MAK195
Lipolysis (Adipocyte) Kit
Sufficient for 5 g of tissue
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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.
Suitability
This kit is suitable for the isolation of adipocytes from tissue and the measurement of lipolysis.
Principle
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
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replaced by
Product No.
Description
Pricing
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Resp. Sens. 1 - Skin Sens. 1
WGK
WGK 3
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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