Related Experiment Video

Updated: Jul 16, 2026

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
09:41

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro

Published on: March 17, 2023

Adrenomedullin inhibits adipogenesis under transcriptional control of insulin

Romain Harmancey1, Jean-Michel Senard, Philippe Rouet

  • 1I2MR INSERM U858, Laboratoire de Pharmacologie, Faculté de Médecine, Universite Paul Sabatier, Institut Louis Bugnard IFR31, 37 allées Jules Guesde, 31000 Toulouse, France.

Diabetes
|March 1, 2007
PubMed

Insights

Adrenomedullin acts as an antiadipogenic factor, inhibiting fat cell differentiation. Its levels increase in obesity and correlate inversely with insulin, suggesting a role in metabolic regulation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Research

Background:

  • Adrenomedullin (AM) is a peptide hormone with diverse physiological roles.
  • The regulation of adipose tissue differentiation and its relationship with metabolic diseases are critical areas of research.

Purpose of the Study:

  • To investigate the role of adrenomedullin in adipogenesis.
  • To explore the relationship between insulin, adrenomedullin, and insulin resistance.

Main Methods:

  • Generation of preadipocyte cell lines with reduced adrenomedullin production using small interfering RNA.
  • Overexpression of active adrenomedullin peptide.
  • Dose-response studies of insulin on adrenomedullin expression in human adipocytes and in vivo rat models.
  • Analysis of adrenomedullin plasma levels in obese and lean individuals.
  • Luciferase reporter gene assays to study adrenomedullin promoter activity.

Main Results:

  • Reduced adrenomedullin synthesis accelerated adipose differentiation, while its overexpression delayed it, indicating AM is an antiadipogenic factor.
  • Insulin inhibited adrenomedullin expression in a dose-dependent manner, an effect reversed by resistin.
  • Circulating adrenomedullin levels were threefold higher in obese patients compared to lean individuals.
  • Plasma adrenomedullin levels negatively correlated with plasma insulin levels in obese patients.
  • Adrenomedullin expression was upregulated in insulin-resistant adipose cells, and insulin's effect was mediated by insulin-responsive elements.

Conclusions:

  • Adrenomedullin functions as an endogenous antiadipogenic factor.
  • Insulin negatively regulates adrenomedullin expression, potentially contributing to altered fat mass development in obesity and diabetes.
  • Elevated circulating adrenomedullin in obesity may reflect an adaptive response to insulin resistance.

More Related Videos

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance09:48

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Related Concept Videos

Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
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...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Regulation of Food Intake01:30

Regulation of Food Intake

Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
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...