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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 43 out of 100. How common it is

Topic: Brain proteins, microglia and lab models

The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.

Key findings

Why it matters

This review states that dysfunction of fat tissue in obesity may link obesity to several health problems, including dementia. It discusses a possible mechanism and does not test any treatment, cure or prevention for Alzheimer's disease.

Study details

How this study scored 43/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 5 of 6; Cited by studies here 1 of 6; Still being cited 3 of 4; Senior author's track record 1 of 4; Institution's track record 1 of 3; Multi-centre collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 43 of 100.43 of 100 points earned57 not earned

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.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association)
Journal's citation record 1 / 4 Experimental and Clinical Endocrinology & Diabetes: journal h-index 99 (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 2009 — 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 663 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 34.9 citations a year over 19 year(s) since 2009
Impact for its field and year 5 / 6 Cited 26.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 1 / 6 Cited by 2 other studies in this library
Still being cited 3 / 4 Cited 61 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author Mattias Blüher: h-index 6 (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 19358089)
Free to read 0 / 2 Behind a paywall — scores zero
Total 43 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

May need a subscription OpenAlex found no free copy of the full text (checked 6 Feb 1020), so the publisher may charge for it. The PubMed abstract is free.

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. (2009). Adipose tissue dysfunction in obesity. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. https://doi.org/10.1055/s-0029-1192044

Vancouver

Blüher M. Adipose tissue dysfunction in obesity. Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2009. doi:10.1055/s-0029-1192044. PMID: 19358089.

BibTeX

@article{bluher2009-19358089,
  author  = {Blüher, M.},
  title   = {{Adipose tissue dysfunction in obesity}},
  journal = {Experimental and clinical endocrinology \& diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association},
  year    = {2009},
  doi     = {10.1055/s-0029-1192044},
  pmid    = {19358089},
  url     = {https://doi.org/10.1055/s-0029-1192044}
}

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2 studies in the alzhub library list this one in their references.

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