The Association Between Sarcopenia and Diabetes: From Pathophysiology Mechanism to Therapeutic Strategy

Hui-ling, Chen; Huang, Xiaojing; Dong, Meiyuan; Su, Wen; Zhou, Ligang; Yuan, Xinlu

doi:10.2147/dmso.s410834

Cited by 37 publications

(11 citation statements)

References 163 publications

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“…By targeting multiple pathways involved in muscle protein synthesis and glucose metabolism, this combination of nutrients may work synergically to improve glucose uptake by muscle, stimulate muscle protein synthesis, reduce muscle protein degradation, and counteract insulin resistance. By exploring the unique characteristics of each ingredient and its potential synergy, we seek to provide a novel nutritional strategy that addresses the tremendous changes in the skeletal muscle, concerning both muscle atrophy and glucose utilization in diabetic patients [39].…”

Section: Discussionmentioning

confidence: 99%

Arginine and Lysine Supplementation Potentiates the Beneficial β-Hydroxy ß-Methyl Butyrate (HMB) Effects on Skeletal Muscle in a Rat Model of Diabetes

Manzano,

Girón,

Salto

et al. 2023

Nutrients

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Skeletal muscle is the key tissue for maintaining protein and glucose homeostasis, having a profound impact on the development of diabetes. Diabetes causes deleterious changes in terms of loss of muscle mass, which will contribute to reduced glucose uptake and therefore progression of the disease. Nutritional approaches in diabetes have been directed to increase muscle glucose uptake, and improving protein turnover has been at least partially an oversight. In muscle, β-hydroxy β-methyl butyrate (HMB) promotes net protein synthesis, while arginine and lysine increase glucose uptake, albeit their effects on promoting protein synthesis are limited. This study evaluates if the combination of HMB, lysine, and arginine could prevent the loss of muscle mass and function, reducing the progression of diabetes. Therefore, the combination of these ingredients was tested in vitro and in vivo. In muscle cell cultures, the supplementation enhances glucose uptake and net protein synthesis due to an increase in the amount of GLUT4 transporter and stimulation of the insulin-dependent signaling pathway involving IRS-1 and Akt. In vivo, using a rat model of diabetes, the supplementation increases lean body mass and insulin sensitivity and decreases blood glucose and serum glycosylated hemoglobin. In treated animals, an increase in GLUT4, creatine kinase, and Akt phosphorylation was detected, demonstrating the synergic effects of the three ingredients. Our findings showed that nutritional formulations based on the combination of HMB, lysine, and arginine are effective, not only to control blood glucose levels but also to prevent skeletal muscle atrophy associated with the progression of diabetes.

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Section: Discussionmentioning

confidence: 99%

Arginine and Lysine Supplementation Potentiates the Beneficial β-Hydroxy ß-Methyl Butyrate (HMB) Effects on Skeletal Muscle in a Rat Model of Diabetes

Manzano,

Girón,

Salto

et al. 2023

Nutrients

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“…Age- and diabetes-related muscle loss has been associated with mitochondrial abnormalities with respect to content, size, and morphology as well as function. Compared to younger adults, those who are older exhibit lower oxidative capacity per unit muscle, which results in mitochondrial impairment [ 49 , 50 ]. Newer research results indicate that the accumulation of mitochondrial DNA (mtDNA) mutations and mtDNA copy number depletion may contribute to mitochondrial dysfunction in T2DM [ 51 ].…”

Section: Biochemical Mechanisms Underlying Impaired Glucose Regulatio...mentioning

confidence: 99%

The Vicious Cycle of Type 2 Diabetes Mellitus and Skeletal Muscle Atrophy: Clinical, Biochemical, and Nutritional Bases

Lopez-Pedrosa,

Camprubi-Robles,

Guzman-Rolo

et al. 2024

Nutrients

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Today, type 2 diabetes mellitus (T2DM) and skeletal muscle atrophy (SMA) have become increasingly common occurrences. Whether the onset of T2DM increases the risk of SMA or vice versa has long been under investigation. Both conditions are associated with negative changes in skeletal muscle health, which can, in turn, lead to impaired physical function, a lowered quality of life, and an increased risk of mortality. Poor nutrition can exacerbate both T2DM and SMA. T2DM and SMA are linked by a vicious cycle of events that reinforce and worsen each other. Muscle insulin resistance appears to be the pathophysiological link between T2DM and SMA. To explore this association, our review (i) compiles evidence on the clinical association between T2DM and SMA, (ii) reviews mechanisms underlying biochemical changes in the muscles of people with or at risk of T2DM and SMA, and (iii) examines how nutritional therapy and increased physical activity as muscle-targeted treatments benefit this population. Based on the evidence, we conclude that effective treatment of patients with T2DM-SMA depends on the restoration and maintenance of muscle mass. We thus propose that regular intake of key functional nutrients, along with guidance for physical activity, can help maintain euglycemia and improve muscle status in all patients with T2DM and SMA.

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“…The underlying causes of sarcopenia include malnutrition, inactivity, and disease, as well as drugs and hospital admission 2 . Skeletal muscle quality is thus not only lost with old age (primary sarcopenia) but also in association with diseases such as cancer, 5 type 2 diabetes, 6 cardiovascular disease, 7 chronic obstructive pulmonary disease, 8 chronic kidney disease, 9 advanced liver disease, 10 as well as with acute and chronic critical illness 11 . Obesity is an important risk factor for these chronic disorders, and disease‐related secondary sarcopenia also occurs in individuals with excess body fat 12 .…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial involvement in sarcopenia

Affourtit,

Carré

2024

Acta Physiologica

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Sarcopenia lowers the quality‐of‐life for millions of people across the world, as accelerated loss of skeletal muscle mass and function contributes to both age‐ and disease‐related frailty. Physical activity remains the only proven therapy for sarcopenia to date, but alternatives are much sought after to manage this progressive muscle disorder in individuals who are unable to exercise. Mitochondria have been widely implicated in the etiology of sarcopenia and are increasingly suggested as attractive therapeutic targets to help restore the perturbed balance between protein synthesis and breakdown that underpins skeletal muscle atrophy. Reviewing current literature, we note that mitochondrial bioenergetic changes in sarcopenia are generally interpreted as intrinsic dysfunction that renders muscle cells incapable of making sufficient ATP to fuel protein synthesis. Based on the reported mitochondrial effects of therapeutic interventions, however, we argue that the observed bioenergetic changes may instead reflect an adaptation to pathologically decreased energy expenditure in sarcopenic muscle. Discrimination between these mechanistic possibilities will be crucial for improving the management of sarcopenia.

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The Association Between Sarcopenia and Diabetes: From Pathophysiology Mechanism to Therapeutic Strategy

Cited by 37 publications

References 163 publications

Arginine and Lysine Supplementation Potentiates the Beneficial β-Hydroxy ß-Methyl Butyrate (HMB) Effects on Skeletal Muscle in a Rat Model of Diabetes

Arginine and Lysine Supplementation Potentiates the Beneficial β-Hydroxy ß-Methyl Butyrate (HMB) Effects on Skeletal Muscle in a Rat Model of Diabetes

The Vicious Cycle of Type 2 Diabetes Mellitus and Skeletal Muscle Atrophy: Clinical, Biochemical, and Nutritional Bases

Mitochondrial involvement in sarcopenia

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