Carbohydrate and Protein Supplements, an Effective Means for Maintaining Exercise-Induced Glucose Metabolism Homeostasis

2021 ◽  
Vol 11 (6) ◽  
pp. 1120-1128
Author(s):  
Dingguo Ruan ◽  
Hong Deng ◽  
Xiaoyang Xu
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Normal Saline ◽  
Glucose Transporter ◽  
Glycogen Synthesis ◽  
Effective Means ◽  
Recovery Period ◽  
Future Application ◽  
Glut 4 ◽  
Exercise Induced

This study aimed to verify the effects of an independently developed carbohydrate and protein (CHO+P) beverage (7.2% oligosaccharide and 1.6% soy-polypeptide) supplement on exerciseinduced glucose metabolism and associated gene expression. Mice received 1 mL/100 g body weight of normal saline (group C; n = 36) or CHO+P (group E; n = 36) at 30 min before an immediately after exercise. Mice without exercise and supplementation served as normal controls (group NC; n = 9). The expression levels related to glucose metabolism were measured at 0, 4, 12, and 24 h after exercise (n = 9 per group). The blood glucose, insulin, and liver glycogen contents in groups C and E were dramatically lower than group NC immediately after exercise. Those in group E were significantly higher than group C, with few differences between the two. Muscle glycogen was restored more quickly when the CHO+P beverage was consumed compared to normal saline. Furthermore, exercise-induced increase in glucose transporter-4 (GLUT-4) mRNA could be depressed by CHO+P supplementation but enhanced in GLUT-4 protein. Interleukin-6 (IL-6) showed a double peak curve in the recovery period, but IL-6 increased again in group E earlier than group C. These findings confirmed that the beverage has significantly improved time in maintaining blood glucose stability, reducing glycogen consumption, accelerating glycogen resynthesis, and repairing injury in rats. This study suggests the future application of this beverage in humans with experimental support and provides a scientific direction for promoting glycogen synthesis and recovery through nutrition.

Insulin-Sensitive Phospholipid Signaling Systems and Glucose Transport. Update II

2001 ◽  
Vol 226 (4) ◽  
pp. 283-295 ◽  
Author(s):  
Robert V. Farese
Keyword(s):  
Protein Kinase ◽  
Glucose Metabolism ◽  
Glucose Transport ◽  
Intracellular Signaling ◽  
Glucose Transporter ◽  
De Novo ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Cell Types ◽  
Biologically Active

Insulin provokes rapid changes in phospholipid metabolism and thereby generates biologically active lipids that serve as intracellular signaling factors that regulate glucose transport and glycogen synthesis. These changes include: (i) activation of phosphatidylinositol 3-kinase (PI3K) and production of PIP3; (ii) PIP3-dependent activation of atypical protein kinase Cs (PKCs); (iii) PIP3-dependent activation of PKB; (iv) PI3K-dependent activation of phospholipase D and hydrolysis of phosphatidyicholine with subsequent increases in phosphatidic acid (PA) and diacyiglycerol (DAG); (v) PI3K-independent activation of glycerol-3-phosphate acylytansferase and increases in de novo synthesis of PA and DAG; and (vi) activation of DAG-sensitive PKCs. Recent findings suggest that atypical PKCs and PKB serve as important positive regulators of insulin-stimulated glucose metabolism, whereas mechanisms that result in the activation of DAG-sensitive PKCs serve mainly as negative regulators of insulin signaling through PI3K. Atypical PKCs and PKB are rapidly activated by insulin in adipocytes, liver, skeletal muscles, and other cell types by a mechanism requiring PI3K and its downstream effector, 3-phosphoinositide-dependent protein kinase-1 (PDK-1), which, in conjunction with PIP3, phosphorylates critical threonine residues in the activation loops of atypical PKCs and PKB. PIP3 also promotes increases in autophosphorylation and allosteric activation of atypical PKCs. Atypical PKCs and perhaps PKB appear to be required for insulin-induced translocation of the GLUT 4 glucose transporter to the plasma membrane and subsequent glucose transport. PKB also appears to be the major regulator of glycogen synthase. Together, atypical PKCs and PKB serve as a potent, integrated PI3K/PDK-1-directed signaling system that is used by insulin to regulate glucose metabolism.

