The conception of the probable role of the biological active chromium in the emergence of insulin resistance and alimentary obesity

2021 ◽  
Vol 1 (223) ◽  
pp. 34-38
Author(s):  
Bolat Abishev ◽  
Keyword(s):  
Insulin Resistance ◽  
Structural Organization ◽  
Redox State ◽  
Metabolic Response ◽  
Essential Element ◽  
Insulin Receptors ◽  
Trivalent Chromium ◽  
Manual Search ◽  
Alimentary Obesity ◽  
Search And Selection

The conception of probable alimentary chromium role in connection with metabolic reasons emergence of insulin resistance in the alimentary obesity and type 2 diabetes is represented. The violation of insulin receptors structural organization and conformation with these pathological conditions in connection with redox states of chromium is supposed. Based on information from general chemistry and chromium metabolism, higher biological activity of hexavalent chromium when compared to the activity of trivalent chromium is assumed in insulin-resistant conditions. Aim. To analyze the literature data on the a supposed participation of chromium in food and chromium nutraceuticals in connection with insulin resistance at the metabolic level. Material and methods. The analysis of the literature was carried out by the method of manual search and selection of the most important and significant for the analyzed issue monographs and articles up to 60 years in depth. The search criteria were works directly related to the association of food chromium with the insulin-dependent metabolic response of cells and the activity of insulin receptors. No works published over the past 10 years that introduce principled novelty and are of principled importance for the present problem have not been identified. Results and discussion. The concept of the supposed participation of chromium as an essential element in connection with the metabolic reasons for the formation of insulin resistance and the structural organization of insulin receptors depending on the redox state of chromium is presented. Keywords: hexavalent and trivalent chromium, insulin resistance, redox state, insulin receptor, alimentary obesity, diabetes.

scholarly journals Endothelial insulin receptors differentially control insulin signaling kinetics in peripheral tissues and brain of mice

2017 ◽  
Vol 114 (40) ◽  
pp. E8478-E8487 ◽  
Author(s):  
Masahiro Konishi ◽  
Masaji Sakaguchi ◽  
Samuel M. Lockhart ◽  
Weikang Cai ◽  
Mengyao Ella Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
Food Intake ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Brain Regions ◽  
Peripheral Tissues ◽  
Systemic Insulin Resistance

Insulin receptors (IRs) on endothelial cells may have a role in the regulation of transport of circulating insulin to its target tissues; however, how this impacts on insulin action in vivo is unclear. Using mice with endothelial-specific inactivation of the IR gene (EndoIRKO), we find that in response to systemic insulin stimulation, loss of endothelial IRs caused delayed onset of insulin signaling in skeletal muscle, brown fat, hypothalamus, hippocampus, and prefrontal cortex but not in liver or olfactory bulb. At the level of the brain, the delay of insulin signaling was associated with decreased levels of hypothalamic proopiomelanocortin, leading to increased food intake and obesity accompanied with hyperinsulinemia and hyperleptinemia. The loss of endothelial IRs also resulted in a delay in the acute hypoglycemic effect of systemic insulin administration and impaired glucose tolerance. In high-fat diet-treated mice, knockout of the endothelial IRs accelerated development of systemic insulin resistance but not food intake and obesity. Thus, IRs on endothelial cells have an important role in transendothelial insulin delivery in vivo which differentially regulates the kinetics of insulin signaling and insulin action in peripheral target tissues and different brain regions. Loss of this function predisposes animals to systemic insulin resistance, overeating, and obesity.

scholarly journals Insulin Resistance in ICU Patients: Women Have Stronger Metabolic Response

2020 ◽  
Vol 53 (2) ◽  
pp. 16203-16208
Author(s):  
Vincent Uyttendaele ◽  
Jennifer L. Knopp ◽  
Rebecca Gottlieb ◽  
Geoffrey M. Shaw ◽  
Thomas Desaive ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Response ◽  
Icu Patients

Insulin action and resistance in obesity and noninsulin-dependent type II diabetes mellitus

1982 ◽  
Vol 243 (1) ◽  
pp. E15-E30 ◽  
Author(s):  
J. M. Olefsky ◽  
O. G. Kolterman ◽  
J. A. Scarlett
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Action ◽  
Insulin Receptors ◽  
Tissue Level ◽  
Dependent Diabetes Mellitus ◽  
Target Tissue ◽  
Severe Insulin Resistance ◽  
Glucose Clamp Technique

