scholarly journals Magnesium Deficiency Alters Expression of Genes Critical for Muscle Magnesium Homeostasis and Physiology in Mice

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2169
Author(s):  
Dominique Bayle ◽  
Cécile Coudy-Gandilhon ◽  
Marine Gueugneau ◽  
Sara Castiglioni ◽  
Monica Zocchi ◽  
...  
Keyword(s):  
Gastrocnemius Muscle ◽  
Magnesium Deficiency ◽  
Mitochondrial Dynamics ◽  
Body Weight Gain ◽  
Whole Body ◽  
Muscle Physiology ◽  
Deficient Diet ◽  
Muscle Weight ◽  
Magnesium Homeostasis ◽  
Expression Of Genes

Chronic Mg2+ deficiency is the underlying cause of a broad range of health dysfunctions. As 25% of body Mg2+ is located in the skeletal muscle, Mg2+ transport and homeostasis systems (MgTHs) in the muscle are critical for whole-body Mg2+ homeostasis. In the present study, we assessed whether Mg2+ deficiency alters muscle fiber characteristics and major pathways regulating muscle physiology. C57BL/6J mice received either a control, mildly, or severely Mg2+-deficient diet (0.1%; 0.01%; and 0.003% Mg2+ wt/wt, respectively) for 14 days. Mg2+ deficiency slightly decreased body weight gain and muscle Mg2+ concentrations but was not associated with detectable variations in gastrocnemius muscle weight, fiber morphometry, and capillarization. Nonetheless, muscles exhibited decreased expression of several MgTHs (MagT1, CNNM2, CNNM4, and TRPM6). Moreover, TaqMan low-density array (TLDA) analyses further revealed that, before the emergence of major muscle dysfunctions, even a mild Mg2+ deficiency was sufficient to alter the expression of genes critical for muscle physiology, including energy metabolism, muscle regeneration, proteostasis, mitochondrial dynamics, and excitation–contraction coupling.

Decrease in muscle glucose transporter number in chronic physical inactivity in rats

1991 ◽  
Vol 260 (3) ◽  
pp. E403-E410 ◽  
Author(s):  
T. Fushiki ◽  
T. Kano ◽  
K. Inoue ◽  
E. Sugimoto
Keyword(s):  
Glucose Uptake ◽  
Physical Inactivity ◽  
Gastrocnemius Muscle ◽  
Glucose Transporter ◽  
Contractile Activity ◽  
Body Weight Gain ◽  
Muscle Growth ◽  
Whole Body ◽  
Glucose Disposal ◽  
Physically Inactive

In this study, whole body insulin action on glucose uptake and muscle glucose transporter number of rats subjected to 14 days of physical inactivity conditions was examined. Unlike other suspension and denervation models of muscle disuse, this physical inactivity model allows voluntary contractile activity with minimal stress. Minimal depression of body weight gain and significant depression of gastrocnemius muscle growth were observed compared with that of control rats after 14 days of physical inactivity. The whole body insulin sensitivity and responsiveness were determined by the euglycemic clamp technique, with 1.4, 3.6, and 14 mU insulin.kg-1.min-1 perfusion and 2-deoxy-D-[3H]glucose incorporation. The rates of glucose disposal were the same in the restrained rats as in the controls with the 1.4 and 3.6 mU insulin perfusion; however, glucose disposal significantly decreased with 14 mU insulin perfusion. 2-Deoxy-D-[3H]glucose uptake into the gastrocnemius muscle was higher in the control rats than in the physically inactive rats. Glucose transporters in the gastrocnemius and quadriceps muscles, measured by means of the D-glucose-inhibitable cytochalasin B binding assay, were significantly decreased in number in the physically inactive rats. These findings suggest that the decrease in whole body glucose uptake might in part be explained by the decreases in the total glucose transporter number in muscles.

scholarly journals Tungstate Decreases Weight Gain and Adiposity in Obese Rats through Increased Thermogenesis and Lipid Oxidation