In vitro and in vivo culture effects on mRNA expression of genes involved in metabolism and apoptosis in bovine embryos

2005 ◽  
Vol 17 (8) ◽  
pp. 775 ◽  
Author(s):  
Hiemke M. Knijn ◽  
Christine Wrenzycki ◽  
Peter J. M. Hendriksen ◽  
Peter L. A. M. Vos ◽  
Elly C. Zeinstra ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Mrna Expression ◽  
Critical Period ◽  
Glucose Transporter ◽  
Expression Patterns ◽  
Culture Conditions ◽  
Glut 4 ◽  
Gene Transcripts

Bovine blastocysts produced in vitro differ substantially from their in vivo-derived counterparts with regard to glucose metabolism, level of apoptosis and mRNA expression patterns. Maternal embryonic genomic transition is a critical period in which these changes could be induced. The goals of the present study were twofold: (1) to identify the critical period of culture during which the differences in expression of gene transcripts involved in glucose metabolism are induced; and (2) to identify gene transcripts involved in apoptosis that are differentially expressed in in vitro- and in vivo-produced blastocysts. Relative abundances of transcripts for the glucose transporters Glut-1, Glut-3, Glut-4 and Glut-8, and transcripts involved in the apoptotic cascade, including BAX, BCL-XL, XIAP and HSP 70.1, were analysed by a semiquantitative reverse transcription–polymerase chain reaction assay in single blastocysts produced in vitro or in vivo for specific time intervals, that is, before or after maternal embryonic transition. Whether the culture environment was in vitro or in vivo affected the expression of glucose transporter transcripts Glut-3, Glut-4 and Glut-8. However, the critical period during culture responsible for these changes, before or after maternal embryonic transition, could not be determined. With the exception of XIAP, no effects of culture system on the mRNA expression patterns of BAX, BCL-XL and HSP 70.1 could be observed. These data show that expression of XIAP transcripts in expanded blastocysts is affected by in vitro culture. These findings add to the list of bovine genes aberrantly expressed in culture conditions, but do not support the hypothesis that maternal embryonic transition is critical in inducing the aberrations in gene expression patterns studied here.

scholarly journals Polysaccharides fromEnteromorpha proliferaImprove Glucose Metabolism in Diabetic Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Wenting Lin ◽  
Wenxiang Wang ◽  
Dongdong Liao ◽  
Damiao Chen ◽  
Pingping Zhu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Mrna Expression ◽  
Glucose Transporter ◽  
Fasting Blood Glucose ◽  
Diabetic Rats ◽  
High Dose ◽  
Sensitivity Index ◽  
Serum Samples ◽  
Glut 4

This study investigated the effects of polysaccharides fromEnteromorpha prolifera(PEP) on glucose metabolism in a rat model of diabetes mellitus (DM). PEP (0, 150, 300, and 600 mg/kg) was administered intragastrically to rats for four weeks. After treatment, fasting blood glucose (FBG) and insulin (INS) levels were measured, and the insulin sensitivity index (ISI) was calculated. The morphopathological changes in the pancreas were observed. Serum samples were collected to measure the oxidant-antioxidant status. The mRNA expression levels of glucokinase (GCK) and insulin receptor (InsR) in liver tissue and glucose transporter type 4 (GLUT-4) and adiponectin (APN) in adipose tissue were determined. Compared with the model group, the FBG and INS levels were lower, the ISI was higher, and the number of isletβ-cells was significantly increased in all the PEP groups. In the medium- and high-dose PEP groups, MDA levels decreased, and the enzymatic activities of SOD and GSH-Px increased. The mRNA expression of InsR and GCK increased in all the PEP groups; APN mRNA expression increased in the high-dose PEP group, and GLUT-4 mRNA expression increased in adipose tissue. These findings suggest that PEP is a potential therapeutic agent that can be utilized to treat DM.

