scholarly journals Cell models for studying muscle insulin resistance

2021 ◽  
Vol 72 (1) ◽  
pp. 50-57
Author(s):  
Kasja Pavlović ◽  
Nebojša Lalić
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Glucose Disposal ◽  
Controlled Environment ◽  
Cell Models ◽  
Muscle Insulin Resistance ◽  
Biological Reality ◽  
High Insulin

Type 2 diabetes is one of the most prevalent chronic diseases in the world today. Insulin resistance - a reduced responsiveness of tissues to insulin - is a hallmark of type 2 diabetes pathology. Skeletal muscle plays a pivotal role in glucose homeostasis - it is responsible for the majority of insulin-mediated glucose disposal and thus is one of the tissues most affected by insulin resistance. To study the molecular mechanisms of a disease, researchers often turn to cell models - they are inexpensive, easy to use, and exist in a controlled environment with few unknown variables. Cell models for exploring muscle insulin resistance are constructed using primary cell cultures or immortalised cell lines and treating them with fatty acids, high insulin or high glucose concentrations. The choice of cell culture, concentration and duration of the treatment and the methods for measuring insulin sensitivity, in order to confirm the model, are rarely discussed. Choosing an appropriate and physiologically relevant model for a particular topic of interest is required in order for the results to be reproducible, relevant, comparable and translatable to more complex biological systems. Cell models enable research that would otherwise be inaccessible but, especially when studying human disease, they do not serve a purpose if they are not in line with the biological reality. This review aims to summarise and critically evaluate the most commonly used cell models of muscle insulin resistance: the rationale for choosing these exact treatments and conditions, the protocols for constructing the models and the measurable outcomes used for confirming insulin resistance in the cells.

298-OR: Disruption of Multiple Cell-Autonomous Protein Phosphorylation Networks Underlies Muscle Insulin Resistance in Type 2 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 298-OR
Author(s):  
THIAGO M. BATISTA ◽  
NICOLAI J. WEWER ALBRECHTSEN ◽  
JULEEN R. ZIERATH ◽  
MATTHIAS MANN ◽  
C. RONALD KAHN
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Protein Phosphorylation ◽  
Muscle Insulin Resistance ◽  
Multiple Cell

scholarly journals Insulin Resistance and Diabetes Mellitus in Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1236
Author(s):  
Jesús Burillo ◽  
Patricia Marqués ◽  
Beatriz Jiménez ◽  
Carlos González-Blanco ◽  
Manuel Benito ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Progressive Disease

Type 2 diabetes mellitus is a progressive disease that is characterized by the appearance of insulin resistance. The term insulin resistance is very wide and could affect different proteins involved in insulin signaling, as well as other mechanisms. In this review, we have analyzed the main molecular mechanisms that could be involved in the connection between type 2 diabetes and neurodegeneration, in general, and more specifically with the appearance of Alzheimer’s disease. We have studied, in more detail, the different processes involved, such as inflammation, endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction.

Lipid-Induced Insulin Resistance Mechanisms: The Link to Inflammation and Type 2 Diabetes.

2021 ◽  
pp. 1-9
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fatty Acid ◽  
Molecular Mechanisms ◽  
Laboratory Data ◽  
Phosphatidyl Inositol ◽  
Resistance Mechanisms ◽  
Cellular Mechanisms ◽  
Insulin Resistant

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus [T2DM] onset. It occurs as a result of disturbances in lipid metabolism and increased levels of circulating free fatty acids [FFAs]. FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased fatty acid flux has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes development. FFAs appear to cause this defect in glucose transport by inhibiting insulin –stimulated tyrosine phosphorylation of insulin receptor substrate-1 [IRS-1] and IRS-1 associated phosphatidyl-inositol 3-kinase activity. A number of different metabolic abnormalities may increase intramyocellular or intrahepatic fatty acid metabolites that induce insulin resistance through different cellular mechanisms. The current review point out the link between enhanced FFAs flux and activation of PKC and how it impacts on both the insulin signaling in muscle and liver as shown from our laboratory data and highlighting the involvement of the inflammatory pathways importance. This embarks the importance of measuring the inflammatory biomarkers in clinical settings.

IL-6 as a Surrogate Biomarker: The IL-6 Clinical Value for the Diagnosis of Insulin Resistance and Type 2 Diabetes.