Endocrinology ◽  
2005 ◽  
Vol 146 (10) ◽  
pp. 4362-4369 ◽  
Author(s):  
Marc Claret ◽  
Helena Corominola ◽  
Ignasi Canals ◽  
Josep Saura ◽  
Silvia Barcelo-Batllori ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Molecular Mechanisms ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Whole Body ◽  
Mitochondrial Uncoupling ◽  
Novel Therapy ◽  
Expression Of Genes ◽  
Obese Rats

The increasing worldwide incidence of obesity and the limitations of current treatments raise the need for finding novel therapeutic approaches to treat this disease. The purpose of the current study was first to investigate the effects of tungstate on body weight and insulin sensitivity in a rat model of diet-induced obesity. Second, we aimed to gain insight into the molecular mechanisms underlying its action. Oral administration of tungstate significantly decreased body weight gain and adiposity without modifying caloric intake, intestinal fat absorption, or growth rate in obese rats. Moreover, the treatment ameliorated dislipemia and insulin resistance of obese rats. These effects were mediated by an increase in whole-body energy dissipation and by changes in the expression of genes involved in the oxidation of fatty acids and mitochondrial uncoupling in adipose tissue. Furthermore, treatment increased the number of small adipocytes with a concomitant induction of apoptosis. Our results indicate that tungstate treatment may provide the basis for a promising novel therapy for obesity.

scholarly journals Tart Cherry (Fruit of Prunus cerasus) Concentrated Powder (TCcp) Ameliorates Glucocorticoid-Induced Muscular Atrophy in Mice

Medicina ◽  
2021 ◽  
Vol 57 (5) ◽  
pp. 485
Author(s):  
Sae-Kwang Ku ◽  
Jong-Min Lim ◽  
Hyung-Rae Cho ◽  
Khawaja Muhammad Imran Bashir ◽  
Young Suk Kim ◽  
...  
Keyword(s):  
Gastrocnemius Muscle ◽  
Muscular Atrophy ◽  
Muscle Protein ◽  
Oral Treatment ◽  
Calf Muscle ◽  
Prunus Cerasus ◽  
Tart Cherry ◽  
Muscle Weight ◽  
Beneficial Effects ◽  
Antioxidant Defense Systems

Background and Objectives: The present study investigated the beneficial effects of tart cherry (fruit of Prunus cerasus) concentrated powder (TCcp) on glucocorticoid (GLU)-induced catabolic muscular atrophy in the skeletal muscle of mice. Furthermore, its potential mechanism was also studied. Materials and Methods: Changes in calf thickness, calf muscle weight, calf muscle strength, body weight, gastrocnemius muscle histology, immunohistochemistry, serum creatinine, creatine kinase, lactate dehydrogenase, and antioxidant defense systems were measured. Malondialdehyde, reactive oxygen species, glutathione content, catalase, and superoxide dismutase activities in the gastrocnemius muscle, and muscle-specific mRNA expressions were evaluated. Results: After 24 days, GLU control mice showed muscular atrophy at all criteria of indexes. The muscular atrophy symptoms were significantly inhibited by oral treatment with 250 mg/kg and 500 mg/kg of TCcp through antioxidative and anti-inflammatory modulated expression of genes involved in muscle protein degradation (myostatin, atrogin-1, SIRT1, and MuRF1) and synthesis (A1R, Akt1, TRPV4, and PI3K). Conclusions: This study shows that the TCcp (500 mg/kg and 250 mg/kg) could improve muscular atrophies caused by various etiologies.

scholarly journals Non-alcoholic fatty liver disease in mice with hepatocyte-specific deletion of mitochondrial fission factor

Diabetologia ◽  
2021 ◽  
Author(s):  
Yukina Takeichi ◽  
Takashi Miyazawa ◽  
Shohei Sakamoto ◽  
Yuki Hanada ◽  
Lixiang Wang ◽  
...  
Keyword(s):  
Er Stress ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Primary Hepatocytes ◽  
Alcoholic Fatty Liver ◽  
Expression Of Genes ◽  
Specific Deletion

