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Adipose tissue dysfunction contributes to obesity related metabolic diseases
Blüher M.. Best practice & research. Clinical endocrinology & metabolism, 2013-03-06
Topic: Brain proteins, microglia and lab models
Obesity significantly increases the risk of developing type 2 diabetes, hypertension, coronary heart disease, stroke, fatty liver disease, dementia, obstructive sleep apnea and several types of cancer. Adipocyte and adipose tissue dysfunction represent primary defects in obesity and may link obesity to metabolic and cardiovascular diseases. Adipose tissue (AT) dysfunction manifests by a proinflammatory adipokine secretion pattern that mediate auto/paracrine and endocrine communication and by inflammatory cell infiltration, particularly in intra-abdominal fat. Impaired AT function is caused by the interaction of genetic, behavioral and environmental factors which lead to adipocyte hypertrophy, ectopic fat accumulation, hypoxia, AT stresses, impaired AT mitochondrial function and inflammatory processes within adipose tissue. Recently, increased autophagy has been linked to obesity and AT dysfunction and may represent a mechanism to compensate for AT stresses. A better understanding of mechanisms causing or maintaining AT dysfunction may provide new therapeutic strategies in the treatment of obesity-induced metabolic diseases.
Key findings
- Obesity significantly increases the risk of developing type 2 diabetes, hypertension, coronary heart disease, stroke, fatty liver disease, dementia, obstructive sleep apnea and several types of cancer.
Why it matters
This review states that obesity significantly increases the risk of developing dementia, among other diseases. It suggests that a better understanding of adipose tissue dysfunction may provide new therapeutic strategies for treating obesity-induced metabolic diseases.
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Study details
- Evidence strengthLow
How this study scored 46/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Best practice & research. Clinical endocrinology & metabolism) |
| Journal's citation record | 2 / 4 | Best Practice & Research Clinical Endocrinology & Metabolism: journal h-index 152 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2013 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 408 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 27.2 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 5 / 6 | Cited 20.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 3 / 4 | Cited 89 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Matthias Blüher: h-index 123 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Leipzig University: institution h-index 763 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23731879) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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Read the original
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Blüher, M. (2013). Adipose tissue dysfunction contributes to obesity related metabolic diseases. Best practice & research. Clinical endocrinology & metabolism. https://doi.org/10.1016/j.beem.2013.02.005
Vancouver
Blüher M. Adipose tissue dysfunction contributes to obesity related metabolic diseases. Best practice & research. Clinical endocrinology & metabolism. 2013. doi:10.1016/j.beem.2013.02.005. PMID: 23731879.
BibTeX
@article{bluher2013-23731879,
author = {Blüher, M.},
title = {{Adipose tissue dysfunction contributes to obesity related metabolic diseases}},
journal = {Best practice \& research. Clinical endocrinology \& metabolism},
year = {2013},
doi = {10.1016/j.beem.2013.02.005},
pmid = {23731879},
url = {https://doi.org/10.1016/j.beem.2013.02.005}
}
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