Resistance to the action of insulin can result from a variety of causes, including the formation of abnormal insulin or proinsulin molecules, the presence of circulating antagonists to insulin or the insulin receptor, or defects in insulin action at the target tissue level. Defects of the latter type are characteristic of obesity and of noninsulin-dependent diabetes mellitus. Analysis of the nature of the insulin resistance in those disorders has been investigated in intact subjects with the use of the euglycemic glucose clamp technique, and both insulin receptors and insulin-mediated glucose metabolism have been studied in adipocytes and monocytes from affected individuals. In both conditions, the cause of insulin resistance is heterogeneous. In some, insulin resistance appears to be due to a defect in the insulin receptor, whereas others have a defect both in the receptor and at the postreceptor level. In both groups, more severe insulin resistance is due to the postreceptor lesion and is correctable with appropriate therapy.

Abstract 18289: New Roles of the Interplay Between Endothelin and Insulin-like Growth Factor 1 in the Regulation of Vascular Redox State in Patients With Type 2 Diabetes and Coronary Atherosclerosis

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ioannis Akoumianakis ◽  
Marios Margaritis ◽  
Fabio Sanna ◽  
Laura Herdman ◽  
Constantinos Psarros ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Growth Factor ◽  
Nadph Oxidase ◽  
Redox State ◽  
Vascular Complications ◽  
Positive Association ◽  
Elevated Plasma ◽  
Enos Uncoupling

Background: Insulin resistance (IR) is associated with increased cardiovascular risk. Given that plasma endothelin (ET) is elevated in IR, we explored whether the variations in ET levels mediate the vascular complications of type 2 diabetes (T2DM), by exploring its links with vascular redox state in human vessels. Methods: The study population consisted of 383 patients undergoing coronary bypass surgery (CABG), 30% with T2DM. Levels of ET, insulin growth factor 1 (IGF1), insulin and glucose (to calculate HOMA-IR as an index of insulin resistance) were measured in plasma, while vascular superoxide (O2) was measured in saphenous vein segments obtained during surgery. Results: Patients with untreated T2DM had elevated plasma ET, contrary to treated patients with T2DM (A). A positive association was observed between plasma endothelin and IGF1 levels in non-T2DM, which was reversed in T2DM (B). Elevated plasma ET was associated with increased NADPH-stimulated O2- (indicative of higher NADPH oxidase activity) and more LNAME inhibitable O2- (suggestive of more eNOS uncoupling) in human vessels (C, D). Conclusions: We demonstrate that circulating ET is elevated in untreated T2DM but its levels are normalised after intensive glycaemic control. We also document a striking effect of DM on the balance between ET and IGF1, and we demonstrate for the first time in humans, that elevated plasma ET is associated with increased O2- generation in the vascular wall through activation of NADPH-oxidase and uncoupling of eNOS. This study shows that ET and its interplay with IGF1 is possibly a key mechanism linking T2DM with its vascular complications in humans

Effect of Subtoxic DDT Exposure on Glucose Uptake and Insulin Signaling in Rat L6 Myoblast-Derived Myotubes

2019 ◽  
Vol 38 (4) ◽  
pp. 303-311 ◽  
Author(s):  
Vijay Kumar Singh ◽  
Sajib Kumar Sarkar ◽  
Alpana Saxena ◽  
Bidhan Chandra Koner
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Tyrosine Phosphorylation ◽  
Insulin Signaling ◽  
Messenger Rna ◽  
Insulin Receptors ◽  
Serine Phosphorylation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Antioxidant Content ◽  
L6 Myoblast

Exposure to persistent organic pollutants including dichlorodiphenyltrichloroethane (DDT) induces insulin resistance. But the mechanism is not clearly known. The present study was designed to explore the effect of subtoxic DDT exposure on (1) insulin-stimulated glucose uptake, (2) malondialdehyde (MDA) level and total antioxidant content, (3) activation of redox sensitive kinases (RSKs), and (4) insulin signaling in rat L6 myoblast-derived myotubes. Exposure to 30 mg/L and 60 mg/L of DDT for 18 hours dose dependently decreased glucose uptake and antioxidant content in myotubes and increased MDA levels. The exposures did not alter tumor necrosis factor α (TNF-α) level as determined by enzyme-linked immunosorbent assay, despite decreased messenger RNA expression following DDT exposures. Phosphorylation of c-Jun N-terminal kinases and IκBα, an inhibitory component of nuclear factor κB (NFκB), was increased, suggesting activation of RSKs. The level of tyrosine phosphorylation of insulin receptor substrate 1 and serine phosphorylation of protein kinase B (Akt) on insulin stimulation decreased in myotubes with exposure to subtoxic concentrations of DDT, but there was no change in tyrosine phosphorylation level of insulin receptors. We conclude that subtoxic DDT exposure impairs insulin signaling and thereby induces insulin resistance in muscle cells. Data show that oxidative stress-induced activation of RSKs is responsible for impairment of insulin signaling on DDT exposure.

