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Merck
CN

MAK195

Lipolysis (Adipocyte) Kit

Sufficient for 5 g of tissue

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About This Item

UNSPSC Code:
12352200
EC Number:
259-322-7
NACRES:
NA.25
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detection method

colorimetric, fluorometric

relevant disease(s)

endocrinological disorders, diabetes; obesity

storage temp.

−20°C

General description

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.

Application

This kit is suitable for the isolation of adipocytes from tissue and the measurement of lipolysis.

Biochem/physiol Actions

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.

Kit Components Only

Product No.
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

See All (10)

pictograms

Health hazard

signalword

Danger

hcodes

Hazard Classifications

Resp. Sens. 1 - Skin Sens. 1

Storage Class

10 - Combustible liquids

Regulatory Information

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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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