Insulin resistance in Type 2 diabetes and obesity: implications for endothelial function

2011 ◽  
Vol 9 (4) ◽  
pp. 403-407 ◽  
Author(s):  
Amir Aziz ◽  
Stephen Wheatcroft
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Endothelial Function ◽  
Diabetes And Obesity

Vascular dysfunction and insulin stimulated blood flow : impact of physical inactivity and type 2 diabetes

2014 ◽  
Author(s):  
◽  
Leryn J. Boyle
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Blood Flow ◽  
Insulin Sensitivity ◽  
Endothelial Function ◽  
Physical Inactivity ◽  
Vascular Dysfunction ◽  
Insulin Stimulation

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Individuals with type 2 diabetes (T2D) have blunted femoral artery insulin mediated blood flow which is critical for the delivery and uptake of glucose into skeletal muscle. However, it is unclear in humans the precise mechanisms by which insulin resistance impairs insulin stimulated blood flow. Further, chronic physical inactivity is a powerful stimulus for reduced insulin sensitivity and vascular dysfunction; however, the effects of short term, modest reductions in physical activity are limited. Thus, we examined 1) if inactivity for 5 days would impair endothelial function in healthy individuals (study one) 2) if reducing whole body insulin sensitivity, via 5 days of inactivity, would impair the blood flow response to insulin stimulation in parallel with glycemic control (study two) and 3) phosphorylation of endothelial nitric oxide (eNOS) and endothelin-1 (ET-1) production to insulin stimulation would be decreased and increased, respectively, in insulin resistant individuals (study three). We demonstrated significant reductions in endothelial function with only 5 days of reduced daily steps while blood flow to glucose ingestion was unaltered. Further, in obese humans with type 2 diabetes it does not appear that that the reduction in blood flow to 1 hr of insulin stimulation is due to altered peNOS or ET-1. Collectively, these data suggest that reduced daily physical activity and chronic insulin resistance mediate negative impacts on vascular function and insulin stimulated blood flow and signaling.

scholarly journals MicroRNAs in Insulin Resistance and Obesity

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Michael D. Williams ◽  
Geraldine M. Mitchell
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Messenger Rna ◽  
Physiological Role ◽  
Mrna Translation ◽  
Aberrant Expression ◽  
Peripheral Tissues ◽  
Pancreatic Islets Of Langerhans ◽  
Diabetes And Obesity

MicroRNAs (miRNAs) are a class of short, single-stranded non-protein coding gene products which can regulate the gene expression through post-transcriptional inhibition of messenger RNA (mRNA) translation. They are known to be involved in many essential biological processes including development, insulin secretion, and adipocyte differentiation. miRNAs are involved in complex metabolic processes, such as energy and lipid metabolism, which have been studied in the context of diabetes and obesity. Obesity, hyperlipidemia (elevated levels of blood lipids), and insulin resistance are strongly associated with the onset of type 2 diabetes. These conditions are also associated with aberrant expression of multiple essential miRNAs in pancreatic islets of Langerhans and peripheral tissues, including adipose tissue. A thorough understanding of the physiological role these miRNAs play in these tissues, and changes to their expression under pathological conditions, will allow researchers to develop new therapeutics with the potential to correct the aberrant expression of miRNAs in type 2 diabetes and obesity.

Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease

2004 ◽  
Vol 287 (6) ◽  
pp. E1209-E1215 ◽  
Author(s):  
Thomas Nyström ◽  
Mark K. Gutniak ◽  
Qimin Zhang ◽  
Fan Zhang ◽  
Jens Juul Holst ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Healthy Subjects ◽  
Stable Coronary Artery Disease ◽  
Artery Disease ◽  
Type 2 Diabetic ◽  
Diabetes Patients

