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Exercise, Diet and Type 2 Diabetes

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Diabetes".

Deadline for manuscript submissions: 25 February 2025 | Viewed by 2296

Special Issue Editor


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Guest Editor
1. Department of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
2. Department of Diabetology, Kameoka Municipal Hospital, Kameoka 621-8585, Japan
Interests: nutrient; diabetes; immune metabolism; exercise in diabetes; slowly progressive insulin-dependent diabetes mellitus
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Special Issue Information

Dear Colleagues,

We are setting a Special Issue in Nutrients dedicated to the interaction of exercise and type 2 diabetes on skeletal muscle. The loss of skeletal muscle mass or locomotor function is associated with insulin resistance and/or chronic inflammation, which induce several diseases such as type 2 diabetes and cardiovascular disease. Although several exercise therapy approaches, with or without diet manipulation, could prevent or reduce the progression towards type 2 diabetes, the ideal exercise therapy has not been fully elucidated. Therefore, new innovation is needed to establish the ideal exercise approach. This Special Issue welcomes original research articles or clinical trials highlighting new biomarkers or development of therapeutic agents targeting skeletal muscle following exercise with or without diet manipulations in type 2 diabetes or related obesity metabolic disorders We look forward to your submissions.

Dr. Noriyuki Kitagawa
Guest Editor

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Keywords

  • exercise
  • diet
  • type 2 diabetes
  • skeletal muscle mass
  • sarcopenia

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Published Papers (2 papers)

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Research

16 pages, 2018 KiB  
Article
Effect of Isoflavone on Muscle Atrophy in Ovariectomized Mice
by Sayaka Kawai, Takuro Okamura, Chihiro Munekawa, Yuka Hasegawa, Ayaka Kobayashi, Hanako Nakajima, Saori Majima, Naoko Nakanishi, Ryoichi Sasano, Masahide Hamaguchi and Michiaki Fukui
Nutrients 2024, 16(19), 3295; https://doi.org/10.3390/nu16193295 - 28 Sep 2024
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Abstract
Background: Sarcopenia, characterized by muscle mass decline due to aging or other causes, is exacerbated by decreased estrogen levels after menopause in women. Isoflavones, a class of flavonoids acting on estrogen receptors, may have beneficial effects on metabolic disorders. We examined these effects [...] Read more.
Background: Sarcopenia, characterized by muscle mass decline due to aging or other causes, is exacerbated by decreased estrogen levels after menopause in women. Isoflavones, a class of flavonoids acting on estrogen receptors, may have beneficial effects on metabolic disorders. We examined these effects in ovariectomized mice fed a high-fat, high-sucrose diet (HFHSD). Methods: At 7 weeks old, female C57BL6/J mice (18–20 g, n = 12) underwent bilateral ovariectomy (OVX), and were then fed a high-fat, high-sucrose diet starting at 8 weeks of age. Half of the mice received isoflavone water (0.1%). Metabolic analyses, including glucose and insulin tolerance tests, were conducted. Muscle analysis involved grip strength assays, next-generation sequencing, quantitative RT–PCR, and western blotting of skeletal muscle after euthanizing the mice at 14 weeks old. Additionally, 16S rRNA gene sequence analysis of the gut microbiota was performed. Results: The results demonstrated that isoflavone administration did not affect body weight, glucose tolerance, or lipid metabolism. In contrast, isoflavone-treated mice had higher grip strength. Gene expression analysis of the soleus muscle revealed decreased Trim63 expression, and western blotting showed inactivation of muscle-specific RING finger protein 1 in isoflavone-treated mice. Gut microbiota analysis indicated higher Bacteroidetes and lower Firmicutes abundance in the isoflavone group, along with increased microbiota diversity. Gene sets related to TNF-α signaling via NF-κB and unfolded protein response were negatively associated with isoflavones. Conclusions: Isoflavone intake alters gut microbiota and increases muscle strength, suggesting a potential role in improving sarcopenia in menopausal women. Full article
(This article belongs to the Special Issue Exercise, Diet and Type 2 Diabetes)
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12 pages, 2791 KiB  
Article
Daidzein Inhibits Muscle Atrophy by Suppressing Inflammatory Cytokine- and Muscle Atrophy-Related Gene Expression
by Chihiro Munekawa, Takuro Okamura, Saori Majima, Budau River, Sayaka Kawai, Ayaka Kobayashi, Hanako Nakajima, Nobuko Kitagawa, Hiroshi Okada, Takafumi Senmaru, Emi Ushigome, Naoko Nakanishi, Masahide Hamaguchi and Michiaki Fukui
Nutrients 2024, 16(18), 3084; https://doi.org/10.3390/nu16183084 - 13 Sep 2024
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Abstract
Background: Sarcopenic obesity, which is associated with a poorer prognosis than that of sarcopenia alone, may be positively affected by soy isoflavones, known inhibitors of muscle atrophy. Herein, we hypothesize that these compounds may prevent sarcopenic obesity by upregulating the gut metabolites with [...] Read more.
Background: Sarcopenic obesity, which is associated with a poorer prognosis than that of sarcopenia alone, may be positively affected by soy isoflavones, known inhibitors of muscle atrophy. Herein, we hypothesize that these compounds may prevent sarcopenic obesity by upregulating the gut metabolites with anti-inflammatory effects. Methods: To explore the effects of soy isoflavones on sarcopenic obesity and its mechanisms, we employed both in vivo and in vitro experiments. Mice were fed a high-fat, high-sucrose diet with or without soy isoflavone supplementation. Additionally, the mouse C2C12 myotube cells were treated with palmitic acid and daidzein in vitro. Results: The isoflavone considerably reduced muscle atrophy and the expression of the muscle atrophy genes in the treated group compared to the control group (Fbxo32, p = 0.0012; Trim63, p < 0.0001; Foxo1, p < 0.0001; Tnfa, p = 0.1343). Elevated levels of daidzein were found in the muscles and feces of the experimental group compared to the control group (feces, p = 0.0122; muscle, p = 0.0020). The real-time PCR results demonstrated that the daidzein decreased the expression of the palmitate-induced inflammation and muscle atrophy genes in the C2C12 myotube cells (Tnfa, p = 0.0201; Il6, p = 0.0008; Fbxo32, p < 0.0001; Hdac4, p = 0.0002; Trim63, p = 0.0114; Foxo1, p < 0.0001). Additionally, it reduced the palmitate-induced protein expression related to the muscle atrophy in the C2C12 myotube cells (Foxo1, p = 0.0078; MuRF1, p = 0.0119). Conclusions: The daidzein suppressed inflammatory cytokine- and muscle atrophy-related gene expression in the C2C12 myotubes, thereby inhibiting muscle atrophy. Full article
(This article belongs to the Special Issue Exercise, Diet and Type 2 Diabetes)
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