Type 2 diabetes-related sarcopenia: role of nitric oxide
Abstract Sarcopenia, characterized by progressive and generalized loss of skeletal muscle (SkM) mass, strength, and physical performance, is a prevalent complication in type 2 diabetes (T2D). Nitric oxide (NO), a multifunctional gasotransmitter involved in whole-body glucose and insulin homeostasis,...
Saved in:
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2024-12-01
|
| Series: | Nutrition & Metabolism |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s12986-024-00883-z |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1846112777511370752 |
|---|---|
| author | Zahra Bahadoran Parvin Mirmiran Asghar Ghasemi |
| author_facet | Zahra Bahadoran Parvin Mirmiran Asghar Ghasemi |
| author_sort | Zahra Bahadoran |
| collection | DOAJ |
| description | Abstract Sarcopenia, characterized by progressive and generalized loss of skeletal muscle (SkM) mass, strength, and physical performance, is a prevalent complication in type 2 diabetes (T2D). Nitric oxide (NO), a multifunctional gasotransmitter involved in whole-body glucose and insulin homeostasis, plays key roles in normal SkM physiology and function. Here, we highlight the role of NO in SkM mass maintenance and its potential contribution to the development of T2D-related sarcopenia. Physiologic NO level, primarily produced by sarcolemmal neuronal nitric oxide synthase (nNOSμ isoform), is involved in protein synthesis in muscle fibers and maintenance of SkM mass. The observed effect of nNOSμ on SkM mass is muscle-type specific and sex-dependent. Impaired NO homeostasis [due to a diminished nNOSμ-NO availability and excessive NO production through inducible NOS (iNOS) in response to atrophic stimuli, e.g., inflammatory cytokines] in SkM occurred during the development and progression of T2D, may cause sarcopenia. Theoretically, restoration of NO through nNOS overexpression, supplying NOS substrates (e.g., L-arginine and L-citrulline), phosphodiesterase (PDE) inhibition, and supplementation with NO donors (e.g., inorganic nitrate) may be potential therapeutic approaches to preserve SkM mass and prevents sarcopenia in T2D. |
| format | Article |
| id | doaj-art-6b103bbea04d472a8d1d91b572bd2f47 |
| institution | Kabale University |
| issn | 1743-7075 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Nutrition & Metabolism |
| spelling | doaj-art-6b103bbea04d472a8d1d91b572bd2f472024-12-22T12:19:16ZengBMCNutrition & Metabolism1743-70752024-12-0121111510.1186/s12986-024-00883-zType 2 diabetes-related sarcopenia: role of nitric oxideZahra Bahadoran0Parvin Mirmiran1Asghar Ghasemi2Micronutrient Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical SciencesNutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical SciencesEndocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical SciencesAbstract Sarcopenia, characterized by progressive and generalized loss of skeletal muscle (SkM) mass, strength, and physical performance, is a prevalent complication in type 2 diabetes (T2D). Nitric oxide (NO), a multifunctional gasotransmitter involved in whole-body glucose and insulin homeostasis, plays key roles in normal SkM physiology and function. Here, we highlight the role of NO in SkM mass maintenance and its potential contribution to the development of T2D-related sarcopenia. Physiologic NO level, primarily produced by sarcolemmal neuronal nitric oxide synthase (nNOSμ isoform), is involved in protein synthesis in muscle fibers and maintenance of SkM mass. The observed effect of nNOSμ on SkM mass is muscle-type specific and sex-dependent. Impaired NO homeostasis [due to a diminished nNOSμ-NO availability and excessive NO production through inducible NOS (iNOS) in response to atrophic stimuli, e.g., inflammatory cytokines] in SkM occurred during the development and progression of T2D, may cause sarcopenia. Theoretically, restoration of NO through nNOS overexpression, supplying NOS substrates (e.g., L-arginine and L-citrulline), phosphodiesterase (PDE) inhibition, and supplementation with NO donors (e.g., inorganic nitrate) may be potential therapeutic approaches to preserve SkM mass and prevents sarcopenia in T2D.https://doi.org/10.1186/s12986-024-00883-zType 2 diabetesSarcopeniaSkeletal muscle massNitric oxideL-arginineNitrate |
| spellingShingle | Zahra Bahadoran Parvin Mirmiran Asghar Ghasemi Type 2 diabetes-related sarcopenia: role of nitric oxide Nutrition & Metabolism Type 2 diabetes Sarcopenia Skeletal muscle mass Nitric oxide L-arginine Nitrate |
| title | Type 2 diabetes-related sarcopenia: role of nitric oxide |
| title_full | Type 2 diabetes-related sarcopenia: role of nitric oxide |
| title_fullStr | Type 2 diabetes-related sarcopenia: role of nitric oxide |
| title_full_unstemmed | Type 2 diabetes-related sarcopenia: role of nitric oxide |
| title_short | Type 2 diabetes-related sarcopenia: role of nitric oxide |
| title_sort | type 2 diabetes related sarcopenia role of nitric oxide |
| topic | Type 2 diabetes Sarcopenia Skeletal muscle mass Nitric oxide L-arginine Nitrate |
| url | https://doi.org/10.1186/s12986-024-00883-z |
| work_keys_str_mv | AT zahrabahadoran type2diabetesrelatedsarcopeniaroleofnitricoxide AT parvinmirmiran type2diabetesrelatedsarcopeniaroleofnitricoxide AT asgharghasemi type2diabetesrelatedsarcopeniaroleofnitricoxide |