Evidence map›Paper›PMID 34731089›Full record

ArticleAging2021

Impaired glucose metabolism reduces the neuroprotective action of adipocytokines in cognitively normal older adults with insulin resistance.

Karel M Lopez-Vilaret, Jose L Cantero, Marina Fernandez-Alvarez, Miguel Calero, Olga Calero, Mónica Lindín, Montserrat Zurrón, Fernando Díaz, Mercedes Atienza

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Karel M Lopez-VilaretLaboratory of Functional Neuroscience, Universidad Pablo de Olavide, Seville, Spain.
Jose L CanteroLaboratory of Functional Neuroscience, Universidad Pablo de Olavide, Seville, Spain.
Marina Fernandez-AlvarezLaboratory of Functional Neuroscience, Universidad Pablo de Olavide, Seville, Spain.
Miguel CaleroCIBERNED, Network Center for Biomedical Research in Neurodegenerative Diseases, Madrid, Spain.
Olga CaleroCIBERNED, Network Center for Biomedical Research in Neurodegenerative Diseases, Madrid, Spain.
Mónica LindínCognitive Neuroscience Laboratory, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Montserrat ZurrónCognitive Neuroscience Laboratory, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Fernando DíazCognitive Neuroscience Laboratory, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
Mercedes AtienzaLaboratory of Functional Neuroscience, Universidad Pablo de Olavide, Seville, Spain.
Universidad Pablo de Olavide · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESInstituto de Salud Carlos III · ESUniversidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence suggests that aging-related dysfunctions of adipose tissue and metabolic disturbances increase the risk of diabetes and metabolic syndrome (MtbS), eventually leading to cognitive impairment and dementia. However, the neuroprotective role of adipocytokines in this process has not been specifically investigated. The present study aims to identify metabolic alterations that may prevent adipocytokines from exerting their neuroprotective action in normal ageing. We hypothesize that neuroprotection may occur under insulin resistance (IR) conditions as long as there are no other metabolic alterations that indirectly impair the action of adipocytokines, such as hyperglycemia. This hypothesis was tested in 239 cognitively normal older adults (149 females) aged 52 to 87 years (67.4 ± 5.9 yr). We assessed whether the homeostasis model assessment-estimated insulin resistance (HOMA-IR) and the presence of different components of MtbS moderated the association of plasma adipocytokines (i.e., adiponectin, leptin and the adiponectin to leptin [Ad/L] ratio) with cognitive functioning and cortical thickness. The results showed that HOMA-IR, circulating triglyceride and glucose levels moderated the neuroprotective effect of adipocytokines. In particular, elevated triglyceride levels reduced the beneficial effect of Ad/L ratio on cognitive functioning in insulin-sensitive individuals; whereas under high IR conditions, it was elevated glucose levels that weakened the association of the Ad/L ratio with cognitive functioning and with cortical thickness of prefrontal regions. Taken together, these findings suggest that the neuroprotective action of adipocytokines is conditioned not only by whether cognitively normal older adults are insulin-sensitive or not, but also by the circulating levels of triglycerides and glucose, respectively.

Indexed as

AdipokinesBlood GlucoseAdipose TissueAgedAged, 80 and overAgingCognitionFemaleHumansInsulin ResistanceMaleMetabolic SyndromeMiddle AgedNeuroprotectionNeuroprotective AgentsTriglyceridesAdipokinesBlood GlucoseNeuroprotective AgentsTriglyceridesadiponectincognitive functioncortical thicknessleptinmetabolism

Identifiers

PMID34731089
PMCPMC8610113
OpenAlexW3210186873

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.