ApoB100-LDL and Its Role in Fat Cell Lipolysis
Author Information
Author(s): Josefin Skogsberg, Andreas Dicker, Mikael Rydén, Gaby Åström, Roland Nilsson, Hasanuzzaman Bhuiyan, Sigurd Vitols, Aline Mairal, Dominique Langin, Peteris Alberts, Erik Walum, Jesper Tegnér, Anders Hamsten, Peter Arner, Johan Björkegren
Primary Institution: Karolinska Institutet, Karolinska University Hospital, Sweden
Hypothesis
ApoB-containing lipoproteins affect adipocyte lipolysis, serving as a signal from the liver to peripheral fat deposits.
Conclusion
ApoB100-LDL inhibits lipolysis in adipocytes, linking dyslipidemias to metabolic syndrome.
Supporting Evidence
- ApoB100-LDL binding to adipocytes inhibits lipolysis.
- LDL receptor is necessary for the inhibition of lipolysis by ApoB100-LDL.
- Human primary adipocytes showed a concentration-dependent inhibition of lipolysis by LDL.
- Mice lacking ApoB100 had increased lipolysis and energy expenditure.
- LDL did not affect lipolysis in 3T3-L1 cells when ApoB48 was present.
- Inverse correlation between plasma ApoB levels and lipolysis rate was observed in human subjects.
- LDL receptor deficiency led to increased lipolysis in mice.
Takeaway
This study found that a type of fat in the blood, called ApoB100-LDL, tells fat cells to stop breaking down fat, which could be important for understanding certain health problems.
Methodology
The study involved human and mouse adipocytes to assess the effects of ApoB100-LDL on lipolysis.
Potential Biases
Potential bias in participant selection as only healthy men were included.
Limitations
The study primarily focused on male subjects and may not generalize to females.
Participant Demographics
48 overweight but otherwise healthy Scandinavian men, aged 23–72 years.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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