Nicotinamide protects against skeletal muscle atrophy in streptozotocin-induced diabetic mice

被引：30
作者：
Guo, Shizhe [1 ]
Chen, Qingyan [2 ]
Sun, Yaying [3 ]
Chen, Jiwu [3 ]
机构：
[1] Fudan Univ, Huashan Hosp, Dept Endocrinol & Metab, Shanghai, Peoples R China
[2] Boston Univ, Dept Biol, Coll Arts & Sci, 5 Cummington St, Boston, MA 02215 USA
[3] Fudan Univ, Huashan Hosp, Dept Sports Med, 12 Middle Wulumuqi Rd, Shanghai 200040, Peoples R China
来源：
ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY | 2019年 / 125卷 / 05期
基金：
中国国家自然科学基金;
关键词：
Nicotinamide; diabetes mellitus; skeletal muscle; atrophy; TGF-beta; 1; TGF-BETA; SHORT-TERM; NAD(+); EXPRESSION; METABOLISM; ACTIVATION; FIBROSIS; CACHEXIA; PATHWAY; MASS;
D O I：
10.1080/13813455.2019.1638414
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Context: Skeletal muscle atrophy is a complication of diabetes, partially induced by nicotinamide adenine dinucleotide (NAD(+)) deficiency. Objective: This study investigates the potential of nicotinamide (NAM) supplementation, a precursor of NAD(+), against muscle atrophy. Methods: Mice were separated into normal control group, normal control with NAM administration group, diabetic group, and diabetic mice with NAM administration group. Basic characteristics, muscle weight, maximal grip strength, and myofibers cross-sectional area were analysed. Markers reflecting muscle atrophy and hypertrophy, and transforming growth factor beta 1/Smad2 (TGF-beta 1/Smad2) pathway were examined. Results: NAM did not influence body weight and blood glucose. In diabetic mice, NAM increased NAD(+) level, rescued muscle weight and strength loss, and increased myofibers cross-sectional area. NAM inhibited MuRF1 and Atrogin1, while elevated phosphorylation of Akt. Overactivation of TGF-beta 1/Smad2 pathway was repressed by NAM. Conclusion: NAM ameliorated diabetic muscle atrophy by rebalancing protein anabolism and catabolism, probably through de-activation of TGF-beta 1/Smad2 signaling.
引用
收藏
页码：470 / 477
页数：8
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