Europe PMC

This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our privacy notice and cookie policy.

Expression of ob mRNA and its encoded protein in rodents. Impact of nutrition and obesity.

Author information

Affiliations

  • 1. Division of Endocrinology, Beth Israel Hospital (Research North), Boston, Massachusetts 02215, USA.
      Authors
    • Frederich RC 1
    (1 author)

The Journal of Clinical Investigation, 01 Sep 1995, 96(3):1658-1663
https://doi.org/10.1172/jci118206 PMID: 7657836 PMCID: PMC185793

Free full text in Europe PMC

Abstract 

The mutant gene responsible for obesity in the ob/ob mouse was recently identified by positional cloning (Zhang Y., R. Proenca, M. Maffel, M. Barone, L. Leopold, and J.M. Friedman. 1994. Nature (Lond.) 372:425). The encoded protein and to represent and "adipostat" signal reflecting the state of energy stores. We confirm that the adipocyte is the source of ob mRNA and that the predicted 16-kD ob protein is present in rodent serum as detected by Western blot. To evaluate the hypothesis that it might represent an adipostat, we assessed serum levels of ob protein and expression of ob mRNA in adipose cells and tissue of rodents in response to a variety of perturbations which effect body fat mass. Both ob protein and ob mRNA expression are markedly increased in obesity. The levels of ob protein are approximately 5-10-fold elevated in serum of db/db mice, in mice with hypothalamic lesions caused by neonatal administration of monosodium glutamate (MSG), and in mice with toxigene induced brown fat ablation, (UCP-DTA). Very parallel changes are observed in adipocyte ob mRNA expression in these models and in ob/ob mice. As predicted however, no serum ob protein could be detected in the ob/ob mice. By contrast to obesity, starvation of normal rats and mice for 1-3 d markedly suppresses ob mRNA abundance, and this is reversed with refeeding. Similarly, ob protein concentration in normal mice falls to undetectable levels with starvation. In the ob/ob, UCP-DTA and MSG models, overexpression of ob mRNA is reversed by caloric restriction. These data support the hypothesis that expression of ob mRNA and protein are regulated as a function of energy stores, and that ob serves as a circulating feedback signal to sites involved in regulation of energy homeostasis.

Free full text 

Logo of jcinvestThe Journal of Clinical Investigation
J Clin Invest. 1995 Sep; 96(3): 1658–1663.
PMCID: PMC185793
PMID: 7657836

Expression of ob mRNA and its encoded protein in rodents. Impact of nutrition and obesity.

R C Frederich, B Löllmann, A Hamann, A Napolitano-Rosen, B B Kahn, B B Lowell, and J S Flier
Author information Copyright and License information Disclaimer

Abstract

The mutant gene responsible for obesity in the ob/ob mouse was recently identified by positional cloning (Zhang Y., R. Proenca, M. Maffel, M. Barone, L. Leopold, and J.M. Friedman. 1994. Nature (Lond.) 372:425). The encoded protein and to represent and "adipostat" signal reflecting the state of energy stores. We confirm that the adipocyte is the source of ob mRNA and that the predicted 16-kD ob protein is present in rodent serum as detected by Western blot. To evaluate the hypothesis that it might represent an adipostat, we assessed serum levels of ob protein and expression of ob mRNA in adipose cells and tissue of rodents in response to a variety of perturbations which effect body fat mass. Both ob protein and ob mRNA expression are markedly increased in obesity. The levels of ob protein are approximately 5-10-fold elevated in serum of db/db mice, in mice with hypothalamic lesions caused by neonatal administration of monosodium glutamate (MSG), and in mice with toxigene induced brown fat ablation, (UCP-DTA). Very parallel changes are observed in adipocyte ob mRNA expression in these models and in ob/ob mice. As predicted however, no serum ob protein could be detected in the ob/ob mice. By contrast to obesity, starvation of normal rats and mice for 1-3 d markedly suppresses ob mRNA abundance, and this is reversed with refeeding. Similarly, ob protein concentration in normal mice falls to undetectable levels with starvation. In the ob/ob, UCP-DTA and MSG models, overexpression of ob mRNA is reversed by caloric restriction. These data support the hypothesis that expression of ob mRNA and protein are regulated as a function of energy stores, and that ob serves as a circulating feedback signal to sites involved in regulation of energy homeostasis.

Full text

Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.5M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.
 
icon of scanned page 1658
1658
icon of scanned page 1659
1659
icon of scanned page 1660
1660
icon of scanned page 1661
1661
icon of scanned page 1662
1662
icon of scanned page 1663
1663
 

Images in this article

Image
Image
on p.1659
Image
Image
on p.1660
Image
Image
on p.1660
Image
Image
on p.1660
Image
Image
on p.1661
Image
Image
on p.1661
Image
Image
on p.1662
Click on the image to see a larger version.

