The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review

Sarcopenia is a common muscular affection among elderly individuals. More recently, it has been recognized as the skeletal muscle (SM) expression of the metabolic syndrome. The prevalence of sarcopenia is increasing along with visceral obesity, to which it is tightly associated. Nonetheless, it is a...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Angelo Armandi, Chiara Rosso, Gian Paolo Caviglia, Davide Giuseppe Ribaldone, Elisabetta Bugianesi
Formato: article
Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://doaj.org/article/64783f3376bf425cbd7b7ec8fc8ad4c5
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:64783f3376bf425cbd7b7ec8fc8ad4c5
record_format dspace
spelling oai:doaj.org-article:64783f3376bf425cbd7b7ec8fc8ad4c52021-11-10T06:17:52ZThe Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review1664-239210.3389/fendo.2021.716533https://doaj.org/article/64783f3376bf425cbd7b7ec8fc8ad4c52021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fendo.2021.716533/fullhttps://doaj.org/toc/1664-2392Sarcopenia is a common muscular affection among elderly individuals. More recently, it has been recognized as the skeletal muscle (SM) expression of the metabolic syndrome. The prevalence of sarcopenia is increasing along with visceral obesity, to which it is tightly associated. Nonetheless, it is a still underreported entity by clinicians, despite the worsening in disease burden and reduced patient quality of life. Recognition of sarcopenia is clinically challenging, and variability in study populations and diagnostic methods across the clinical studies makes it hard to reach a strong evidence. Impaired insulin activity in SM is responsible for the altered molecular pathways and clinical manifestations of sarcopenia, which is morphologically expressed by myosteatosis. Lipotoxicity, oxidative stress and adipose tissue-derived inflammation lead to both alterations in glucose disposal and protein synthesis in SM, with raising insulin resistance (IR) and SM atrophy. In particular, hyperleptinemia and leptin resistance interfere directly with SM activity, but also with the release of Growth Hormone from the hypohysis, leading to a lack in its anabolic effect on SM. Moreover, sarcopenia is independently associated to liver fibrosis in Non-Alcoholic Fatty Liver Disease (NAFLD), which in turn worsens SM functionality through the secretion of proinflammatory heptokines. The cross-talk between the liver and SM in the IR setting is of crucial relevance, given the high prevalence of NAFLD and the reciprocal impact of insulin-sensitive tissues on the overall disease burden. Along with the efforts of non-invasive diagnostic approaches, irisin and myostatin are two myokines currently evaluated as potential biomarkers for diagnosis and prognostication. Decreased irisin levels seem to be potentially associated to sarcopenia, whereas increased myostatin has shown to negatively impact on sarcopenia in pre-clinical studies. Gene variants in irisin have been explored with regard to the impact on the liver disease phenotype, with conflicting results. The gut-muscle axis has gain relevance with the evidence that insulin resistance-derived gut dysbiosis is responsible for increased endotoxemia and reduction in short-chain free fatty acids, directly affecting and predisposing to sarcopenia. Based on the current evidence, more efforts are needed to increase awareness and improve the management of sarcopenic patients. Angelo ArmandiChiara RossoGian Paolo CavigliaDavide Giuseppe RibaldoneElisabetta BugianesiFrontiers Media S.A.articlesarcopeniainsulin resistanceobesityNAFLDleptinmicrobiotaDiseases of the endocrine glands. Clinical endocrinologyRC648-665ENFrontiers in Endocrinology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic sarcopenia
insulin resistance
obesity
NAFLD
leptin
microbiota
Diseases of the endocrine glands. Clinical endocrinology
RC648-665
spellingShingle sarcopenia
insulin resistance
obesity
NAFLD
leptin
microbiota
Diseases of the endocrine glands. Clinical endocrinology
RC648-665
Angelo Armandi
Chiara Rosso
Gian Paolo Caviglia
Davide Giuseppe Ribaldone
Elisabetta Bugianesi
The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
description Sarcopenia is a common muscular affection among elderly individuals. More recently, it has been recognized as the skeletal muscle (SM) expression of the metabolic syndrome. The prevalence of sarcopenia is increasing along with visceral obesity, to which it is tightly associated. Nonetheless, it is a still underreported entity by clinicians, despite the worsening in disease burden and reduced patient quality of life. Recognition of sarcopenia is clinically challenging, and variability in study populations and diagnostic methods across the clinical studies makes it hard to reach a strong evidence. Impaired insulin activity in SM is responsible for the altered molecular pathways and clinical manifestations of sarcopenia, which is morphologically expressed by myosteatosis. Lipotoxicity, oxidative stress and adipose tissue-derived inflammation lead to both alterations in glucose disposal and protein synthesis in SM, with raising insulin resistance (IR) and SM atrophy. In particular, hyperleptinemia and leptin resistance interfere directly with SM activity, but also with the release of Growth Hormone from the hypohysis, leading to a lack in its anabolic effect on SM. Moreover, sarcopenia is independently associated to liver fibrosis in Non-Alcoholic Fatty Liver Disease (NAFLD), which in turn worsens SM functionality through the secretion of proinflammatory heptokines. The cross-talk between the liver and SM in the IR setting is of crucial relevance, given the high prevalence of NAFLD and the reciprocal impact of insulin-sensitive tissues on the overall disease burden. Along with the efforts of non-invasive diagnostic approaches, irisin and myostatin are two myokines currently evaluated as potential biomarkers for diagnosis and prognostication. Decreased irisin levels seem to be potentially associated to sarcopenia, whereas increased myostatin has shown to negatively impact on sarcopenia in pre-clinical studies. Gene variants in irisin have been explored with regard to the impact on the liver disease phenotype, with conflicting results. The gut-muscle axis has gain relevance with the evidence that insulin resistance-derived gut dysbiosis is responsible for increased endotoxemia and reduction in short-chain free fatty acids, directly affecting and predisposing to sarcopenia. Based on the current evidence, more efforts are needed to increase awareness and improve the management of sarcopenic patients.
format article
author Angelo Armandi
Chiara Rosso
Gian Paolo Caviglia
Davide Giuseppe Ribaldone
Elisabetta Bugianesi
author_facet Angelo Armandi
Chiara Rosso
Gian Paolo Caviglia
Davide Giuseppe Ribaldone
Elisabetta Bugianesi
author_sort Angelo Armandi
title The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
title_short The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
title_full The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
title_fullStr The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
title_full_unstemmed The Impact of Dysmetabolic Sarcopenia Among Insulin Sensitive Tissues: A Narrative Review
title_sort impact of dysmetabolic sarcopenia among insulin sensitive tissues: a narrative review
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/64783f3376bf425cbd7b7ec8fc8ad4c5
work_keys_str_mv AT angeloarmandi theimpactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT chiararosso theimpactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT gianpaolocaviglia theimpactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT davidegiusepperibaldone theimpactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT elisabettabugianesi theimpactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT angeloarmandi impactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT chiararosso impactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT gianpaolocaviglia impactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT davidegiusepperibaldone impactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
AT elisabettabugianesi impactofdysmetabolicsarcopeniaamonginsulinsensitivetissuesanarrativereview
_version_ 1718440473615400960