GLP-1 stimulates insulin secretion, suppresses glucagon secretion, delays gastric emptying, and inhibits small bowel motility, all actions contributing to the anti-diabetogenic peptide effect. Endothelial dysfunction is strongly associated with insulin resistance and type 2 diabetes mellitus and may cause the angiopathy typifying this debilitating disease. Therefore, interventions affecting both endothelial dysfunction and insulin resistance may prove useful in improving survival in type 2 diabetes patients. We investigated GLP-1's effect on endothelial function and insulin sensitivity (SI) in two groups: 1) 12 type 2 diabetes patients with stable coronary artery disease and 2) 10 healthy subjects with normal endothelial function and SI. Subjects underwent infusion of recombinant GLP-1 or saline in a random crossover study. Endothelial function was measured by postischemic FMD of brachial artery, using ultrasonography. SI [in (10−4 dl·kg−1·min−1)/(μU/ml)] was measured by hyperinsulinemic isoglycemic clamp technique. In type 2 diabetic subjects, GLP-1 infusion significantly increased relative changes in brachial artery diameter from baseline FMD(%) (3.1 ± 0.6 vs. 6.6 ± 1.0%, P < 0.05), with no significant effects on SI (4.5 ± 0.8 vs. 5.2 ± 0.9, P = NS). In healthy subjects, GLP-1 infusion affected neither FMD(%) (11.9 ± 0.9 vs. 10.3 ± 1.0%, P = NS) nor SI (14.8 ± 1.8 vs. 11.6 ± 2.0, P = NS). We conclude that GLP-1 improves endothelial dysfunction but not insulin resistance in type 2 diabetic patients with coronary heart disease. This beneficial vascular effect of GLP-1 adds yet another salutary property of the peptide useful in diabetes treatment.

scholarly journals Vitamin D 3, osteoprotegerin and other hormonal and metabolic parameters in female patients with type 2 diabetes

2012 ◽  
Vol 9 (4) ◽  
pp. 23-27 ◽  
Author(s):  
A F Verbovoi ◽  
L A Sharonova ◽  
A V Kapishnikov ◽  
D V Demidova
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Vitamin D3 ◽  
Metabolic Parameters ◽  
Female Patients ◽  
Vitamin D 3 ◽  
Diabetes And Obesity

The article presents the results of evaluation of vitamin D3, osteoprotegerin, carbohydrate and fat metabolic parameters in women with type 2 diabetes and obesity. The study subjects showed an increase of osteoprotegerin, decrease of vitamin D3, insulin resistance and compensatory hyperinsulinemia.

scholarly journals Role of GALNT2 on Insulin Sensitivity, Lipid Metabolism and Fat Homeostasis

2022 ◽  
Vol 23 (2) ◽  
pp. 929
Author(s):  
Alessandra Antonucci ◽  
Antonella Marucci ◽  
Vincenzo Trischitta ◽  
Rosa Di Paola
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Common Ground ◽  
Metabolic Diseases ◽  
Atherogenic Dyslipidemia ◽  
Physiological Processes ◽  
Protein Functions ◽  
Heavy Burden ◽  
Diabetes And Obesity

O-linked glycosylation, the greatest form of post-translational modifications, plays a key role in regulating the majority of physiological processes. It is, therefore, not surprising that abnormal O-linked glycosylation has been related to several human diseases. Recently, GALNT2, which encodes the GalNAc-transferase 2 involved in the first step of O-linked glycosylation, has attracted great attention as a possible player in many highly prevalent human metabolic diseases, including atherogenic dyslipidemia, type 2 diabetes and obesity, all clustered on the common ground of insulin resistance. Data available both in human and animal models point to GALNT2 as a molecule that shapes the risk of the aforementioned abnormalities affecting diverse protein functions, which eventually cause clinically distinct phenotypes (a typical example of pleiotropism). Pathways linking GALNT2 to dyslipidemia and insulin resistance have been partly identified, while those for type 2 diabetes and obesity are yet to be understood. Here, we will provide a brief overview on the present knowledge on GALNT2 function and dysfunction and propose novel insights on the complex pathogenesis of the aforementioned metabolic diseases, which all impose a heavy burden for patients, their families and the entire society.

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