2021 ◽  
pp. 1-13
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Diagnostic Value ◽  
Low Grade ◽  
Clinical Value ◽  
Insulin Resistant ◽  
Tnf Α ◽  
Low Grade Inflammation

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus (T2D). It occurs as a result of lipid disorders and increased levels of circulating free fatty acids (FFAs). FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased levels fatty acid has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes. Among the biomarkers that are accompanying low grade inflammation include IL-1β, IL-6 and TNF-α. The current review point out the importance of measuring the inflammatory biomarkers especially focusing on the conductance and measurement for IL-6 as a screening laboratory test and its diagnostic value in clinical practice.

scholarly journals Insulin therapy in patients with type 2 diabetes and high insulin resistance is associated with increased risk of complications and mortality

2019 ◽  
Vol 131 (6) ◽  
pp. 376-382 ◽  
Author(s):  
Carlos E. Mendez ◽  
Rebekah J. Walker ◽  
Christian R. Eiler ◽  
Basem M. Mishriky ◽  
Leonard E. Egede
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Therapy ◽  
Increased Risk ◽  
High Insulin ◽  
Complications And Mortality

scholarly journals Selenoprotein P as a significant regulator of pancreatic β cell function

2019 ◽  
Author(s):  
Yoshiro Saito
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Insulin Signalling ◽  
Selenoprotein P ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Β Cell Function

Abstract Selenoprotein P (SeP; encoded by SELENOP) is selenium (Se)-rich plasma protein that is mainly produced in the liver. SeP functions as a Se-transport protein to deliver Se from the liver to other tissues, such as the brain and testis. The protein plays a pivotal role in Se metabolism and antioxidative defense, and it has been identified as a ‘hepatokine’ that causes insulin resistance in type 2 diabetes. SeP levels are increased in type 2 diabetes patients, and excess SeP impairs insulin signalling, promoting insulin resistance. Furthermore, increased levels of SeP disturb the functioning of pancreatic β cells and inhibit insulin secretion. This review focuses on the biological function of SeP and the molecular mechanisms associated with the adverse effects of excess SeP on pancreatic β cells’ function, particularly with respect to redox reactions. Interactions between the liver and pancreas are also discussed.

scholarly journals Pathophysiology of Type 2 Diabetes Mellitus

2020 ◽  
Vol 21 (17) ◽  
pp. 6275 ◽  
Author(s):  
Unai Galicia-Garcia ◽  
Asier Benito-Vicente ◽  
Shifa Jebari ◽  
Asier Larrea-Sebal ◽  
Haziq Siddiqi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Release ◽  
Molecular Mechanisms ◽  
Metabolic Memory ◽  
Insulin Metabolism ◽  
Insulin Synthesis

Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin. Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the synthesis and release of insulin, as well as in its detection are tightly regulated. Defects in any of the mechanisms involved in these processes can lead to a metabolic imbalance responsible for the development of the disease. This review analyzes the key aspects of T2DM, as well as the molecular mechanisms and pathways implicated in insulin metabolism leading to T2DM and insulin resistance. For that purpose, we summarize the data gathered up until now, focusing especially on insulin synthesis, insulin release, insulin sensing and on the downstream effects on individual insulin-sensitive organs. The review also covers the pathological conditions perpetuating T2DM such as nutritional factors, physical activity, gut dysbiosis and metabolic memory. Additionally, because T2DM is associated with accelerated atherosclerosis development, we review here some of the molecular mechanisms that link T2DM and insulin resistance (IR) as well as cardiovascular risk as one of the most important complications in T2DM.

scholarly journals Integration of microRNA changes in vivo identifies novel molecular features of muscle insulin resistance in type 2 diabetes

10.1186/gm130 ◽  
2010 ◽  
Vol 2 (2) ◽  
pp. 9 ◽  
Author(s):  
Iain J Gallagher ◽  
Camilla Scheele ◽  
Pernille Keller ◽  
Anders R Nielsen ◽  
Judit Remenyi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Muscle Insulin Resistance ◽  
Molecular Features

scholarly journals Obesity and Insulin Resistance: An Abridged Molecular Correlation

2013 ◽  
Vol 6 ◽  
pp. LPI.S10805 ◽  
Author(s):  
Biswajit Mukherjee ◽  
Chowdhury M. Hossain ◽  
Laboni Mondal ◽  
Paramita Paul ◽  
Miltu K. Ghosh
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
Cardiovascular Complications ◽  
Vital Role ◽  
Diabetic Patients ◽  
Predisposing Factor ◽  
Main Culprit

A relationship between obesity and type 2 diabetes is now generally well accepted. This relationship represents several major health hazards including morbid obesity and cardiovascular complications worldwide. Diabetes mellitus is a complex metabolic disorder characterized by impaired insulin release and insulin resistance. Lipids play an important physiological role in skeletal muscle, heart, liver and pancreas. Deregulation of fatty acid metabolism is the main culprit for developing insulin resistance and type 2 diabetes. A predominant predisposing factor to developing obesity, insulin resistance and type 2 diabetes is the permanent elevation of free fatty acids in plasma followed by impaired utilization of lipids by muscle. Diabetes-induced inflammation and oxidative stress have also vital role for development of insulin resistance in diabetic patients. The present review is intended to describe the correlation between lipids, obesity and insulin resistance based on current literature, in order to elucidate involved molecular mechanisms in depth.

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