scholarly journals Alterations in Glucose Metabolism During the Transition to Heart Failure: The Contribution of UCP-2

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 552 ◽  
Author(s):  
Hanna Sarah Kutsche ◽  
Rolf Schreckenberg ◽  
Martin Weber ◽  
Christine Hirschhäuser ◽  
Susanne Rohrbach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Contractile Function ◽  
Uncoupling Protein ◽  
Left Ventricular ◽  
Mitochondrial Uncoupling ◽  
Glut 4

The cardiac expression of the mitochondrial uncoupling protein (UCP)-2 is increased in patients with heart failure. However, the underlying causes as well as the possible consequences of these alterations during the transition from hypertrophy to heart failure are still unclear. To investigate the role of UCP-2 mechanistically, expression of UCP-2 was silenced by small interfering RNA in adult rat ventricular cardiomyocytes. We demonstrate that a downregulation of UCP-2 by siRNA in cardiomyocytes preserves contractile function in the presence of angiotensin II. Furthermore, silencing of UCP-2 was associated with an upregulation of glucose transporter type (Glut)-4, increased glucose uptake, and reduced intracellular lactate levels, indicating improvement of the oxidative glucose metabolism. To study this adaptation in vivo, spontaneously hypertensive rats served as a model for cardiac hypertrophy due to pressure overload. During compensatory hypertrophy, we found low UCP-2 levels with an upregulation of Glut-4, while the decompensatory state with impaired function was associated with an increase of UCP-2 and reduced Glut-4 expression. By blocking the aldosterone receptor with spironolactone, both cardiac function as well as UCP-2 and Glut-4 expression levels of the compensated phase could be preserved. Furthermore, we were able to confirm this by left ventricular (LV) biopsies of patients with end-stage heart failure. The results of this study show that UCP-2 seems to impact the cardiac glucose metabolism during the transition from hypertrophy to failure by affecting glucose uptake through Glut-4. We suggest that the failing heart could benefit from low UCP-2 levels by improving the efficiency of glucose oxidation. For this reason, UCP-2 inhibition might be a promising therapeutic strategy to prevent the development of heart failure.

scholarly journals Alpha Mangostin and Xanthone from Mangosteen (Garcinia mangostana l.) Role on Glucose Tolerance and Glucose Transporter-4 in Diabetes Mellitus

2017 ◽  
Vol 9 (09) ◽  
Author(s):  
Ratwita W. ◽  
Sukandar E. Y. ◽  
Adnyana I. K. ◽  
Kurniati N. F.
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Transporter ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Positive Control ◽  
Control Group ◽  
Cardiac Cell ◽  
Glut 4 ◽  
Adipocyte Cell

