MAK195
Lipolysis (Adipocyte) Kit
Sufficient for 5 g of tissue
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About This Item
Produits recommandés
Méthode de détection
colorimetric
fluorometric
Maladie(s) pertinente(s)
endocrinological disorders, diabetes; obesity
Température de stockage
−20°C
Description générale
Lipolysis is the process of hydrolyzing triglycerides to free fatty acids and glycerol. This process involves the action of adipose TG lipase (ATGL), hormone-sensitive lipase (HSL), and monoglyceride lipase. Lipolysis maintains the energy balance during fasting and exercise by providing a substrate for oxidative metabolism. Lipolysis is regulated by nutritional factors and hormones. Problems with the regulation of lipolysis are associated with obesity, diabetes, and metabolic syndromes.
Adéquation
This kit is suitable for the isolation of adipocytes from tissue and the measurement of lipolysis.
Principe
The Lipolysis (Adipocyte) Kit provides contains synthetic catecholamine (isoproterenol) that activates β-adrenergic receptors. This results in the activation of adenylate cyclase that converts ATP to cAMP. cAMP then activates the hydrolysis of triglycerides by hormone-sensitive lipase. Lipolysis is determined by measuring a fluorescent (λex = 535/ λem = 587 nm) or colorimetric (570 nm) product proportional to the amount of glycerol present.
Composants de kit seuls
Réf. du produit
Description
- Collagenase (0.2%)
- Collagenase Stop Buffer
- Adipocyte Wash Buffer
- Adipocyte Lipolysis Buffer
- Glycerol Assay Buffer
- Glycerol Probe, in DMSO
- Glycerol Enzyme Mix
- Glycerol Standard, 100 mM
- Isoproterenol, 10 mM
- Cell Strainer
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Remplacé(e)(s) par
Réf. du produit
Description
Tarif
Mention d'avertissement
Danger
Mentions de danger
Conseils de prudence
Classification des risques
Resp. Sens. 1 - Skin Sens. 1
Code de la classe de stockage
10 - Combustible liquids
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Les clients ont également consulté
José M Bravo-San Pedro et al.
Cell metabolism, 30(4), 754-767 (2019-08-20)
Autophagy facilitates the adaptation to nutritional stress. Here, we show that short-term starvation of cultured cells or mice caused the autophagy-dependent cellular release of acyl-CoA-binding protein (ACBP, also known as diazepam-binding inhibitor, DBI) and consequent ACBP-mediated feedback inhibition of autophagy.
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