Related Experiment Video

Updated: Aug 18, 2026

Measurement of Basal and Forskolin-stimulated Lipolysis in Inguinal Adipose Fat Pads
07:59

Measurement of Basal and Forskolin-stimulated Lipolysis in Inguinal Adipose Fat Pads

Published on: July 21, 2017

The effect of antilipolytic agents on cyclic AMP, free fatty acid and total catecholamine concentrations in plasma

R C Strange, M J Rowe, O D Mjos

    Acta Medica Scandinavica
    |January 1, 1976
    PubMed

    More Related Videos

    Assessing Whole-Body Lipid-Handling Capacity in Mice07:57

    Assessing Whole-Body Lipid-Handling Capacity in Mice

    Published on: November 24, 2020

    Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro09:41

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

    Published on: March 17, 2023

    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,...
    Adrenergic Agonists: Direct-Acting Agents01:30

    Adrenergic Agonists: Direct-Acting Agents

    Drugs that mimic the action of endogenous catecholamines like noradrenaline and adrenaline are called adrenergic agonists or sympathomimetics. Based on their mechanism of action, sympathomimetics can be classified as direct-, indirect-, or mixed-acting sympathomimetics. Direct-acting adrenergic agonists activate adrenoceptors without affecting presynaptic neurons, making them independent of neuronal catecholamine-depleting agents like reserpine and guanethidine.
    These agents can be classified...
    Adrenergic Agonists: Indirect-Acting Agents01:25

    Adrenergic Agonists: Indirect-Acting Agents

    Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
    One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
    Adrenergic Agonists: Mixed-Action Agents01:28

    Adrenergic Agonists: Mixed-Action Agents

    Mixed-action adrenergic agonists, like ephedrine and pseudoephedrine, directly and indirectly affect adrenergic receptors. These agents stimulate adrenoceptors and indirectly release stored neurotransmitters, amplifying the adrenergic response.
    Ephedrine and pseudoephedrine lack a catecholamine group, making them less susceptible to degradation by metabolic enzymes. They have increased oral bioavailability and lipophilicity, resulting in a longer duration of action. Their response is reduced by...
    Drugs Affecting Neurotransmitter Release or Uptake01:21

    Drugs Affecting Neurotransmitter Release or Uptake

    Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...