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Effects of parabiosis of obese with diabetes and normal mice

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  • Published: August 1973
  • Volume 9, pages 294–298, (1973)
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Effects of parabiosis of obese with diabetes and normal mice
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  • D. L. Coleman1 
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Parabiosis of obese (ob/ob) with diabetes (db 2J/db2J) mice caused the obese partner to become hypoglycemic, to lose weight and to die of starvation, while no abnormal changes were observed in the diabetes partner. The striking similarity of this response to that observed in normal mice in parabiosis with diabetes mice suggests that obese mice are like normal mice in having normal satiety centers sensitive to the satiety factor produced by the diabetes partner. In contrast, parabiosis of obese with normal mice is a fully viable combination suggesting that the obese partner does not produce sufficient satiety factor to turn off the normal partner's eating drive. However, obese mice in parabiosis with normal mice gain weight less rapidly and eat less than obese mice in parabiosis with obese mice. These observations suggest that some humoral factor is provided by the normal partner that regulates food consumption in the obese partner. To explain the identical obese-hyperglycemic syndromes produced by these two unrelated and separate genes when on identical genetic backgrounds, it is postulated that the obese mouse is unable to produce sufficient satiety factor to regulate its food consumption, whereas the diabetes mouse produces satiety factor, but cannot respond to it because of a defective satiety center.

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References

  1. Chlouverakis, C.: Insulin resistance of parabiotic obese-obob. Horm. Metab. Res.4, 143–148 (1972).

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  2. Coleman, D.L., Hummel, K.P.: Studies with the mutation, diabetes, in the mouse. Diabetologia3, 238–248 (1967).

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  3. Coleman, D.L., Hummel, K.P.: Effects of parabiosis of normal with genetically diabetic mice. Amer. J. Physiol.217, 1298–1304 (1969).

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  4. Coleman, D.L., Hummel, K.P.: The influence of genetic background on the expression of the obese (ob) gene in the mouse. Diabetologia,9, 287–293 (1973).

    Google Scholar 

  5. Haessler, H.A., Crawford, J.D.: Alterations in the fatty acid composition of depot fat associated with obesity. Ann. N. Y. Acad. Sci.131, 476–484 (1965).

    Google Scholar 

  6. Hausberger, F.X.: Parabiosis and transplantation experiments in hereditary obese mice. Anat. Rec.130, 313 abstr. (1958).

    Google Scholar 

  7. Hummel, K.P., Coleman, D.L., Lane, P.W.: The influence of genetic background on expression of mutations at the diabetes locus in the mouse. Biochem. Genet.7, 1–13 (1972).

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  8. Strautz, R.L.: Studies of hereditary-obese mice (obob) after implantation of pancreatic islets in millipore filter capsules. Diabetologia6, 306–312 (1970).

    Google Scholar 

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Author information

Authors and Affiliations

  1. The Jackson Laboratory, 04609, Bar Harbor, Maine, USA

    D. L. Coleman

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  1. D. L. Coleman
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Additional information

Supported in part by NIH Research Grant AM 14461 from the National Institute of Arthritis, Metabolism, and Digestive Diseases and by an allocation from the South Waite Foundation.

The Jackson Laboratory is fully accredited by the American Association for Accreditation of Laboratory Animal Care.

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Coleman, D.L. Effects of parabiosis of obese with diabetes and normal mice. Diabetologia 9, 294–298 (1973). https://doi.org/10.1007/BF01221857

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  • Received: 01 March 1973

  • Accepted: 10 April 1973

  • Issue date: August 1973

  • DOI: https://doi.org/10.1007/BF01221857

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Key words

  • Parabiosis
  • obese mice
  • diabetes mice
  • satiety factor
  • satiety center
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