Effects of luseogliflozin treatment on hyperglycemia-induced muscle atrophy in rats

Diabetes mellitus is recognized as a risk factor for sarcopenia. Luseogliflozin, a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, reduces inflammation and oxidative stress by improving hyperglycemia, subsequently improving hepatosteatosis or kidney dysfunction. However, the effects of S...

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Published in:Journal of Clinical Biochemistry and Nutrition 2023, Vol.72(3), pp.248-255
Main Authors: Xie, Keyu, Sugimoto, Ken, Tanaka, Minoru, Akasaka, Hiroshi, Fujimoto, Taku, Takahashi, Toshimasa, Onishi, Yuri, Minami, Tomohiro, Yoshida, Shino, Takami, Yoichi, Yamamoto, Koichi, Rakugi, Hiromi
Format: Article
Language:English
Subjects:
Advanced glycosylation end products
Atrophy
Beta cells
Biodegradation
Degradation
Diabetes mellitus
Glycosylation
Hyperglycemia
Inhibitors
Kidney diseases
Mitochondria
mitochondrial function
muscle atrophy
Muscles
Original
Oxidative stress
protein degradation
Risk factors
Sarcopenia
Skeletal muscle
Sodium-glucose cotransporter
sodium-glucose cotransporter 2 inhibitor
Streptozocin
Toxicity
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Summary:Diabetes mellitus is recognized as a risk factor for sarcopenia. Luseogliflozin, a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, reduces inflammation and oxidative stress by improving hyperglycemia, subsequently improving hepatosteatosis or kidney dysfunction. However, the effects of SGLT2 inhibitor on the regulation of skeletal muscle mass or function in hyperglycemia are still unknown. In this study, we investigated the effects of luseogliflozin-mediated attenuation of hyperglycemia on the prevention of muscle atrophy. Twenty-four male Sprague–Dawley rats were randomly divided into four groups: control, control with SGLT2 inhibitor treatment, hyperglycemia, and hyperglycemia with SGLT2 inhibitor treatment. The hyperglycemic rodent model was established using a single injection of streptozotocin, a compound with preferential toxicity toward pancreatic beta cells. Muscle atrophy in streptozotocin-induced hyperglycemic model rats was inhibited by the suppression of hyperglycemia using luseogliflozin, which consequently suppressed hyperglycemia-mediated increase in the levels of advanced glycation end products (AGEs) and activated the protein degradation pathway in muscle cells. Treatment with luseogliflozin can restore the hyperglycemia-induced loss in the muscle mass to some degree partly through the inhibition of AGEs-induced or homeostatic disruption of mitochondria-induced activation of muscle degradation.
ISSN:0912-0009
1880-5086
DOI:10.3164/jcbn.22-58