Abstract:Background:
Patients with type 2 diabetes mellitus (T2DM) have an increased risk of
muscle mass reduction. However, the association between muscle mass and
mortality in T2DM remains unknown.
Methods:
This was a historical cohort study with the endpoint of all-cause mortality.
This study included 163 Japanese men and 141 postmenopausal women with T2DM
whose body compositions were evaluated using dual-energy X-ray
absorptiometry. Low muscle mass was defined as a skeletal … Show more
“…Protein synthesis in skeletal muscle is decreased by type 1 DM (T1DM) due to loss of insulin signaling, and protein degradation is enhanced with myostatin-mediated autophagy in type 2 DM (T2DM) ( Sala and Zorzano, 2015 ). Particularly, an age-adjusted study reported that muscle wasting is an independent risk for all-cause mortality in patients with T2DM ( Miyake et al, 2019 ). Prevention of DM-associated muscle loss is an important subject but there is no efficacious drugs, because it is still a complicated pathology and underlying mechanism has not been fully understood.…”
Skeletal muscle wasting in patients with diabetes mellitus (DM) is a complication of decreased muscle mass and strength, and is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle wasting. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8 (IL-8). iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat muscle wasting in patients with DM.
“…Protein synthesis in skeletal muscle is decreased by type 1 DM (T1DM) due to loss of insulin signaling, and protein degradation is enhanced with myostatin-mediated autophagy in type 2 DM (T2DM) ( Sala and Zorzano, 2015 ). Particularly, an age-adjusted study reported that muscle wasting is an independent risk for all-cause mortality in patients with T2DM ( Miyake et al, 2019 ). Prevention of DM-associated muscle loss is an important subject but there is no efficacious drugs, because it is still a complicated pathology and underlying mechanism has not been fully understood.…”
Skeletal muscle wasting in patients with diabetes mellitus (DM) is a complication of decreased muscle mass and strength, and is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle wasting. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8 (IL-8). iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat muscle wasting in patients with DM.
“…Aging and obesity are major risk factors in diabetes mellitus (DM), and the number of patients with DM is increasing worldwide. Muscle wasting is associated with the risk of mortality in patients with DM (Miyake et al, 2019). Therefore, the prevention and treatment of DM-associated sarcopenic obesity is important for public health (Wang et al, 2020).…”
Sarcopenic obesity is a complication of decreased muscle mass and strength associated with obesity, and sarcopenia associated with diabetes mellitus (DM) is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle atrophy. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8. iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat sarcopenic obesity.
“…Muscle is a major organ for glucose metabolism [ 9 ]; therefore, muscle is an important target for treatment of patients with T2D. It has been reported that muscle mass loss is associated with low quality of life [ 28 ], cardiovascular disease [ 29 , 30 ], and mortality [ 31 ]. Previous studies revealed that muscle mass of patients with T2D is unchanged or slightly decreased in the natural course [ 32 , 33 , 34 ].…”
Background: The aim of this study was to investigate the effect of the coronavirus disease (COVID-19) pandemic restrictions on the change in muscle mass in older patients with type 2 diabetes (T2D), who were not infected with COVID-19. Methods: In this retrospective cohort study, data were obtained from outpatients who underwent bioelectrical impedance analysis at least twice before April 2020 and at least once thereafter. Skeletal muscle mass index (SMI, kg/m2) was calculated as appendicular muscle mass (kg) divided by height squared (m2). Change in SMI (kg/m2/year) was calculated as (follow-up SMI—baseline SMI/follow-up period). The differences between the changes in SMI before and after the start of the COVID-19 pandemic were evaluated using paired t test. Results: This study recruited 56 patients, with a mean (SD) age of 75.2 (7.1) years. SMI changed from 6.7 (0.9) to 6.8 (0.9) kg/m2 before the COVID-19 pandemic, whereas SMI changed from 6.8 (0.9) to 6.6 (0.9) kg/m2 after the start of the COVID-19 pandemic. SMI decreased after the start of the COVID-19 pandemic compared with before the pandemic (−0.117 (0.240) vs. 0.005 (0.289) kg/m2/year, p = 0.049). This decrease was observed in men (−0.159 (0.257) vs. 0.031 (0.325) kg/m2/year, p = 0.038), patients with poor glycemic control (−0.170 (0.264) vs. 0.031 (0.285) kg/m2/year, p = 0.042), and those with a long diabetes duration (−0.153 (0.229) vs. 0.082 (0.291) kg/m2, p = 0.049). Conclusions: The COVID-19 pandemic restrictions caused muscle mass loss in older patents with T2D. Actions, including recommendation of exercise and adequate diet intake, are needed to prevent loss of muscle mass.
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