scholarly journals Nicotinamide riboside supplementation to improve skeletal muscle mitochondrial health and whole‐body glucose homeostasis: does it actually work in humans?

2020 ◽  
Vol 598 (4) ◽  
pp. 619-620
Author(s):  
Jean‐Philippe Leduc‐Gaudet ◽  
Maude Dulac ◽  
Olivier Reynaud ◽  
Marie‐Belle Ayoub ◽  
Gilles Gouspillou
Keyword(s):  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Whole Body ◽  
Nicotinamide Riboside

Insulin resistance: cross-talk between adipose tissue and skeletal muscle, through free fatty acids, liver X receptor, and peroxisome proliferator-activated receptor-α signaling

2013 ◽  
Vol 15 (3) ◽  
Author(s):  
Ann Louise Olson
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Glucose Homeostasis ◽  
Glucose Transporter ◽  
Control Point ◽  
Nuclear Hormone Receptor ◽  
Whole Body ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

AbstractSkeletal muscle and adipose tissue play a major role in the regulation of whole-body glucose homeostasis. Much of the coordinated regulation of whole-body glucose homeostasis results from the regulation of lipid storage and release by adipose tissue and efficient switching between glucose oxidation and fatty acid oxidation in skeletal muscle. A control point for these biochemical actions center around the regulation of the insulin responsive glucose transporter, GLUT4. This review examines the regulation of GLUT4 in adipose tissue and skeletal muscle, in the context of the steroid nuclear hormone receptor signaling.

scholarly journals Exercising for Insulin Sensitivity – Is There a Mechanistic Relationship With Quantitative Changes in Skeletal Muscle Mass?

2021 ◽  
Vol 12 ◽  
Author(s):  
Jasmine Paquin ◽  
Jean-Christophe Lagacé ◽  
Martin Brochu ◽  
Isabelle J. Dionne
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Metabolic Health ◽  
Whole Body ◽  
Future Research ◽  
Level Of Evidence ◽  
Exercise Interventions ◽  
Quantitative Changes ◽  
The Impact

Skeletal muscle (SM) tissue has been repetitively shown to play a major role in whole-body glucose homeostasis and overall metabolic health. Hence, SM hypertrophy through resistance training (RT) has been suggested to be favorable to glucose homeostasis in different populations, from young healthy to type 2 diabetic (T2D) individuals. While RT has been shown to contribute to improved metabolic health, including insulin sensitivity surrogates, in multiple studies, a universal understanding of a mechanistic explanation is currently lacking. Furthermore, exercised-improved glucose homeostasis and quantitative changes of SM mass have been hypothesized to be concurrent but not necessarily causally associated. With a straightforward focus on exercise interventions, this narrative review aims to highlight the current level of evidence of the impact of SM hypertrophy on glucose homeostasis, as well various mechanisms that are likely to explain those effects. These mechanistic insights could provide a strengthened rationale for future research assessing alternative RT strategies to the current classical modalities, such as low-load, high repetition RT or high-volume circuit-style RT, in metabolically impaired populations.

scholarly journals Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

2020 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Yasir S. Elhassan ◽  
Gareth G. Lavery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Endurance Capacity ◽  
Similar Response ◽  
Transcriptional Responses ◽  
Nicotinamide Riboside ◽  
Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

Antioxidant supplemention in the treatment of skeletal muscle insulin resistance: potential mechanisms and clinical relevance

2008 ◽  
Vol 33 (1) ◽  
pp. 21-31 ◽  
Author(s):  
David Wright ◽  
Lindsey Sutherland
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Whole Body ◽  
Antioxidant Compounds ◽  
Muscle Insulin Resistance ◽  
Beneficial Effects ◽  
Skeletal Muscle Insulin Resistance

The incidence of type 2 diabetes has increased dramatically over the past several decades and this trend is projected to continue into the foreseeable future. Skeletal muscle insulin resistance is thought to be a key development in the pathogenesis of type 2 diabetes. Given this fact, interventions that prevent or reverse impairments in skeletal muscle action can have profound effects on whole-body glucose homeostasis. Traditional approaches used in this regard include exercise, weight loss, and insulin-sensitizing drugs such as thiazolidinediones (TZDs). Although these interventions have proven effective in improving glucose homeostasis, there are adherence issues seen with lifestyle interventions and undesirable side effects have been reported with TZDs. With these points in mind, the development of alternative strategies to maintain or improve skeletal muscle insulin sensitivity is warranted. In this context, the purpose of the present review is to highlight the role of antioxidant compounds in the prevention and treatment of skeletal muscle insulin resistance. Specifically, we will briefly describe the mechanisms of insulin-stimulated skeletal muscle glucose uptake and the potential mediators of oxidative stress induced insulin resistance, highlight data suggesting that antioxidant compounds can have beneficial effects on skeletal muscle insulin action, and discuss potential mechanisms mediating this effect.

