Level A· Stronger Clinical EvidenceMeta-analysisEurope PMCOpen access

Further evidence supporting a potential role for ADH1B in obesity

Morales LD., Cromack DT., Tripathy D., Fourcaudot M., Kumar S., Curran JE.

Meta-analysis on Type 2 Diabetes, published in Sci Rep (2021) — summary generated from the PubMed abstract.

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Level A· Stronger Clinical EvidenceEvidence level of this study

Relatively higher-quality human studies compared with other topics in this database, e.g. multiple RCTs or systematic reviews. This does not mean it is standard or approved care.

  • 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
Meta-analysis
Journal
Sci Rep (2021)
Reported sample size
—
Source database
Europe PMC
PMID
33479282
PMCID
PMC7820614
DOI
10.1038/s41598-020-80563-z
Citations
22

Abstract (original English)

Insulin is an essential hormone that regulates glucose homeostasis and metabolism. Insulin resistance (IR) arises when tissues fail to respond to insulin, and it leads to serious health problems including Type 2 Diabetes (T2D). Obesity is a major contributor to the development of IR and T2D. We previously showed that gene expression of alcohol dehydrogenase 1B (ADH1B) was inversely correlated with obesity and IR in subcutaneous adipose tissue of Mexican Americans. In the current study, a meta-analysis of the relationship between ADH1B expression and BMI in Mexican Americans, African Americans, Europeans, and Pima Indians verified that BMI was increased with decreased ADH1B expression. Using established human subcutaneous pre-adipocyte cell lines derived from lean (BMI -2 ) or obese (BMI ≥ 30 kg m -2 ) donors, we found that ADH1B protein expression increased substantially during differentiation, and overexpression of ADH1B inhibited fatty acid binding protein expression. Mature adipocytes from lean donors expressed ADH1B at higher levels than obese donors. Insulin further induced ADH1B protein expression as well as enzyme activity. Knockdown of ADH1B expression decreased insulin-stimulated glucose uptake. Our findings suggest that ADH1B is involved in the proper development and metabolic activity of adipose tissues and this function is suppressed by obesity.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Relatively higher-quality human studies compared with other topics in this database, e.g. multiple RCTs or systematic reviews. This does not mean it is standard or approved care.

How we grade evidence
Adipose TissueAdipocytesHumansDiabetes Mellitus, Type 2Insulin ResistanceObesityInsulinAlcohol DehydrogenaseBody Mass IndexAdult

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