炎症与胰岛素抵抗：肥胖和肌肉减少症的纽带

赵 士君, 丁印 鲁*
山东大学第二医院

摘要


在老龄化背景下，肥胖与肌肉减少症的共病显著增加老年人代谢紊乱与失能风险。本文聚焦肥胖相关脂
肪-肌肉交互机制，系统阐述内脏脂肪堆积驱动的慢性炎症及成胰岛素抵抗的核心病理关联。研究表明，肥胖状态
下脂肪组织分泌的促炎因子通过诱导胰岛素抵抗与抑制蛋白合成加速肌肉流失，而骨骼肌质量下降进一步加重脂质
异位沉积，形成恶性循环本综述为肥胖相关肌肉退行性疾病的防治提供机制-临床转化新视角，助力实现代谢健康
老龄化目标。

关键词


肥胖；肌肉减少症；慢性炎症；胰岛素抵抗

全文:

PDF


参考


[1]Safiri S, Grieger JA, Ghaffari Jolfayi A, et al. Burden

of diseases attributable to excess body weight in 204 countries

and territories, 1990-2019. Nutr J. 2025;24(1):23.

[2]Lopez-Pedrosa JM, Camprubi-Robles M, GuzmanRolo G, et al. The Vicious Cycle of Type 2 Diabetes Mellitus

and Skeletal Muscle Atrophy: Clinical, Biochemical, and

Nutritional Bases. Nutrients. 2024;16(1):172

[3]Petermann-Rocha F, Balntzi V, Gray SR, et

al. Global prevalence of sarcopenia and severe sarcopenia: a

systematic review and meta-analysis. J Cachexia Sarcopenia

Muscle. 2022;13(1):86-99.

[4]Zeng Q, Li N, Pan XF, et al. Clinical management

and treatment of obesity in China. Lancet Diabetes

Endocrinol. 2021;9(6):393-405.

[5]Ren X, Zhang X, He Q, et al. Prevalence of

sarcopenia in Chinese community-dwelling elderly: a

systematic review. BMC Public Health. 2022;22:1702.

[6]Khanal P, Williams AG, He L, et al. Sarcopenia,

Obesity, and Sarcopenic Obesity: Relationship with Skeletal

Muscle Phenotypes and Single Nucleotide Polymorphisms. J

Clin Med. 2021;10(21):4933. doi:10.3390/jcm1021493

[7]Wunderle C, Stumpf F, Schuetz P. Inflammation and

response to nutrition interventions. JPEN J Parenter Enteral

Nutr. 2024;48(1):27-36.

[8]Wu Y, Yao X, Shi X, et al. Myeloma extracellular

vesicle-derived RAGE increases inflammatory responses and

myotube atrophy in multiple myeloma through activation of

the TLR4/NF-κB p65 pathway. Apoptosis. 2024;29(5-

6):849-864. doi:10.1007/s10495-023-01920-7

[9]Cavaliere G, Cimmino F, Trinchese G, et al. From

Obesity-Induced Low-Grade Inflammation to Lipotoxicity

and Mitochondrial Dysfunction: Altered Multi-Crosstalk

between Adipose Tissue and Metabolically Active Organs. An

tioxidants. 2023;12(6):1172.

[10]Aisike G, Kuerbanjiang M, Muheyati D, et

al. Correlation analysis of obesity phenotypes with leptin and

adiponectin. Sci Rep. 2023;13(1):17718.

[11]Yang S, Yang G, Wu H, et al. IL-6 Deficiency

Attenuates Skeletal Muscle Atrophy by Inhibiting Mitochondrial

ROS Production through the Upregulation of PGC-1α inSeptic Mice. Oxid Med Cell Longev. 2022; 2022: 9148246.

[12]Shen KC, Collins KH, Ferey JLA, et al. Excess

intramyocellular lipid in metabolically abnormal

obesity. Diabetes. 2025;73(8):1266-1277.

[13]Huang H, Zheng X, Wen X, et al. Visceral fat

correlates with insulin secretion and sensitivity independent

of BMI and subcutaneous fat in Chinese with type 2

diabetes. Front Endocrinol. 2023;14:1144834.

[14]Cao C, Koh HE, Van Vliet S, et al. Increased plasma

fatty acid clearance, not fatty acid concentration, is associated

with muscle insulin resistance in people with obesity. Metabol

ism. 2022;132:155216. doi:10.1016/j.metabol.2022.155216

[15]蔡永东, 黄彩华. 2型糖尿病性肌少症及其运动

干预研究进展. 福建体育科技. 2023;(5):32-37.

[16]Carvalho LP, Basso-Vanelli RP, Di ThommazoLuporini L, et al. Myostatin and adipokines: The

role of the metabolically unhealthy obese phenotype

in muscle function and aerobic capacity in young

adults. Cytokine. 2018;107:118-124.

[17]Liu ZJ, Zhu CF. Causal relationship between

insulin resistance and sarcopenia. Diabetol Metab

Syndr. 2023;15(1):46.

[18]Ding Q, Sun B, Wang M, et al. N-acetylcysteine

alleviates oxidative stress and apoptosis and prevents skeletal

muscle atrophy in type 1 diabetes mellitus through the

NRF2/HO-1 pathway. Life Sci. 2023;329:121975.

[19]Yang L, Liu D, Jiang S, et al. SIRT1 signaling

pathways in sarcopenia: Novel mechanisms and potential

therapeutic targets. Biomed Pharmacother. 2024;177:116917.


Refbacks

  • 当前没有refback。