scholarly journals Delivery of adiponectin gene to skeletal muscle using ultrasound targeted microbubbles improves insulin sensitivity and whole body glucose homeostasis

2013 ◽  
Vol 304 (2) ◽  
pp. E168-E175 ◽  
Author(s):  
Vivian Vu ◽  
Ying Liu ◽  
Sanjana Sen ◽  
Aimin Xu ◽  
Gary Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Homeostasis ◽  
Fluorescent Protein ◽  
Systemic Circulation ◽  
Tolerance Test ◽  
Whole Body ◽  
Glucose Disposal ◽  
Adiponectin Gene ◽  
Green Fluorescent

Numerous studies have shown that adiponectin confers antidiabetic effects via both insulin-like and insulin-sensitizing actions. The majority of adiponectin in circulation is derived from adipocytes; however, other tissues such as skeletal muscle can produce adiponectin. This study was designed to investigate the functional significance of adiponectin produced by skeletal muscle. We encapsulated the adiponectin gene in lipid-coated microspheres filled with octafluoropropane gas that were injected into the systemic circulation and destroyed within the microvasculature of skeletal muscle using ultrasound. We first demonstrated safe and successful targeting of luciferase and green fluorescent protein reporter genes to skeletal muscle using this approach and then confirmed efficient overexpression of adiponectin mRNA and oligomeric protein forms. Glucose tolerance test indicated that overexpression of adiponectin in skeletal muscle was able to improve glucose intolerance induced by feeding mice a high-fat diet (HFD), and this correlated with improved skeletal muscle insulin signaling. We then performed hyperinsulinemic-euglycemic clamp studies and demonstrated that adiponectin overexpression attenuated the decreases in glucose infusion rate, glucose disposal, and increase in glucose appearance induced by HFD. Ultrasound-targeted microbubble destruction (UTMD) delivery of adiponectin to skeletal muscle also enhanced serum adiponectin levels and improved hepatic insulin sensitivity. In conclusion, our data show that UTMD efficiently delivers adiponectin to skeletal muscle and that this improves insulin sensitivity and glucose homeostasis.

scholarly journals Soya protein reverses dyslipidaemia and the altered capacity of insulin-stimulated glucose utilization in the skeletal muscle of sucrose-rich diet-fed rats

2008 ◽  
Vol 102 (1) ◽  
pp. 60-68 ◽  
Author(s):  
María E. Oliva ◽  
Adriana G. Chicco ◽  
Yolanda B. Lombardo
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Glucose Utilization ◽  
Body Weight Gain ◽  
Protein Isolate ◽  
Soya Protein ◽  
Whole Body ◽  
Control Group ◽  
Soya Protein Isolate

The present study investigates the benefits of dietary intake of soya protein upon dyslipidaemia and insulin resistance in rats chronically (8 months) fed a sucrose-rich (63 %) diet (SRD). For this purpose, we analysed the effectiveness of soya protein isolate in improving or reversing these metabolic abnormalities. Wistar rats were fed a SRD for 4 months. By the end of this period, stable dyslipidaemia and insulin resistance were present in the animals. From months 4 to 8, half the animals continued with the SRD and the other half were fed a SRD in which the source of protein casein was substituted by soya. The control group received a diet in which the source of carbohydrate was maize starch. The results showed that: (1) soya protein normalized plasma TAG, cholesterol and NEFA levels in the SRD-fed rats. Moreover, the addition of soya protein reversed the hepatic steatosis. (2) Glucose homeostasis was normalized without changes in circulating insulin levels. Whole-body peripheral insulin sensitivity substantially improved. Besides, soya protein moderately decreases body weight gain limiting the accretion of visceral fat. (3) By shifting the source of dietary protein from casein to soya during the last 4 months of the feeding period it was possible to reverse both the diminished insulin-stimulated glucose oxidation and disposal in the skeletal muscle of SRD-fed rats. This study provides new data showing the beneficial effect of soya protein upon lipid and glucose homeostasis in the experimental model of dyslipidaemia and insulin resistance.

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