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Related Experiment Videos

Is leptin a key factor which develops obesity by ovariectomy?

Kenju Shimomura1, Hiroyuki Shimizu, Takahumi Tsuchiya

  • 1First Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.

Endocrine Journal
|October 31, 2002
PubMed
Summary

Ovariectomy increases adiposity by reducing leptin levels, contributing to obesity. Leptin supplementation mitigates some weight gain, suggesting its crucial role in estrogen withdrawal-induced obesity.

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Area of Science:

  • Endocrinology
  • Obesity Research
  • Reproductive Biology

Background:

  • Estrogen withdrawal via ovariectomy is linked to increased adiposity.
  • Decreased circulating leptin levels, a product of the ob gene, accompany ovariectomy and may contribute to obesity.
  • Leptin is known to inhibit food intake.

Purpose of the Study:

  • To investigate the role of reduced circulating leptin in ovariectomy-induced obesity.
  • To examine body weight changes in leptin-deficient obese mice after ovariectomy with leptin supplementation.

Main Methods:

  • Genetically obese (ob/ob) mice and lean littermates were used.
  • Obese mice received recombinant mouse leptin supplementation prior to surgery.
  • Mice underwent bilateral ovariectomy, and body weight changes were monitored for 56 days.

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Main Results:

  • Ovariectomy significantly increased body weight in lean mice without leptin treatment starting at 16 days post-operation.
  • Leptin-treated obese mice showed significant body weight gain from 44 days after ovariectomy.
  • Ovariectomy increased retroperitoneal white adipose tissue in lean mice but not in leptin-treated obese mice.

Conclusions:

  • Reduced circulating leptin levels play a significant role in the acute phase of ovariectomy-induced body weight gain.
  • During the static phase, estrogen withdrawal effects on body weight may occur independently of leptin-mediated effects.