Level C· Early human research exploring benefitsProspective StudyEurope PMCOpen access

Elevated expression of osteopontin may be related to adipose tissue macrophage accumulation and liver steatosis in morbid obesity

Bertola A., Deveaux V., Bonnafous S., Rousseau D., Anty R., Anty R.

Prospective Study on Type 2 Diabetes, published in Diabetes (2009) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

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
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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
Diabetes (2009)
Reported sample size
—
Source database
Europe PMC
PMID
18952835
PMCID
PMC2606860
DOI
10.2337/db08-0400
Citations
109

Abstract (original English)

Objective Osteopontin (OPN) plays an important role in the development of insulin resistance and liver complications in dietary murine models. We aimed to determine the expression pattern of OPN and its receptor CD44 in obese patients and mice according to insulin resistance and liver steatosis. Research design and methods OPN and CD44 expressions were studied in 52 morbidly obese patients and in mice. Cellular studies were performed in HepG2 cells. Results Hepatic OPN and CD44 expressions were strongly correlated with liver steatosis and insulin resistance in obese patients and mice. This increased OPN expression could be due to the accumulation of triglycerides, since fat loading in HepG2 promotes OPN expression. In contrast, OPN expression in adipose tissue (AT) was enhanced independently of insulin resistance and hepatic steatosis in obese patients. The elevated OPN expression in AT was paralleled with the AT macrophage infiltration, and both phenomena were reversed after weight loss. The circulating OPN level was slightly elevated in obese patients and was not related to liver steatosis. Further, AT did not appear to secrete OPN. In contrast, bariatric surgery-induced weight loss induced a strong increase in circulating OPN. Conclusions The modestly elevated circulating OPN levels in morbidly obese patients were not related to liver steatosis and did not appear to result f

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.

How we grade evidence
LiverAdipose TissueCell Line, TumorMacrophagesAnimalsMice, Inbred C57BLHumansMiceFatty LiverObesity, Morbid

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