Abstract Aims/hypothesis Mitochondria are highly dynamic organelles continuously undergoing fission and fusion, referred to as mitochondrial dynamics, to adapt to nutritional demands. Evidence suggests that impaired mitochondrial dynamics leads to metabolic abnormalities such as non-alcoholic steatohepatitis (NASH) phenotypes. However, how mitochondrial dynamics are involved in the development of NASH is poorly understood. This study aimed to elucidate the role of mitochondrial fission factor (MFF) in the development of NASH. Methods We created mice with hepatocyte-specific deletion of MFF (MffLiKO). MffLiKO mice fed normal chow diet (NCD) or high-fat diet (HFD) were evaluated for metabolic variables and their livers were examined by histological analysis. To elucidate the mechanism of development of NASH, we examined the expression of genes related to endoplasmic reticulum (ER) stress and lipid metabolism, and the secretion of triacylglycerol (TG) using the liver and primary hepatocytes isolated from MffLiKO and control mice. Results MffLiKO mice showed aberrant mitochondrial morphologies with no obvious NASH phenotypes during NCD, while they developed full-blown NASH phenotypes in response to HFD. Expression of genes related to ER stress was markedly upregulated in the liver from MffLiKO mice. In addition, expression of genes related to hepatic TG secretion was downregulated, with reduced hepatic TG secretion in MffLiKO mice in vivo and in primary cultures of MFF-deficient hepatocytes in vitro. Furthermore, thapsigargin-induced ER stress suppressed TG secretion in primary hepatocytes isolated from control mice. Conclusions/interpretation We demonstrated that ablation of MFF in liver provoked ER stress and reduced hepatic TG secretion in vivo and in vitro. Moreover, MffLiKO mice were more susceptible to HFD-induced NASH phenotype than control mice, partly because of ER stress-induced apoptosis of hepatocytes and suppression of TG secretion from hepatocytes. This study provides evidence for the role of mitochondrial fission in the development of NASH. Graphical abstract

Effect of growth hormone on gastrocnemius muscle of aged rats after immobilization: biochemistry and morphology

1993 ◽  
Vol 75 (4) ◽  
pp. 1529-1535 ◽  
Author(s):  
E. Carmeli ◽  
Z. Hochberg ◽  
E. Livne ◽  
I. Lichtenstein ◽  
C. Kestelboim ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gastrocnemius Muscle ◽  
Muscle Protein ◽  
Aged Rats ◽  
Muscle Weight ◽  
Hindlimb Muscles ◽  
Capillary Blood Volume ◽  
Rat Growth ◽  
Old Rats ◽  
Limb Immobilization

Immobilization of limbs of aged animals is associated with swift muscular damage and atrophy. We investigated the effect of rat growth hormone (rGH) on immobilized hindlimb muscles of 26-mo-old rats. Administration of rGH significantly reduced muscle weight loss and muscle protein oxidation caused by immobilization. Capillary blood volume, measured by photoplethysmography of the hindlimb, showed a 34% reduction in immobilized animals, which was eliminated by rGH. The activity of creatine phosphokinase in immobilized gastrocnemius muscle was significantly reduced by immobilization. This damage was diminished by rGH administration. Similarly, the increase in acid phosphatase activity in immobilized muscle was reduced after rGH treatment. Morphologically, marked muscle atrophy and fiber disorientation were observed in immobilized limbs. Therapy with rGH prevented some of these changes. These results indicate that administration of rGH may provide a useful means to attenuate the degenerative effects of limb immobilization of aged rats, as evident from physiological, biochemical, and morphological parameters.

scholarly journals Antiobesity Effect of a Novel Herbal Formulation LI85008F in High-Fat Diet-Induced Obese Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Hak Joo Choi ◽  
Hwa Young Kim ◽  
Kyoung Sik Park
Keyword(s):  
Weight Gain ◽  
Body Fat ◽  
Fat Mass ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Whole Body ◽  
Body Fat Mass ◽  
Obese Mice ◽  
High Fat ◽  
Herbal Formulation

