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Journal of Lipid Research, Vol. 43, 835-860, June 2002
Copyright © 2002 by Lipid Research, Inc.

Review

Understanding adipose tissue development from transgenic animal models

Philippe Valet¹, Geneviève Tavernier, Isabelle Castan-Laurell, Jean Sébastien Saulnier-Blache and Dominique Langin¹

INSERM Unit 317, Louis Bugnard Institute, Paul Sabatier University, Bldg. L3, Rangueil University Hospital, 31403 Toulouse Cedex 4, France

¹ To whom correspondence should be addressed. e-mail: valet{at}toulouse.inserm.fr, langin{at}toulouse.inserm.fr

The World Health Organization has recognized obesity as a health problem of pandemic proportions. Recent work led to major breakthroughs in the understanding of the molecular basis of adipose tissue development with the cloning and characterization of numerous genes involved in fat cell differentiation and metabolism. Transgenesis has proved very useful in establishing the physiological roles of these genes. Here we review transgenic models made to study adipose tissue's metabolic and trophic responses. Genetic modifications unexpectedly associated to alterations of adipose tissue development are also examined because of their potential involvement in obesity and energy balance regulation. After a description of the methodologies commonly used, we review the data obtained on transcription factors, metabolism, signal transduction, secreted products, and models of lipodystrophy. An overview of such integrative studies leads to a better understanding of the physiology of adipose tissue development.

Alterations in expression levels of proteins involved at different steps of a regulatory pathway highlight the complementary roles of genes in the regulation of adipose tissue development. However, lack of phenotypes also illustrates the capacity of animals to set up adaptive mechanisms.

Abbreviations: ACC, acetylCoA carboxylase; ADD1, adipocyte determination and differentiation factor 1; AGT, angiotensinogen; aP2/ALBP, adipocyte lipid binding protein; AR, adrenergic receptor; ASP, acylation-stimulating protein; AT, adipose tissue; BAT, brown adipose tissue; 11ß HSD-1, 11ß hydroxysteroid deshydrogenase type 1; C/EBP, CCAAT-enhancer binding protein; CMV, cytomegalovirus; DGAT, diacylglycerotransferase; Cre, cyclization recombination; DT-A, diphtheria toxin A; EDG, endothelial differentiation gene; ES, embryonic stem; FAS, fatty acid synthase; FAT, fatty acid transporter; FOXC2, Forkhead box C2; GH, growth hormone; GLUT 4, glucose transporter 4; HMG, high mobility group protein; HSL, hormone sensitive lipase; IGF, insulin growth factor; IR, insulin receptor; IRES, internal ribosome entry site; IRS, insulin receptor substrate; iNOS, inducible NO synthase; PEPCK, phosphoenolpyruvate carboxykinase; PPAR, peroxisome-proliferator activated receptors; PTP1B, protein tyrosine phosphatase 1B; RXR, retinoid X receptor; SREBP, sterol responsive element binding protein; TNF, tumor necrosis factor ; TZD, thiazolidinediones; UCP, uncoupling protein; WAT, white adipose tissue

Supplementary key words fat cell • obesity • gene invalidation • additive or random insertional transgenesis • targeted transgenesis

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