Abstract:Two highly prevalent and growing global diseases impacted by skeletal muscle atrophy are chronic heart failure (HF) and type 2 diabetes mellitus (DM). The presence of either condition increases the likelihood of developing the other, with recent studies revealing a large and relatively poorly characterized clinical population of patients with coexistent HF and DM (HFDM). HFDM results in worse symptoms and poorer clinical outcomes compared with DM or HF alone, and cardiovascular‐focused disease‐modifying agents… Show more
“…Diabetes and heart failure synergistically contribute to severely decreased physical function through skeletal muscle atrophy, inflammation, and metabolic dysfunction. 21 Levels of cardiac dysfunction may correlate poorly with symptoms, 22,23 and exercise training, although associated with improved physical function, 6 has relatively little effect on cardiac function in heart failure. 24,25 The benefits of physical rehabilitation and exercise are thought to be primarily through peripheral mechanisms such as improved skeletal muscle, mitochondrial, and microvascular function.…”
Section: Discussionmentioning
confidence: 99%
“…Muscle strength among heart failure patients with diabetes is impaired compared with patients without diabetes, 28 potentially as a result of mitochondrial dysfunction, reactive oxygen species generation, insulin resistance, lipotoxicity, and inflammation. 21 Other complications of diabetes can lead to significant impairments in mobility and physical function. Patients with diabetes often have concurrent peripheral neuropathy, which can impair balance and proprioception, leading to reduced functional performance and stability.…”
“…Diabetes and heart failure synergistically contribute to severely decreased physical function through skeletal muscle atrophy, inflammation, and metabolic dysfunction. 21 Levels of cardiac dysfunction may correlate poorly with symptoms, 22,23 and exercise training, although associated with improved physical function, 6 has relatively little effect on cardiac function in heart failure. 24,25 The benefits of physical rehabilitation and exercise are thought to be primarily through peripheral mechanisms such as improved skeletal muscle, mitochondrial, and microvascular function.…”
Section: Discussionmentioning
confidence: 99%
“…Muscle strength among heart failure patients with diabetes is impaired compared with patients without diabetes, 28 potentially as a result of mitochondrial dysfunction, reactive oxygen species generation, insulin resistance, lipotoxicity, and inflammation. 21 Other complications of diabetes can lead to significant impairments in mobility and physical function. Patients with diabetes often have concurrent peripheral neuropathy, which can impair balance and proprioception, leading to reduced functional performance and stability.…”
“…Thus, the serum cystatin C level might be elevated by an increase in the BMI, possibly through subclinical inflammation ( 10 , 19 - 21 ) but not a decline in the renal function, leading to discordance between eGFRcre and eGFRcys. In addition, muscle wasting is frequently observed in patients with DM, regardless of increased fat mass, which is called sarcopenic obesity; this effect contributes to the co-existence of a reduced Scr level and increased body weight ( 23 - 25 ). Importantly, a reduction in hemoglobin levels and elevation in BUN levels, markers of malnutrition, are not typically found at this stage of DM if patients do not have advanced-stage diabetic nephropathy.…”
Section: Discussionmentioning
confidence: 99%
“…Intriguingly, the utility of the eGFR for assessing the renal function in diabetic patients is a matter of debate ( 25 ). The results of a cross-sectional study by Luis-Lima et al showed that there was poor agreement between eGFRcre or eGFRcys and the GFR measured by the plasma clearance of iohexol (“measured GFR”), which was greater in patients with a measured GFR <60 mL/min, leading to misclassification of CKD stages in approximately 30% of the study subjects ( 26 ).…”
Objective
We recently reported a novel score for the detection of glomerular filtration rate (GFR) overestimation using a creatinine-based equation. We examined the utility of this score in patients with cardiovascular/renal diseases and diabetes mellitus.
Methods
We enrolled 1,425 patients (65±15 years old; 37% women) who were admitted to our hospital for the management of cardiovascular and renal diseases and their risk factors. Overestimation of the GFR (OE) was defined as a creatinine-based GFR (eGFRcre) ≥120% of the cystatin C-based estimated GFR. The OE score was calculated as the sum of the scores for the body weight, hemoglobin concentration, and blood urea nitrogen (BUN)/serum creatinine (Scr), totaling 1 point if the body weight was <63.0 kg in men or <42.0 kg in women, 1 point if the hemoglobin concentration was <12.4 g/dL in men or <11.0 g/dL in women, and 1 point if the BUN/Scr was >26.5.
Results
The proportion of patients with OE was 14.2%. The score predicted OE with a sensitivity of 70.8% and a specificity of 99.6%, and the sensitivity was increased in patients ≥75 years old (88.3%) and decreased in diabetics (58.6%). When patients were divided into subgroups by the total score, the frequencies of OE were 8% (59/754), 14% (72/502), 38% (58/151), and 72% (13/18) in patients with scores of 0, 1, 2, and 3, respectively.
Conclusion
The OE score is useful for detecting elderly cases of cardiovascular and renal diseases in which eGFRcre overestimates the GFR, although its utility is limited in diabetics.
“…Many metabolic diseases, including diabetes, chronic kidney disease, and cancer, can cause whole-body muscle atrophy and make people become emaciated [ 34 , 35 ]. This situation can not only lead to the loss of body muscle mass, but also increase the mortality of humans.…”
Eggs are rich in nutrients and contain a lot of protein. Although eggs have proved to accelerate the growth of C2C12 cells, the regulatory and mechanism of fertilized egg yolk extract (FEYE) on skeletal muscle development and fat metabolism remains unclearly. The mice were treated with FEYE by gavage for 24 d, we found that FEYE can inhibit the expression of skeletal muscle atrophy genes such as MSTN and Murf-1, and up-regulate the expression levels of MYOD, MYOG and Irisin. In addition, the treatment of FEYE induced UCP1 and PGC1α high expression in WAT, thereby causing WAT browning reaction. In order to confirm the composition of FEYE, we performed protein full spectrum identification (LC MS/MS) analysis and found the most enriched component is vitellogenin 2 (VTG2). Therefore, we added the recombinant protein VTG2 to C2C12 cells and found that VTG2 promoted the proliferation and differentiation of C2C12 cells. After that, we further proved that VTG2 inhibited the expression of MSTN and improved the expression of MYOD and Irisin. Finally, the dual luciferase test proved that VTG2 directly inhibited the transcriptional activity of MSTN. Our results conclude that FEYE inhibits the expression of MSTN in muscle tissues by delivering VTG2, thereby promoting skeletal muscle development, and can also promote the expression level of FNDC5 in serum. Then, FNDC5 acts on the fat through the serum, stimulating the browning reaction of white adipocytes. Therefore, VTG2 can be used to stop muscle consumption, improve skeletal muscle aging, and prevent obesity.
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