A variety of natural products have been explored for their antiobesity potential and widely used to develop dietary supplements for the prevention of weight gain from excess body fat. In an attempt to find a natural antiobesity agent, this study was designed to evaluate the antiobesity activity of a novel herbal formulation LI85008F composed of extracts from three medicinal plants in high-fat diet- (HFD-) induced obese mice. After the thirteen-week oral administration of the test materials to mice, the body weight gain, whole-body fat mass, adipose tissue weight, and the expression levels of obesity-related proteins were measured. Our results indicated that LI85008F can suppress body weight gain and lower whole-body fat mass in HFD-induced obese mice. Significant decreases in epididymal and retroperitoneal fat mass were observed in LI85008F-treated groups compared with the HFD-fed control group ( p < 0.05 ). Furthermore, the oral administration of LI85008F caused significant decreases in the expression level of adipogenic (C/EBPα and PPARγ) and lipogenic (ACC) markers and notable increases in the production level of thermogenetic (AMPKα, PGC1α and UCP1) and lipolytic (HSL) proteins. These findings suggest that LI85008F holds great promise for a novel herbal formulation with antiobesity activities, preventing body fat accumulation and altering lipid metabolism.

scholarly journals Metabolic tracing reveals novel adaptations to skeletal muscle cell energy production pathways in response to NAD+ depletion

2019 ◽  
Vol 3 ◽  
pp. 147 ◽  
Author(s):  
Lucy A. Oakey ◽  
Rachel S. Fletcher ◽  
Yasir S. Elhassan ◽  
David M. Cartwright ◽  
Craig L. Doig ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Carbon Metabolism ◽  
Energy Production ◽  
Quantum Coherence ◽  
Metabolic Energy ◽  
Whole Body ◽  
Muscle Physiology ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Central Carbon ◽  
Metabolic Tracing

Background: Skeletal muscle is central to whole body metabolic homeostasis, with age and disease impairing its ability to function appropriately to maintain health. Inadequate NAD+ availability is proposed to contribute to pathophysiology by impairing metabolic energy pathway use. Despite the importance of NAD+ as a vital redox cofactor in energy production pathways being well-established, the wider impact of disrupted NAD+ homeostasis on these pathways is unknown. Methods: We utilised skeletal muscle myotube models to induce NAD+ depletion, repletion and excess and conducted metabolic tracing to provide comprehensive and detailed analysis of the consequences of altered NAD+ metabolism on central carbon metabolic pathways. We used stable isotope tracers, [1,2-13C] D-glucose and [U-13C] glutamine, and conducted combined 2D-1H,13C-heteronuclear single quantum coherence (HSQC) NMR spectroscopy and GC-MS analysis. Results: NAD+ excess driven by nicotinamide riboside (NR) supplementation within skeletal muscle cells resulted in enhanced nicotinamide clearance, but had no effect on energy homeostasis or central carbon metabolism. Nicotinamide phosphoribosyltransferase (NAMPT) inhibition induced NAD+ depletion and resulted in equilibration of metabolites upstream of glyceraldehyde phosphate dehydrogenase (GAPDH). Aspartate production through glycolysis and TCA cycle activity was increased in response to low NAD+, which was rapidly reversed with repletion of the NAD+ pool using NR. NAD+ depletion reversibly inhibits cytosolic GAPDH activity, but retains mitochondrial oxidative metabolism, suggesting differential effects of this treatment on sub-cellular pyridine pools. When supplemented, NR efficiently reversed these metabolic consequences. However, the functional relevance of increased aspartate levels after NAD+ depletion remains unclear, and requires further investigation. Conclusions: These data highlight the need to consider carbon metabolism and clearance pathways when investigating NAD+ precursor usage in models of skeletal muscle physiology.

scholarly journals High Sugar Intake and Development of Skeletal Muscle Insulin Resistance and Inflammation in Mice: A Protective Role for PPAR-δAgonism

