Hostname: page-component-8448b6f56d-c4f8m Total loading time: 0 Render date: 2024-04-18T02:06:08.913Z Has data issue: false hasContentIssue false

Successful lactation in leptin-deficient obese (ob/ob) mice

Published online by Cambridge University Press:  20 November 2017

C. H. Knight
Affiliation:
Hannah Research Institute, Ayr KA6 5HL, U.K.
E. Ong
Affiliation:
Hannah Research Institute, Ayr KA6 5HL, U.K.
R.G. Vernon
Affiliation:
Hannah Research Institute, Ayr KA6 5HL, U.K.
A. Sorensen
Affiliation:
Hannah Research Institute, Ayr KA6 5HL, U.K.
Get access

Extract

Mice lacking a functional leptin gene (ob/ob) are obese and sterile. Treatment with exogenous leptin will restore fertility and allow full-term pregnancy, but when leptin is withdrawn at parturition the young die, apparently as a result of total lactation failure (Chehab et al., 1996). From this one could hypothesise that leptin is an essential requirement for mammary development and/or initiation of milk secretion. Since a few of the mice used in this work were subsequently able to rear pups following a second pregnancy and parturition, we decided to re-examine this hypothesis.

Type
Theatre Presentations
Copyright
Copyright © The British Society of Animal Science 2002

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Chehab, F. F., Lim, M. E. and Lu, R. 1996. Correction of the sterility defect in homozygous obese female mice by treatment with the human recombinant leptin. Nature Genetics 12: 318320.CrossRefGoogle ScholarPubMed