scholarly journals Interleukin-4 Promotes Myogenesis and Boosts Myocyte Insulin Efficacy

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yih-Hsin Chang ◽  
Jen-Ning Tsai ◽  
Tzu-Lin Chen ◽  
Kuo-Ting Ho ◽  
Hsin-Yi Cheng ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Insulin Signaling ◽  
Energy Homeostasis ◽  
Interleukin 4 ◽  
Whole Body ◽  
Myocyte Differentiation ◽  
Anti Inflammatory Cytokine

Anti-inflammatory cytokine interleukin-4 (IL-4) promotes glucose tolerance and insulin sensitivity while reduces lipid deposits. However, the effects of IL-4 on energy metabolism in muscle, the largest insulin-targeting organ, remain obscure. The study aimed at addressing the roles of IL-4 in myocyte differentiation (myogenesis) and energy metabolism of muscle cells. Effects of IL-4 on myogenesis, and interaction between IL-4 and insulin on glucose metabolism of C2C12 myoblasts and the terminal differentiated myocytes were analyzed. IL-4 improved GLUT4 translocation and tended to elevate glucose uptake by boosting insulin signaling. In diabetic mice, transient and long-term IL-4 showed differential effects on insulin signaling and efficacy. The study provides evidence to address the roles of IL-4 in mediating whole-body muscle reservoir and glucose metabolism, as well as the interaction between immune responses and energy homeostasis. IL-4 has dual potential to act as an adjuvant therapeutic target for sarcopenia to preserve muscle mass and insulin resistance to improve insulin sensitivity, which implicates the regulation of immune system to the muscle differentiation and exercise performance.

scholarly journals Cross-Talk between PPARγand Insulin Signaling and Modulation of Insulin Sensitivity

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-12 ◽  
Author(s):  
Anna Leonardini ◽  
Luigi Laviola ◽  
Sebastio Perrini ◽  
Annalisa Natalicchio ◽  
Francesco Giorgino
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Beneficial Effects ◽  
Major Mediator

PPARγactivation in type 2 diabetic patients results in a marked improvement in insulin and glucose parameters, resulting from an improvement of whole-body insulin sensitivity. Adipose tissue is the major mediator of PPARγaction on insulin sensitivity. PPARγactivation in mature adipocytes induces the expression of a number of genes involved in the insulin signaling cascade, thereby improving insulin sensitivity. PPARγis the master regulator of adipogenesis, thereby stimulating the production of small insulin-sensitive adipocytes. In addition to its importance in adipogenesis, PPARγplays an important role in regulating lipid, metabolism in mature adipocytes by increasing fatty acid trapping. Finally, adipose tissue produces several cytokines that regulate energy homeostasis, lipid and glucose metabolism. Disturbances in the production of these factors may contribute to metabolic abnormalities, and PPARγactivation is also associated with beneficial effects on expression and secretion of a whole range of cytokines.

Abstract P247: Gut Microbiota From A Rat Model Of Metabolic Syndrome Lowers Fitness Of High Exercise Capacity Rats (HCR/ Tol ) By Impairing Energy Homeostasis And Increasing Blood Pressure

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Guannan Zhou ◽  
Tao Yang ◽  
Sivarajan Kumarasamy ◽  
Bina Joe ◽  
Lauren G Koch
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Energy Metabolism ◽  
Gut Microbiota ◽  
Exercise Capacity ◽  
Energy Homeostasis ◽  
Current Knowledge ◽  
Strong Predictor ◽  
Whole Body ◽  
Acid Oxidation