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Elisa Benetti ◽  
Raffaella Mastrocola ◽  
Mara Rogazzo ◽  
Fausto Chiazza ◽  
Manuela Aragno ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Gastrocnemius Muscle ◽  
Metabolic Diseases ◽  
Whole Body ◽  
Intercellular Adhesion Molecule ◽  
Fibroblast Growth Factor 21 ◽  
Peroxisome Proliferator ◽  
Intercellular Adhesion Molecule 1 ◽  
Peroxisome Proliferator Activated Receptor

Peroxisome Proliferator Activated Receptor (PPAR)-δagonists may serve for treating metabolic diseases. However, the effects of PPAR-δagonism within the skeletal muscle, which plays a key role in whole-body glucose metabolism, remain unclear. This study aimed to investigate the signaling pathways activated in the gastrocnemius muscle by chronic administration of the selective PPAR-δagonist, GW0742 (1 mg/kg/day for 16 weeks), in male C57Bl6/J mice treated for 30 weeks with high-fructose corn syrup (HFCS), the major sweetener in foods and soft-drinks (15% wt/vol in drinking water). Mice fed with the HFCS diet exhibited hyperlipidemia, hyperinsulinemia, hyperleptinemia, and hypoadiponectinemia. In the gastrocnemius muscle, HFCS impaired insulin and AMP-activated protein kinase signaling pathways and reduced GLUT-4 and GLUT-5 expression and membrane translocation. GW0742 administration induced PPAR-δupregulation and improvement in glucose and lipid metabolism. Diet-induced activation of nuclear factor-κB and expression of inducible-nitric-oxide-synthase and intercellular-adhesion-molecule-1 were attenuated by drug treatment. These effects were accompanied by reduction in the serum concentration of interleukin-6 and increase in muscular expression of fibroblast growth factor-21. Overall, here we show that PPAR-δactivation protects the skeletal muscle against the metabolic abnormalities caused by chronic HFCS exposure by affecting multiple levels of the insulin and inflammatory cascades.

scholarly journals Effects of gut microbiota on leptin expression and body weight are lessened by high-fat diet in mice

2020 ◽  
Vol 124 (4) ◽  
pp. 396-406 ◽  
Author(s):  
Hongyang Yao ◽  
Chaonan Fan ◽  
Xiuqin Fan ◽  
Yuanyuan Lu ◽  
Yuanyuan Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Hepatic Expression ◽  
Reduced Body ◽  
Expression Of Genes ◽  
Underlying Mechanisms ◽  
Leptin Expression

AbstractAberration in leptin expression is one of the most frequent features in the onset and progression of obesity, but the underlying mechanisms are still unclear and need to be clarified. This study investigated the effects of the absence of gut microbiota on body weight and the expression and promoter methylation of the leptin. Male C57 BL/6 J germ-free (GF) and conventional (CV) mice (aged 4–5 weeks) were fed either a normal-fat diet (NFD) or a high-fat diet (HFD) for 16 weeks. Six to eight mice from each group, at 15 weeks, were administered exogenous leptin for 7 d. Leptin expression and body weight gain in GF mice were increased by NFD with more CpG sites hypermethylated at the leptin promoter, whereas there was no change with HFD, compared with CV mice. Adipose or hepatic expression of genes associated with fat synthesis (Acc1, Fas and Srebp-1c), hydrolysis and oxidation (Atgl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was lower, and hypothalamus expression of Pomc and Socs3 was higher in GF mice than levels in CV mice, particularly with NFD feeding. Exogenous leptin reduced body weight in both types of mice, with a greater effect on CV mice with NFD. Adipose Lep-R expression was up-regulated, and hepatic Fas and hypothalamic Socs3 were down-regulated in both types of mice. Expression of fat hydrolysis and oxidative genes (Atgl, Hsl, Cpt1a, Cpt1c, Ppar-α and Pgc-1α) was up-regulated in CV mice. Therefore, the effects of gut microbiota on the leptin expression and body weight were affected by dietary fat intake.

Sign in / Sign up

Export Citation Format

Share Document