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Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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...
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...
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and produces two-second...

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Updated: May 15, 2026

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
07:22

Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells

Published on: March 28, 2013

Prostaglandins as PPARγ Modulators in Adipogenesis.

Ko Fujimori1

  • 1Laboratory of Biodefense and Regulation, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.

PPAR Research
|January 16, 2013
PubMed
Summary

Prostaglandins (PGs) modulate adipocyte differentiation and energy homeostasis by interacting with PPARγ. Specific PGs promote or suppress adipogenesis, highlighting their role in obesity regulation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolism

Background:

  • Adipocytes regulate energy homeostasis through adipogenesis, a process influenced by gene expression and hormone sensitivity.
  • Peroxisome proliferator-activated receptor gamma (PPARγ) is a key transcription factor in adipogenesis, promoting adipogenic and lipogenic gene expression.

Purpose of the Study:

  • To investigate the role of Prostaglandins (PGs) as modulators of PPARγ activity in adipogenesis.
  • To explore the potential of PGs in regulating obesity through their effects on adipocyte differentiation.

Main Methods:

  • Analysis of Prostaglandin (PG) involvement in adipocyte differentiation pathways.
  • Examination of Prostaglandin (PG) interactions with PPARγ and its downstream targets.
  • Investigating the impact of specific Prostaglandins (PGs) on adipocyte precursor cell differentiation.

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Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
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Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues

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Isolation and Differentiation of Stromal Vascular Cells to Beige/Brite Cells
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Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
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Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

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Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues
09:20

Isolation and Differentiation of Adipose-Derived Stem Cells from Porcine Subcutaneous Adipose Tissues

Published on: March 31, 2016

Main Results:

  • Prostacyclin promotes adipocyte differentiation by upregulating C/EBPβ and δ, which in turn activate PPARγ.
  • Prostaglandin E2 (PGE2) and Prostaglandin F2α (PGF2α) inhibit early adipogenesis by increasing cyclooxygenase-2 expression and suppressing PPARγ function.
  • Prostaglandin D2 (PGD2) and Δ(12)-PGJ2 activate middle-late adipogenesis via DP2 receptors and PPARγ.

Conclusions:

  • Prostaglandins (PGs) differentially regulate adipogenesis, acting as crucial modulators of PPARγ activity.
  • Understanding these Prostaglandin (PG)-PPARγ interactions is vital for developing strategies to manage obesity.