Introduction: Low exercise capacity is a strong predictor of cardiovascular disease and overall mortality. Previously we have shown that rats artificially selected for low intrinsic exercise capacity (LCR) have reduced longevity and develop features consistent with metabolic syndrome (MetS) compared to high intrinsic exercise capacity rats (HCR). Current knowledge suggests that gut microbiota is an important contributor for host fitness. Thus, we hypothesized that transferring gut microbiota from LCR rats into inbred high capacity runner (HCR /Tol ) rats would increase risk factors for MetS, including high blood pressure (BP), gain in body weight (BW), and altered resting energy metabolism. Methods: Gut microbiota was depleted in male HCR/ Tol rats (4 mo.) by an antibiotic cocktail given orally (50mg/kg of BW/day) for 5 days, followed by weekly fecal microbiota transfer (FMT) from male LCR or HCR rats (13 mo.) to generate HCR/ Tol -LCR FMT (n = 5) or HCR/ Tol -HCR FMT (n = 6) groups. BW was measured every 4 weeks. At week 11, whole body metabolism was measured by indirect calorimetry (Oxymax, Columbus Instruments). Respiratory Exchange Ratio (RER), Energy Expenditure (EE), glucose and fat oxidation were calculated from oxygen consumption and carbon dioxide release (VO 2 and VCO 2 ). At week 12, BP was measured by tail-cuff method (Kent Scientific) and treadmill exercise test was done at week 13. Results: Compared to HCR/ Tol -HCR FMT , HCR/ Tol -LCR FMT showed a significant gain in BW (7.2% vs 1.9%, P<0.05), elevated systolic BP (147 vs 120 mmHg, P<0.0001), diastolic BP (112 vs 91 mmHg, P<0.01), and mean BP (123 vs 100 mmHg, P<0.001). BP changes in HCR/ Tol -LCR FMT associated with 1) increased VO 2 (355 vs 320 ml/hr, P<0.05), 2) elevated VCO 2 (350 vs 298 ml/hr, P<0.01), 3) increased EE (1.8 vs 1.6 kcal/hr, P<0.01), 4) higher RER (0.96 vs 0.91, P<0.001), 5) higher glucose oxidation (1.36 vs 1.12 g/kg/hr, P<0.001) and 6) reduced fatty acid oxidation (0.09 vs 0.15 g/kg/hr, P<0.01) and a 23% lower exercise capacity. Conclusions: Gut microbiota from LCR rats strongly associated with poor health outcomes, notably elevated BP and impaired energy metabolism. These findings suggest that altered energy homeostasis by microbiota is mechanistically linked to host BP regulation within MetS.

Effect of needle biopsy from the vastus lateralis muscle on insulin-stimulated glucose metabolism in humans

1994 ◽  
Vol 267 (4) ◽  
pp. E544-E548 ◽  
Author(s):  
P. Holck ◽  
N. Porksen ◽  
M. F. Nielsen ◽  
B. Nyholm ◽  
J. F. Bak ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Muscle Biopsy ◽  
Needle Biopsy ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Vastus Lateralis Muscle ◽  
Lateralis Muscle ◽  
Glucose Output

To examine the cellular mechanisms behind conditions characterized by insulin resistance, the clamp technique is often combined with muscle biopsies. To test whether the trauma of a needle biopsy from the vastus lateralis muscle per se may influence insulin-stimulated glucose uptake, eight healthy subjects underwent two randomly sequenced hyperinsulinemic (insulin infusion rate: 0.6 mU.kg-1.min-1 for 150 min) euglycemic clamps with an interval of 4-6 wk. In one study (study B) a muscle biopsy (approximately 250 mg, i.e., larger than normal standard) was taken in the basal state just before the clamp procedure, whereas the other was a control study (study C). Insulin-stimulated glucose uptake was significantly reduced in study B (5.36 +/- 0.96 mg.kg-1.min-1) compared with study C (6.06 +/- 0.68 mg.kg-1.min-1; P < 0.05). Nonoxidative glucose disposal (indirect calorimetry) was decreased (2.81 +/- 1.08 vs. 3.64 +/- 1.34 mg.kg-1.min-1; P < 0.05), whereas glucose oxidation was unaltered. Likewise, endogenous glucose output ([3-3H]glucose) was identically suppressed during hyperinsulinemia. Circulating levels of epinephrine, glucagon, and growth hormone did not differ significantly in studies B and C. In contrast, plasma norepinephrine, serum cortisol, and free fatty acid rose after biopsy (P < 0.05). In conclusion, performance of a muscle biopsy may diminish insulin sensitivity by affecting nonoxidative glucose metabolism. This should be considered when assessing whole body insulin sensitivity after a percutaneous needle muscle biopsy.

scholarly journals Resting Whole Body Energy Metabolism in Class 3 Obesity; from Preserved Insulin Sensitivity to Overt Type 2 Diabetes

2020 ◽  
Vol Volume 13 ◽  
pp. 489-497 ◽  
Author(s):  
Giuseppina Manzoni ◽  
Alice Oltolini ◽  
Silvia Perra ◽  
Emanuele Muraca ◽  
Stefano Ciardullo ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Whole Body ◽  
Body Energy

scholarly journals Free leptin index and thyroid function in male highly trained athletes

