Obesity-induced changes in lipid mediators persist after weight loss
Hernandez-Carretero A., Weber N., La Frano MR., Ying W., Lantero Rodriguez J., Sears DD.
Prospective Study, published in Int J Obes (Lond) (2018) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Int J Obes (Lond) (2018)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 29089614
- PMCID
- PMC6055936
- DOI
- 10.1038/ijo.2017.266
- Citations
- 35
Abstract (original English)
Background Obesity induces significant changes in lipid mediators, however, the extent to which these changes persist after weight loss has not been investigated. Subjects/methods We fed C57BL6 mice a high-fat diet to generate obesity and then switched the diet to a lower-fat diet to induce weight loss. We performed a comprehensive metabolic profiling of lipid mediators including oxylipins, endocannabinoids, sphingosines and ceramides in key metabolic tissues (including adipose, liver, muscle and hypothalamus) and plasma. Results We found that changes induced by obesity were largely reversible in most metabolic tissues but the adipose tissue retained a persistent obese metabolic signature. Prostaglandin signaling was perturbed in the obese state and lasting increases in PGD 2 , and downstream metabolites 15-deoxy PGJ 2 and delta-12-PGJ 2 were observed after weight loss. Furthermore expression of the enzyme responsible for PGD 2 synthesis (hematopoietic prostaglandin D synthase, HPGDS) was increased in obese adipose tissues and remained high after weight loss. We found that inhibition of HPGDS over the course of 5 days resulted in decreased food intake in mice. Increased HPGDS expression was also observed in human adipose tissues obtained from obese compared with lean individuals. We then measured circulating levels of PGD 2 in obese patients before and after weight loss and fou
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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