Systematic-analysis of mRNA expression profiles in skeletal muscle of patients with type II diabetes: The glucocorticoid was central in pathogenesis

2017 ◽  
Vol 233 (5) ◽  
pp. 4068-4076 ◽  
Author(s):  
Kan Shao ◽  
Li-Sha Shen ◽  
Hui-Hua Li ◽  
Shan Huang ◽  
Yong Zhang
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Type Ii Diabetes ◽  
Expression Profiles ◽  
Type Ii ◽  
Systematic Analysis

Effect of Forced Treadmill Running on Skeletal Muscle Myokine Levels in Mice with a Model of Type II Diabetes Mellitus

2021 ◽  
Vol 57 (4) ◽  
pp. 904-912
Author(s):  
A. N. Zakharova ◽  
T. A. Kironenko ◽  
K. G. Milovanova ◽  
A. A. Orlova ◽  
E. Yu. Dyakova ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Skeletal Muscle ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Treadmill Running ◽  
Type Ii

scholarly journals Systematic analysis of mRNA expression profiles in NSCLC cell lines to screen metastasis-related genes

2016 ◽  
Vol 14 (6) ◽  
pp. 5093-5103 ◽  
Author(s):  
Ying Liu ◽  
Lei Liu ◽  
Tao Yu ◽  
He-Chun Lin ◽  
Dandan Chu ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cell Lines ◽  
Expression Profiles ◽  
Nsclc Cell ◽  
Systematic Analysis

Skeletal muscle potassium increases after diet and weight reduction in obese subjects with normal and impaired glucose tolerance

1989 ◽  
Vol 121 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Kerstin Landin ◽  
Folke Lindgärde ◽  
Bengt Saltin
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Type Ii Diabetes ◽  
Fasting Blood Glucose ◽  
Dry Weight ◽  
Type Ii ◽  
Total Body Potassium ◽  
Men And Women ◽  
Total Body

Abstract. Body composition calculated from total body potassium and skeletal muscle potassium were studied in middle-aged obese men and women with normal and impaired glucose tolerance as well as Type II diabetes before and after advice on calorie reduction during twelve months. The subjects were compared with healthy lean men and women. Mean weight loss was 6.6 kg (P< 0.05). Lean body mass and body fat decreased 2.0 kg (P< 0.05) and 4.6 kg (P< 0.05), respectively. Total body potassium decreased by a mean of 146 ± 49 mmol (P< 0.01). Obese men with Type II diabetes and impaired glucose tolerance had lower total body potassium and muscle potassium levels than obese healthy men. After dieting, the obese men and women increased their muscle potassium levels with a mean of 2.8 mmol/100 g fat-free dry weight to 42.6 ± 2.6 mmol/100 g fat-free dry weight (P< 0.05), but they were still below the levels of the lean controls, 44.4 ± 1.3 mmol/100 g fat-free dry weight, (P< 0.01). Increase in skeletal muscle potassium was correlated to decrease in body weight, r = 0.55 (P< 0.01) and to decrease in fasting blood glucose, r = 0.42 (P< 0.05).

Insulin signal transduction in human skeletal muscle: identifying the defects in Type II diabetes

2005 ◽  
Vol 33 (2) ◽  
pp. 354-357 ◽  
Author(s):  
M. Björnholm ◽  
J.R. Zierath
Keyword(s):  
Skeletal Muscle ◽  
Type Ii Diabetes ◽  
Insulin Action ◽  
Glucose Transporter ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type Ii ◽  
Peripheral Tissues ◽  
Glucose Homoeostasis ◽  
Insulin Receptor Signalling

Type II diabetes is characterized by defects in insulin action on peripheral tissues, such as skeletal muscle, adipose tissue and liver and pancreatic β-cell defects. Since the skeletal muscle accounts for approx. 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Thus identifying defective steps in this process may reveal attractive targets for drug development to combat insulin resistance and Type II diabetes. This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Evidence for impaired activation of the insulin receptor signalling cascade and defective glucose transporter 4 translocation in the skeletal muscle from Type II diabetic patients will be presented. Through the identification of the intracellular defects in insulin action that control glucose homoeostasis, a better understanding of the disease pathogenesis can be gained and strategies for intervention may be developed.

Effects Of Type II Diabetes On Capillary Hemodynamics In Skeletal Muscle

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S359 ◽  
Author(s):  
Danielle J. Padilla ◽  
Paul McDonough ◽  
Bradley J. Behnke ◽  
Yutaka Kano ◽  
Karen S. Hageman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Type Ii Diabetes ◽  
Type Ii

scholarly journals The effect of weight reduction on skeletal muscle UCP2 and UCP3 mRNA expression and UCP3 protein content in Type II diabetic subjects

