2026-06-14T00:34:10Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/134592025-03-27T09:53:24Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19617
Repisalud
author
Lopez-Vilaret, Karel M
author
Cantero, José Luis
author
Fernandez-Alvarez, Marina
author
Calero, Miguel
author
Calero, Olga
author
Lindín, Mónica
author
Zurrón, Montserrat
author
Díaz, Fernando
author
Atienza, Mercedes
funder
Ministerio de Economía y Competitividad (España)
funder
Centro de Investigación Biomedica en Red - CIBER
funder
International Council on Active Aging
funder
Regional Government of Andalusia (España)
funder
Xunta de Galicia (España)
2021-11-22T15:25:15Z
2021-11-22T15:25:15Z
2021-11-03
Aging (Albany NY). 2021 Nov 3;13(21):23936-23952.
10.18632/aging.203668
1945-4589
Aging
34731089
http://hdl.handle.net/20.500.12105/13459
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.
eng
Adiponectin
Cognitive function
Cortical thickness
Leptin
Metabolism
Impaired glucose metabolism reduces the neuroprotective action of adipocytokines in cognitively normal older adults with insulin resistance
research article
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ImpairedGlucoseMetabolismReduces_2021.pdf
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https://repisalud.isciii.es/bitstreams/6b9c95dd-8d75-4681-b7ee-4a97e7df3e90/download
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text/plain
ImpairedGlucoseMetabolismReduces_2021.pdf.txt