Related Experiment Video
Updated: May 7, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Impaired leptin gene expression and release in cultured preadipocytes isolated from individuals born with low birth
Ninna S Schultz1, Christa Broholm, Linn Gillberg
1Department of Endocrinology, Diabetes and Metabolism, Rigshospitalet, Copenhagen, Denmark.
Insights
Low birth weight (LBW) is linked to higher type 2 diabetes (T2D) risk. LBW impairs preadipocyte maturation, reducing leptin production and increasing T2D susceptibility.
Area of Science:
- Endocrinology
- Metabolic Health
- Developmental Biology
Background:
- Low birth weight (LBW) is a known risk factor for developing type 2 diabetes (T2D).
- Leptin, an appetite-regulating hormone, is produced by mature adipocytes, but its production may be compromised in immature cells from LBW individuals.
- Understanding the mechanisms linking LBW to T2D is crucial for early intervention.
Purpose of the Study:
- To investigate preadipocyte maturation and leptin production in individuals born with LBW compared to normal birth weight (NBW) controls.
- To explore the role of DNA methylation in the leptin promoter in LBW-associated metabolic changes.
- To assess the expression of key adipocyte differentiation markers in LBW subjects.
Main Methods:
- Recruitment of men born with LBW and NBW controls.
- Isolation and culture of subcutaneous abdominal preadipocytes.
- Analysis of leptin and differentiation marker gene expression, leptin secretion, and DNA methylation of the leptin promoter.
Main Results:
- Differentiating preadipocytes from LBW individuals exhibited reduced leptin gene expression and secretion compared to NBW controls.
- Increased DNA methylation of the proximal leptin (LEP) promoter was observed in LBW individuals.
- Lower mRNA expression of adipocyte differentiation markers (FABP4, PPARG, GLUT4) was found in LBW preadipocytes, indicating impaired maturation.
Conclusions:
- Findings suggest impaired preadipocyte maturation in individuals with LBW.
- Epigenetic modifications, such as increased leptin promoter methylation, may contribute to reduced leptin production.
- Impaired adipocyte function in LBW may underlie the increased risk of developing type 2 diabetes.
Abstract:
Low birth weight (LBW) is associated with increased risk of the development of type 2 diabetes (T2D). The appetite-regulating hormone leptin is released from mature adipocytes, and its production may be decreased in immature preadipocytes from LBW individuals. We recruited 14 men born with LBW and 13 controls born with normal birth weight (NBW). Biopsy samples were obtained from subcutaneous abdominal fat depots, and preadipocytes were isolated and cultured. Gene expression of leptin and selected differentiation markers were analyzed during preadipocyte differentiation, and cell culture media were collected to analyze leptin secretion. DNA methylation of CpG sites in the leptin promoter was measured using pyrosequencing. We found that differentiating preadipocytes from LBW individuals showed reduced leptin gene expression and a corresponding reduced leptin release compared with NBW individuals. Mean DNA methylation of the proximal LEP promoter was increased in LBW compared with NBW individuals. The notion of impaired adipocyte maturation in LBW individuals was supported by a lower mRNA expression of the differentiation markers; fatty acid binding protein 4, peroxisome proliferator-activated receptor γ, and GLUT4. Our findings are consistent with impaired preadipocyte maturation, contributing to an increased risk of the development of T2D in LBW subjects.
More Related Videos
06:08Semi-Automated Isolation of the Stromal Vascular Fraction from Murine White Adipose Tissue Using a Tissue Dissociator
Published on: May 19, 2023
06:16White and Brown Adipose Grafts: An Approach to Correct Reproductive, Metabolic, and Renal Deficits in Black and Tan Brachyury (BTBR) Obese Mice
Published on: September 9, 2025
Related Concept Videos
01:58Cell Specific Gene Expression
01:24Obesity
01:30Regulation of Food Intake
01:26Type II Diabetes I: Introduction
02:30Genomic Imprinting and Inheritance
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
02:41Lethal Alleles
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...