Diabetologia ◽  
2000 ◽  
Vol 43 (11) ◽  
pp. 1408-1416 ◽  
Author(s):  
P. Schrauwen ◽  
G. Schaart ◽  
W. H. M. Saris ◽  
L. J. Slieker ◽  
J. F. C. Glatz ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Protein Content ◽  
Weight Reduction ◽  
Type Ii

scholarly journals Hepatic microRNAs in Type II Diabetes Pathogenesis

2020 ◽  
Vol 3 ◽  
Author(s):  
Gene Qian ◽  
Nuria Morral
Keyword(s):  
Fatty Acid ◽  
Insulin Signaling ◽  
Mirna Expression ◽  
Metabolic Pathways ◽  
Type Ii Diabetes ◽  
Expression Profiles ◽  
Future Research ◽  
Acid Oxidation ◽  
Type Ii ◽  
Pubmed Database

Background/Objective:  Diabetes mellitus is a disease with increasing incidence worldwide affecting more than 435 million patients, most of whom have Type II diabetes (T2D). Of the many organs affected by T2D, the liver is responsible for much of the dysregulated metabolic pathways in response to insulin signaling. These include, but are not limited to gluconeogenesis, glycogen storage, fatty acid and cholesterol biosynthesis and transport, and fatty acid oxidation. Recent studies show significant differences in miRNA expression profiles between healthy and disease states of T2D. This implicates an important role of miRNAs in T2D pathogenesis and makes miRNAs an attractive therapeutic target and diagnostic marker for T2D patients. The aim of this review is to provide an overview of the hepatic miRNAs relevant to T2D pathogenesis.    Methods:  We compiled and reviewed articles from the PubMed database that were relevant to miRNAs and T2D pathogenesis in the liver.    Results:  We found that hepatic miRNAs affect most if not all dysregulated metabolic pathways in T2D pathogenesis, which we categorized into carbohydrate metabolism, lipid metabolism, and insulin signaling. The miRNAs that are most represented in our literature include miR-122, miR-33a/b, miR-29, and miR-21. These miRNAs target a variety of molecules, including transcription factors that are master regulators of metabolic pathways (FOXO1, HNF4α), lipid transporters (ABCA1, ABCG1), or key insulin signaling molecules (IRS1/2, caveolin-1). In addition, circulating miR-122 is associated with the risk of developing metabolic syndrome and T2D in the general population.    Conclusion and Potential Impact:  Multiple miRNAs are dysregulated in the liver of animal models of T2D. Administration of miRNA mimics or antagomirs to correct aberrant miRNA expression improved the pathophysiology in vivo. miRNAs are also promising tools as markers for disease development. Ultimately, the identification of miRNAs can guide future research to facilitate the diagnosis and improve the treatment of T2D. 

scholarly journals Placental growth factor levels in quadriceps muscle are reduced by a Western diet in association with advanced glycation end products

2019 ◽  
Vol 317 (4) ◽  
pp. H851-H866
Author(s):  
Asitha T. Silva ◽  
Farzana Rouf ◽  
Oluwayemisi A. Semola ◽  
Mark E. Payton ◽  
Pamela C. Lovern
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Type Ii Diabetes ◽  
Placental Growth Factor ◽  
Western Diet ◽  
Negative Regulator ◽  
Type Ii ◽  
Hindlimb Ischemia ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

In peripheral artery disease (PAD), atherosclerotic occlusion chronically impairs limb blood flow. Arteriogenesis (collateral artery remodeling) is a vital adaptive response to PAD that protects tissue from ischemia. People with type II diabetes have a high risk of developing PAD and would benefit from arteriogenesis. However, arteriogenesis is suppressed in people with diabetes by a multifaceted mechanism which remains incompletely defined. Upregulation of placental growth factor (PLGF) is a key early step in arteriogenesis. Therefore, we hypothesized that metabolic dysfunction would impair PLGF expression in skeletal muscle. We tested this hypothesis in C57BL/6J and ApoE−/− mice of both sexes fed a Western diet (WD) for 24 wk. We first assessed baseline levels of PLGF, vascular endothelial growth factor (VEGF-A), and VEGF receptor 1 (VEGFR1) protein in hindlimb skeletal muscle. Only PLGF was consistently decreased by the WD. We next investigated the effect of 24 wk of the WD on the response of PLGF, VEGF-A, VEGFR1, and monocyte chemoattractant protein-1 (MCP-1) to the physiological stimulus of vascular occlusion. Hindlimb ischemia was induced in mice by gradual femoral artery occlusion using an ameroid constrictor. Growth factor levels were measured 3–28 days postsurgery. In C57BL/6J mice, the WD decreased and delayed upregulation of PLGF and abolished upregulation of VEGF-A and VEGFR1 but had no effect on MCP-1. In ApoE−/− mice fed either diet, all factors tested failed to respond to occlusion. Metabolic phenotyping of mice and in vitro studies suggest that an advanced glycation end product/TNFα-mediated mechanism could contribute to the effects observed in vivo. NEW & NOTEWORTHY In this study, we tested the effect of a Western diet on expression of the arteriogenic growth factor placental growth factor (PLGF) in mouse skeletal muscle. We provide the first demonstration that a Western diet interferes with both baseline expression and hindlimb ischemia-induced upregulation of PLGF. We further identify a potential role for advanced glycation end product/TNFα signaling as a negative regulator of PLGF. These studies provide insight into one possible mechanism by which type II diabetes may limit collateral growth.

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