Related Experiment Video

Updated: Jul 10, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Inhibition of adipogenesis and development of glucose intolerance by soluble preadipocyte factor-1 (Pref-1)

Kichoon Lee1, Josep A Villena, Yang Soo Moon

  • 1Department of Nutritional Sciences and Toxicology, and. Cancer Research Laboratory, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California 94720, USA.

The Journal of Clinical Investigation
|February 18, 2003
PubMed

Insights

Preadipocyte factor-1 (Pref-1) inhibits fat cell development and function. This leads to reduced body fat, impaired glucose metabolism, and insulin resistance in mice.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Background:

  • Preadipocyte factor-1 (Pref-1) is a transmembrane protein crucial for preadipocyte development.
  • Pref-1 expression is downregulated during adipocyte differentiation.
  • Proteolytic cleavage of Pref-1 yields soluble products with potential signaling roles.

Purpose of the Study:

  • To investigate the in vivo function of Pref-1 in adipogenesis and metabolic regulation.
  • To elucidate the effects of Pref-1 expression on adipose tissue mass and function.
  • To determine the systemic metabolic consequences of Pref-1-mediated inhibition of adipogenesis.

Main Methods:

  • Generation of transgenic mice expressing the Pref-1 ectodomain fused to human immunoglobulin-gamma (hFc).
  • Adipose tissue-specific and liver-specific transgene expression driven by adipocyte fatty acid-binding protein (aP2) and albumin promoters, respectively.
  • Analysis of adipose tissue mass, adipocyte marker expression, and metabolic parameters (glucose tolerance, insulin sensitivity, triglyceride levels).

Main Results:

  • Transgenic mice expressing Pref-1/hFc in adipose tissue exhibited reduced fat pad weight and decreased expression of adipocyte markers (leptin, adiponectin).
  • Increased Pref-1 expression in adipose tissue correlated with impaired glucose tolerance, hypertriglyceridemia, and reduced insulin sensitivity.
  • Liver-specific Pref-1/hFc expression also led to decreased adipose mass, suggesting an endocrine role for Pref-1.

Conclusions:

  • Pref-1 actively inhibits adipogenesis and adipocyte function in vivo.
  • Pref-1-induced impairment of adipogenesis leads to metabolic abnormalities, including dyslipidemia and insulin resistance.
  • Pref-1 may act as an endocrine factor influencing systemic metabolism through its effects on adipose tissue.

More Related Videos

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function09:20

An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator06:08

Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator

Published on: May 19, 2023

Related Concept Videos

Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...