of fat as markedly in ob/ob mice as
in chemically-obese mice. The weight-reduced ob/ob mice
displayed a better cold tolerance(3°) than control ob/obs.
The ob/ob mice had lower rectal temperatures at ambient
temperature and, on fasting displayed a greater incidence
of torpor and a slower rate of arousal than their lean
littermates. Further, ob/ob mice exhibited torpor even
when fed ad libitum. The experiments suggest that energy
expenditure and control of lipid deposition is at least as
important in the aetiology of obesity as regulation of
energy intake.

This thesis supplied via ROAR to UEL-registered users is protected by copyright and other intellectual property rights, and duplication of any part of the material is not permitted, except for your personal use for the purposes of non-commercial research and private study in electronic or print form. You must obtain permission from the copyright-holder for any other use. Electronic or print copies may not be offered, for sale or otherwise, to anyone. No quotation from the thesis may be published without proper acknowledgement.