2009 ◽  
Vol 161 (6) ◽  
pp. 871-876 ◽  
Author(s):  
Gianluca Perseghin ◽  
Guido Lattuada ◽  
Francesca Ragogna ◽  
Giampietro Alberti ◽  
Antonio La Torre ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Thyroid Function ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Anaerobic Power ◽  
Biologically Active ◽  
Retinol Binding Protein ◽  
Endocrine Function ◽  
Whole Body ◽  
Retinol Binding Protein 4

ObjectiveExercise training may cause changes in thyroid function. This thyroid response may be due to exercise-induced modulation of energy metabolism but also of the adipocytes endocrine function. In particular, the role of leptin and of circulating soluble leptin receptor (sOB-R) was unexplored. The aim of this study was to assess the relationships between thyroid function, whole body energy metabolism, and adipokines – mainly leptin and its receptor, sOB-R.MethodsWe measured serum TSH, free tri-iodothyronine (FT3), free thyroxine, leptin, and sOB-R and assessed energy homeostasis by means of indirect calorimetry, in 27 highly trained athletes and 27 sedentary, healthy men.ResultsTSH–FT3 ratio was lower in athletes (P<0.03), either in sustained power or anaerobic power-sprint athletes (n=13) or marathon runners (n=14). Whole body respiratory quotient was lower in athletes. Fasting serum sOB-R was higher and leptin lower in athletes than controls. Also serum adiponectin, resistin, and retinol binding protein-4 concentrations were different in athletes than in controls. The ratio between leptin and sOB-R, the free leptin index (FLI), was lower in athletes than in controls (0.025±0.014 vs 0.085±0.049; P<0.001). In multivariate analysis, FLI retained independent association with TSH–FT3 ratio.ConclusionMale, elite athletes had lower TSH–FT3 ratio and FLI than controls while FLI was independently associated with TSH–FT3 ratio supporting the hypothesis that the level of biologically active leptin is involved in the adaptive response of thyroid function in professional athletes.

scholarly journals Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

2019 ◽  
Vol 116 (47) ◽  
pp. 23822-23828 ◽  
Author(s):  
Shintaro Yamaguchi ◽  
Michael P. Franczyk ◽  
Maria Chondronikola ◽  
Nathan Qi ◽  
Subhadra C. Gunawardana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Lipolytic Activity ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Adaptive Thermogenesis ◽  
Body Energy

Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme for cellular energy metabolism. The aim of the present study was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD+ metabolism in regulating whole-body thermogenesis and energy metabolism. Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme. We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in thermogenesis and mitochondrial function in BAT and a blunted thermogenic (rectal temperature, BAT temperature, and whole-body oxygen consumption) response to acute cold exposure, prolonged fasting, and administration of β-adrenergic agonists (norepinephrine and CL-316243). In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activity, likely through inactivation of the NAD+–SIRT1–caveolin-1 axis, which limits an important fuel source fatty acid for BAT thermogenesis. These metabolic abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the block in NAD+ synthesis induced by NAMPT deficiency. Although BANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the ANKO mice, BANKO mice had normal thermogenic and lipolytic responses. We also found NAMPT expression in supraclavicular adipose tissue (where human BAT is localized) obtained from human subjects increased during cold exposure, suggesting our finding in rodents could apply to people. These results demonstrate that adipose NAMPT-mediated NAD+ biosynthesis is essential for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism.

Higher intramuscular triacylglycerol in women does not impair insulin sensitivity and proximal insulin signaling

2009 ◽  
Vol 107 (3) ◽  
pp. 824-831 ◽  
Author(s):  
Louise Høeg ◽  
Carsten Roepstorff ◽  
Maja Thiele ◽  
Erik A. Richter ◽  
Jørgen F. P. Wojtaszewski ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Muscle Fiber ◽  
Insulin Signaling ◽  
Capillary Density ◽  
Follicular Phase ◽  
Activity Level ◽  
Whole Body ◽  
Vastus Lateralis Muscle