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Flier JS. The adipocyte: storage depot or node on the energy information superhighway? Cell. 1995 Jan 13;80(1):15–18. [Abstract] [Google Scholar]
  • Weigle DS. Appetite and the regulation of body composition. FASEB J. 1994 Mar 1;8(3):302–310. [Abstract] [Google Scholar]
  • Hervey GR. Regulation of energy balance. Nature. 1969 May 17;222(5194):629–631. [Abstract] [Google Scholar]
  • Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature. 1994 Dec 1;372(6505):425–432. [Abstract] [Google Scholar]
  • Lowell BB, S-Susulic V, Hamann A, Lawitts JA, Himms-Hagen J, Boyer BB, Kozak LP, Flier JS. Development of obesity in transgenic mice after genetic ablation of brown adipose tissue. Nature. 1993 Dec 23;366(6457):740–742. [Abstract] [Google Scholar]
  • Djazayery A, Miller DS, Stock MJ. Energy balances in obese mice. Nutr Metab. 1979;23(5):357–367. [Abstract] [Google Scholar]
  • Lowell BB, Napolitano A, Usher P, Dulloo AG, Rosen BS, Spiegelman BM, Flier JS. Reduced adipsin expression in murine obesity: effect of age and treatment with the sympathomimetic-thermogenic drug mixture ephedrine and caffeine. Endocrinology. 1990 Mar;126(3):1514–1520. [Abstract] [Google Scholar]
  • Kahn BB, Cushman SW. Mechanism for markedly hyperresponsive insulin-stimulated glucose transport activity in adipose cells from insulin-treated streptozotocin diabetic rats. Evidence for increased glucose transporter intrinsic activity. J Biol Chem. 1987 Apr 15;262(11):5118–5124. [Abstract] [Google Scholar]
  • Flier JS, Cook KS, Usher P, Spiegelman BM. Severely impaired adipsin expression in genetic and acquired obesity. Science. 1987 Jul 24;237(4813):405–408. [Abstract] [Google Scholar]
  • Kahn BB, Charron MJ, Lodish HF, Cushman SW, Flier JS. Differential regulation of two glucose transporters in adipose cells from diabetic and insulin-treated diabetic rats. J Clin Invest. 1989 Aug;84(2):404–411. [Europe PMC free article] [Abstract] [Google Scholar]
  • Coleman DL. Effects of parabiosis of obese with diabetes and normal mice. Diabetologia. 1973 Aug;9(4):294–298. [Abstract] [Google Scholar]
  • Cleary MP, Brasel JA, Greenwood MR. Developmental changes in thymidine kinase, DNA, and fat cellularity in Zucker rats. Am J Physiol. 1979 May;236(5):E508–E513. [Abstract] [Google Scholar]
  • Kahn BB, Simpson IA, Cushman SW. Divergent mechanisms for the insulin resistant and hyperresponsive glucose transport in adipose cells from fasted and refed rats. Alterations in both glucose transporter number and intrinsic activity. J Clin Invest. 1988 Aug;82(2):691–699. [Europe PMC free article] [Abstract] [Google Scholar]
  • Tokuyama K, Himms-Hagen J. Brown adipose tissue thermogenesis, torpor, and obesity of glutamate-treated mice. Am J Physiol. 1986 Oct;251(4 Pt 1):E407–E415. [Abstract] [Google Scholar]
Articles from The Journal of Clinical Investigation are provided here courtesy of American Society for Clinical Investigation

Full text links 

Read article at publisher's site: https://doi.org/10.1172/jci118206

Read article for free, from open access legal sources, via Unpaywall: http://www.jci.org/articles/view/118206/files/pdfUnpaywall

Citations & impact 

Impact metrics

317
Citations
Jump to Citations
1
Data citation
Jump to Data

Citations of article over time

Alternative metrics

Altmetric item for https://www.altmetric.com/details/41655745
Altmetric
Discover the attention surrounding your research
https://www.altmetric.com/details/41655745

Smart citations by scite.ai
Smart citations by scite.ai include citation statements extracted from the full text of the citing article. The number of the statements may be higher than the number of citations provided by EuropePMC if one paper cites another multiple times or lower if scite has not yet processed some of the citing articles.
Explore citation contexts and check if this article has been supported or disputed.
https://scite.ai/reports/10.1172/jci118206

Supporting
Mentioning
Contrasting
27
314
1

Article citations

Go to all (317) article citations

Data 

Similar Articles 

To arrive at the top five similar articles we use a word-weighted algorithm to compare words from the Title and Abstract of each citation.

Funding 

Funders who supported this work.

NHLBI NIH HHS (1)

NIDDK NIH HHS (2)