Objective: This research elaborated role of alpha mangostin and xanthone on glucose tolerance and Glucose Transporter (GLUT)-4 by measuring blood glucose level and GLUT-4 expression on cardiac cell musce and adipocyte cell culture. Methods: Glucose tolerance test were conducted using male wistar rat divided into 9 groups, which were normal, control (D-Glucose induced only), glibenclamide, various doses of -mangostin and xanthone (5, 10, 20 mg/kgbw). All group induced by D-glucose 3 g/kg orally 30 minutes later. Blood glucose levels changes were observed at 90th and 150th minute. GLUT-4 study conducted for 3 weeks on mice that divided into 10 groups which were normal, diabetic control mice (alloxan induced only), metformin, glibenclamide, various doses of -mangostin and xanthone (5, 10, 20 mg/kgbw). GLUT-4 expression than observed on cardiac cell muscle. While other study observed GLUT-4 expression on adipocyte cell culture that treated with -mangostin/xanthone/pioglitazone. Results: Normal group (non-diabetic) responds slightly to the administration of glucose in glucose tolerance test. Blood glucose level in every group in the 90th up to 150th minute decreased significantly when compared to the positive control group (p >0.05). This shows that glucose tolerance does not occur in all treated groups althought they were treated with high glucose consentration. GLUT-4 expressions in mice cardiac-musce cells that treated with -mangostin/xanthone/ glibenclamide/metformin significantly increased when compared to the positive control group, except in group treated with xanthone 5 mg/kgbw. GLUT-4 expressions also increase in adipocytes that treated with 3.125 mM; 6.25 mM and 25 mM 𝛼–mangostin, equivalent to pioglitazone. All treatment group results significantly different when compared with control. The effect of 𝛼–mangostin on GLUT-4 expression better than xanthone’s. Conclusion: Alpha mangostin and xanthone are two substances that showed protective effect to glucose tolerance and also have potential effect to improve insulin resistance by increasing GLUT-4 on cardiac muscle and adipocyte.

Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle

1997 ◽  
Vol 273 (1) ◽  
pp. E185-E191 ◽  
Author(s):  
R. S. Streeper ◽  
E. J. Henriksen ◽  
S. Jacob ◽  
J. Y. Hokama ◽  
D. L. Fogt ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Glucose Transport ◽  
Lipoic Acid ◽  
Glucose Oxidation ◽  
Glucose Transporter ◽  
Glycogen Synthesis ◽  
Racemic Mixture ◽  
Insulin Resistant ◽  
The Individual

The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

Exercise and insulin signaling: a historical perspective

2002 ◽  
Vol 93 (2) ◽  
pp. 765-772 ◽  
Author(s):  
Eva Tomás ◽  
Antonio Zorzano ◽  
Neil B. Ruderman
Keyword(s):  
Insulin Signaling ◽  
Historical Perspective ◽  
Glucose Transporter ◽  
Glycogen Synthesis ◽  
The People ◽  
Current Thinking ◽  
Exercise Induced ◽  
Amp Activated Protein Kinase ◽  
Considerable Body

Over the past 30 years, a considerable body of evidence has revealed that a prior bout of exercise can increase the ability of insulin to stimulate glucose transport and glycogen synthesis in skeletal muscle. Apart from its clinical implications, this work has led to a considerable effort to determine at a molecular level how exercise causes this effect and, in particular, whether it does so by enhancing specific events in the insulin-signaling cascade. The objective of this review is to discuss from a historical perspective how our current thinking in this area has evolved and the people responsible for it. Areas to be discussed include the effect or lack of effect of prior exercise on the insulin-signaling pathway, effects of exercise on the regulation by insulin of the GLUT-4 glucose transporter in muscle, and the emerging role of AMP-activated protein kinase as a mediator of exercise-induced signaling events. In addition, we will discuss briefly some of the avenues that research in this area is likely to follow.

scholarly journals Pengaruh Latihan Fisik terhadap Perbaikan Resistensi Insulin

2021 ◽  
Vol 2 (2) ◽  
pp. 110-114
Author(s):  
Devitya Angielevi Sukarno
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Protein Kinase ◽  
Cell Membrane ◽  
Blood Glucose Level ◽  
Insulin Signaling ◽  
Glucose Transporter ◽  
Insulin Receptor Substrate ◽  
Glucose Transporter 4 ◽  
Glut 4