Women have been shown to have higher muscle triacylglycerol (IMTG) levels than men and could therefore be expected to have lower insulin sensitivity than men, since previous studies have linked high IMTG to decreased insulin sensitivity. Therefore, insulin sensitivity of whole body and leg glucose uptake was studied in 9 women in the follicular phase and 8 men on a controlled diet and matched for maximal oxygen uptake per kilogram of lean body mass and habitual activity level. A 47% higher ( P < 0.05) IMTG level was found in women than in men, and, at the same time, women also displayed 22% higher whole body insulin sensitivity ( P < 0.05) and 29% higher insulin-stimulated leg glucose uptake ( P = 0.05) during an euglycemic-hyperinsulinemic (≈70 μU/ml) clamp compared with matched male subjects. The higher insulin sensitivity in women could not be explained by higher expression of muscle glucose transporter GLUT4, insulin receptor, or Akt expression or by the ability of insulin to stimulate Akt Thr308 or Akt Ser473 phosphorylation. However, a 30% higher ( P < 0.05) capillary density and 31% more type 1 muscle fiber expressed per area in the vastus lateralis muscle were noted in women than in matched men. It is concluded that despite 47% higher IMTG levels in women in the follicular phase, whole body as well as leg insulin sensitivity are higher than in matched men. This was not explained by sex differences in proximal insulin signaling in women. In women, it seems that a high capillary density and type 1 muscle fiber expression may be important for insulin action.

scholarly journals Loss of PDGF-B activity increases hepatic vascular permeability and enhances insulin sensitivity

2011 ◽  
Vol 301 (3) ◽  
pp. E517-E526 ◽  
Author(s):  
Summer M. Raines ◽  
Oliver C. Richards ◽  
Lindsay R. Schneider ◽  
Kathryn L. Schueler ◽  
Mary E. Rabaglia ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Basolateral Membrane ◽  
Tolerance Test ◽  
Whole Body ◽  
Glucose Disposal ◽  
Permeability Barrier ◽  
Loss Of Function ◽  
Transendothelial Transport

Hepatic vasculature is not thought to pose a permeability barrier for diffusion of macromolecules from the bloodstream to hepatocytes. In contrast, in extrahepatic tissues, the microvasculature is critically important for insulin action, because transport of insulin across the endothelial cell layer is rate limiting for insulin-stimulated glucose disposal. However, very little is known concerning the role in this process of pericytes, the mural cells lining the basolateral membrane of endothelial cells. PDGF-B is a growth factor involved in the recruitment and function of pericytes. We studied insulin action in mice expressing PDGF-B lacking the proteoglycan binding domain, producing a protein with a partial loss of function (PDGF-B ret/ ret). Insulin action was assessed through measurements of insulin signaling and insulin and glucose tolerance tests. PDGF-B deficiency enhanced hepatic vascular transendothelial transport. One outcome of this change was an increase in hepatic insulin signaling. This correlated with enhanced whole body glucose homeostasis and increased insulin clearance from the circulation during an insulin tolerance test. In obese mice, PDGF-B deficiency was associated with an 80% reduction in fasting insulin and drastically reduced insulin secretion. These mice did not have significantly higher glucose levels, reflecting a dramatic increase in insulin action. Our findings show that, despite already having a high permeability, hepatic transendothelial transport can be further enhanced. To the best of our knowledge, this is the first study to connect PDGF-B-induced changes in hepatic sinusoidal transport to changes in insulin action, demonstrating a link between PDGF-B signaling and insulin sensitivity.

scholarly journals Relationships between Bone Turnover and Energy Metabolism

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Tânia A. P. Fernandes ◽  
Luísa M. L. Gonçalves ◽  
José A. A. Brito
Keyword(s):  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Bone Turnover ◽  
Osteoporotic Fracture ◽  
Diabetic Complications ◽  
Bone Health ◽  
Conceptual Approach ◽  
Chronic Complications ◽  
Increased Risk

It is well established that diabetes can be detrimental to bone health, and its chronic complications have been associated with an increased risk of osteoporotic fracture. However, there is growing evidence that the skeleton plays a key role in a whole-organism approach to physiology. The hypothesis that bone may be involved in the regulation of physiological functions, such as insulin sensitivity and energy metabolism, has been suggested. Given the roles of insulin, adipokines, and osteocalcin in these pathways, the need for a more integrative conceptual approach to physiology is emphasized. Recent findings suggest that bone plays an important role in regulating intermediary metabolism, being possibly both a target of diabetic complications and a potential pathophysiologic factor in the disease itself. Understanding the relationships between bone turnover and glucose metabolism is important in order to develop treatments that might reestablish energy metabolism and bone health. This review describes new insights relating bone turnover and energy metabolism that have been reported in the literature.

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