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Pharmacologic manipulation of ob expression in a dietary model of obesity.

Publication ,  Journal Article
Collins, S; Surwit, RS
Published in: J Biol Chem
April 19, 1996

Mutation of the obese (ob) gene results in severe hereditary obesity and diabetes in the C57BL/6J and related strains of mice. In this study we examined the expression of the ob gene in a dietary model in which moderate obesity develops in response to fat (58% of calories from fat) without mutation of the ob gene, and in four genetic models of obesity in mice: ob/ob, db/db, tubby, and fat. Several white and brown adipose depots were examined (epididymal, subcutaneous, perirenal, and interscapular). Northern blot analysis shows that levels of ob mRNA are increased in all adipose depots examined in every model of obesity. The average fold increases were 12.0 +/ 2.1 (ob/ob), 4.8 +/- 1.5 (db/db), 2.8 +/- 0.1 (tubby), 2.4 +/- 0.3 (fat), and 2.1 +/- 0.2 (high fat diet-induced A/J). Moreover, we found that the expression of the ob gene could be manipulated by pharmacologically blocking the development of diet-induced obesity. Supplementation of a high fat diet with a beta 3-adrenergic receptor agonist (CL316,243) prevented obesity, but not hyperphagia associated with high fat feeding (body weights of high fat-fed A/J mice = 34.0 +/- 1.0 g; high fat plus CL316,243-fed mice = 26.8 +/- 0.5 g; n = 10). CL316,243-treated, high fat-fed animals contained levels of ob mRNA in all adipose depots that were equal to or less than levels in low fat-fed mice (average levels in high fat plus CL316,243-fed mice relative to low fat-fed mice: 0.93 +/- 0.09). Inasmuch as fat cell size, but not number, was increased in a previous study in diet-induced obese A/J mice, these results indicate that expression of the ob gene serves as a sensor of fat cell hypertrophy, independent of any effects on food intake.

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Published In

J Biol Chem

DOI

ISSN

0021-9258

Publication Date

April 19, 1996

Volume

271

Issue

16

Start / End Page

9437 / 9440

Location

United States

Related Subject Headings

  • Species Specificity
  • RNA, Messenger
  • Proteins
  • Protein Biosynthesis
  • Polymerase Chain Reaction
  • Organ Specificity
  • Obesity
  • Molecular Sequence Data
  • Mice, Obese
  • Mice, Inbred C57BL
 

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Collins, S., & Surwit, R. S. (1996). Pharmacologic manipulation of ob expression in a dietary model of obesity. J Biol Chem, 271(16), 9437–9440. https://doi.org/10.1074/jbc.271.16.9437
Collins, S., and R. S. Surwit. “Pharmacologic manipulation of ob expression in a dietary model of obesity.J Biol Chem 271, no. 16 (April 19, 1996): 9437–40. https://doi.org/10.1074/jbc.271.16.9437.
Collins S, Surwit RS. Pharmacologic manipulation of ob expression in a dietary model of obesity. J Biol Chem. 1996 Apr 19;271(16):9437–40.
Collins, S., and R. S. Surwit. “Pharmacologic manipulation of ob expression in a dietary model of obesity.J Biol Chem, vol. 271, no. 16, Apr. 1996, pp. 9437–40. Pubmed, doi:10.1074/jbc.271.16.9437.
Collins S, Surwit RS. Pharmacologic manipulation of ob expression in a dietary model of obesity. J Biol Chem. 1996 Apr 19;271(16):9437–9440.

Published In

J Biol Chem

DOI

ISSN

0021-9258

Publication Date

April 19, 1996

Volume

271

Issue

16

Start / End Page

9437 / 9440

Location

United States

Related Subject Headings

  • Species Specificity
  • RNA, Messenger
  • Proteins
  • Protein Biosynthesis
  • Polymerase Chain Reaction
  • Organ Specificity
  • Obesity
  • Molecular Sequence Data
  • Mice, Obese
  • Mice, Inbred C57BL