Abstract--Insulin resistance underlies the pathogenesis of chronic disease, such as diabetes mellitus which has high morbidity and mortality rate. Insulin resistance is a pathological condition when cells fail to respond normally to the insulin hormone, because of insulin signaling pathway disruption. Bound between insulin and insulin’s receptor cannot phosphorylate tyrosine and fail to activate insulin receptor substrate-1 (IRS-1). This failure decrease Glucose transporter-4 (GLUT-4) expression on the skeletal muscle’s cell membrane, that leads to decrease glucose influx and increase blood glucose level. A routine physical training which does according to adequate training dose, will activate adenosin 5’monophosphate-activated protein kinase (AMPK) and lead to the translocation of GLUT-4 vesicles without insulin and insulin’s receptor bonding.GLUT-4 expression on the skeletal muscle’s cell membrane which is stimulated by muscle contraction will increase glucose influx and decrease blood glucose level. Keywords: insulin resistance; physical training; insulin signaling pathway   Abstrak--Resistensi insulin merupakan penyebab yang mendasari terjadinya penyakit kronis seperti diabetes melitus yang memiliki angka morbiditas dan mortalitas tinggi.Resistensi insulin merupakan keadaan patologis dimana terjadi kegagalan respon seluler terhadap hormon insulin akibat gangguan pada jalur sinyal insulin.Ikatan insulin pada reseptornya tidak dapat menyebabkan fosforilasi tirosin sehingga tidak dapat mengaktivasi insulin receptor substrate-1 (IRS-1). Kegagalan aktivasi tersebut akan menyebabkan penurunan ekspresi Glucose transporter-4 (GLUT-4) pada membran sel otot rangka sehingga ambilan glukosa oleh sel menurun dan glukosa darah meningkat. Latihan fisik yang dilakukan secara rutin, teratur dan sesuai dengan dosis latihan yang tepat dapat mengaktivasi adenosin 5’monophosphate-activated protein kinase (AMPK), sehingga menyebabkan translokasi vesikel berisi GLUT-4, tanpa melalui ikatan insulin dengan reseptornya. Ekspresi GLUT-4 pada membran sel yang dirangsang oleh kontraksi otot akan meningkatkan ambilan glukosa dan menurunkan glukosa darah. Kata kunci: resistensi insulin; latihan fisik; jalur sinyal insulin

Caveolin gene transfer improves glucose metabolism in diabetic mice

2010 ◽  
Vol 298 (3) ◽  
pp. C450-C456 ◽  
Author(s):  
Koji Otsu ◽  
Yoshiyuki Toya ◽  
Jin Oshikawa ◽  
Reiko Kurotani ◽  
Takuya Yazawa ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Gene Transfer ◽  
Insulin Receptor ◽  
Glycogen Synthesis ◽  
Fasting Blood Glucose ◽  
Hepatic Glycogen ◽  
Diabetic Mice ◽  
Glucose Levels ◽  
Blood Glucose Levels

Caveolin, a member of the membrane-anchoring protein family, accumulates various growth receptors in caveolae and inhibits their function. Upregulation of caveolin attenuates cellular proliferation and growth. However, the role of caveolin in regulating insulin signals remains controversial. Here, we demonstrate that caveolin potently enhances insulin receptor (IR) signaling when overexpressed in the liver in vivo. Adenovirus-mediated gene transfer was used to overexpress caveolin specifically in the liver of diabetic obese mice, which were generated with a high-fat diet. Expression of molecules involved in IR signaling, such as IR or Akt, remained unchanged after gene transfer. However, hepatic glycogen synthesis was markedly increased with a decrease in phosphoenolpyruvate carboxykinase protein expression. Insulin sensitivity was increased after caveolin gene transfer as determined by decreased blood glucose levels in response to insulin injection and fasting blood glucose levels. Glucose tolerant test performance was also improved. Similar improvements were obtained in KKA y genetically diabetic mice. Adenovirus-mediated overexpression of caveolin-3 in hepatic cells also enhanced IR signaling, as shown by increased phosphorylation of IR in response to insulin stimulation and higher glycogen synthesis at baseline. These effects were attributed mostly to increased insulin receptor activity and caveolin-mediated, direct inhibition of protein tyrosine phosphatase 1B, which was increased in obese mouse livers. In conclusion, our results suggest that caveolin is an important regulator of glucose metabolism that can enhance insulin signals.

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