scholarly journals Insulin Resistance and Endometrial Cancer: Emerging Role for microRNA

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2559
Author(s):  
Iwona Sidorkiewicz ◽  
Maciej Jóźwik ◽  
Magdalena Niemira ◽  
Adam Krętowski
Keyword(s):  
Insulin Resistance ◽  
Endometrial Cancer ◽  
Insulin Receptors ◽  
Transcriptional Regulators ◽  
Sex Hormone Binding Globulin ◽  
Female Reproductive System ◽  
Key Factors ◽  
Mirna Expression Pattern ◽  
Reasonable Possibility ◽  
Insulin Like Growth Factors

Endometrial cancer (EC) remains one of the most common cancers of the female reproductive system. Epidemiological and clinical data implicate insulin resistance (IR) and its accompanying hyperinsulinemia as key factors in the development of EC. MicroRNAs (miRNAs) are short molecules of non-coding endogenous RNA that function as post-transcriptional regulators. Accumulating evidence has shown that the miRNA expression pattern is also likely to be associated with EC risk factors. The aim of this work was the verification of the relationships between IR, EC, and miRNA, and, as based on the literature data, elucidation of miRNA’s potential utility for EC prevention in IR patients. The pathways affected in IR relate to the insulin receptors, insulin-like growth factors and their receptors, insulin-like growth factor binding proteins, sex hormone-binding globulin, and estrogens. Herein, we present and discuss arguments for miRNAs as a plausible molecular link between IR and EC development. Specifically, our careful literature search indicated that dysregulation of at least 13 miRNAs has been ascribed to both conditions. We conclude that there is a reasonable possibility for miRNAs to become a predictive factor of future EC in IR patients.

Insulin Receptors in Acute Infection: A Study of Factors Conferring Insulin Resistance*

1984 ◽  
Vol 58 (4) ◽  
pp. 710-716 ◽  
Author(s):  
ELAINE C. DROBNY ◽  
EDITH C. ABRAMSON ◽  
GERHARD BAUMANN
Keyword(s):  
Insulin Resistance ◽  
Acute Infection ◽  
Insulin Receptors

scholarly journals Liraglutide Suppresses Tau Hyperphosphorylation, Amyloid Beta Accumulation through Regulating Neuronal Insulin Signaling and BACE-1 Activity

2020 ◽  
Vol 21 (5) ◽  
pp. 1725 ◽  
Author(s):  
Salinee Jantrapirom ◽  
Wutigri Nimlamool ◽  
Nipon Chattipakorn ◽  
Siriporn Chattipakorn ◽  
Piya Temviriyanukul ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glycogen Synthase ◽  
Insulin Receptors ◽  
Beta Amyloid ◽  
Significant Feature ◽  
Amyloid Formation ◽  
Tau Hyperphosphorylation ◽  
Insulin Resistant ◽  
Neuronal Insulin Resistance ◽  
Bace 1

Neuronal insulin resistance is a significant feature of Alzheimer’s disease (AD). Accumulated evidence has revealed the possible neuroprotective mechanisms of antidiabetic drugs in AD. Liraglutide, a glucagon-like peptide-1 (GLP-1) analog and an antidiabetic agent, has a benefit in improving a peripheral insulin resistance. However, the neuronal effect of liraglutide on the model of neuronal insulin resistance with Alzheimer’s formation has not been thoroughly investigated. The present study discovered that liraglutide alleviated neuronal insulin resistance and reduced beta-amyloid formation and tau hyperphosphorylation in a human neuroblostoma cell line, SH-SY5Y. Liraglutide could effectively reverse deleterious effects of insulin overstimulation. In particular, the drug reversed the phosphorylation status of insulin receptors and its major downstream signaling molecules including insulin receptor substrate 1 (IRS-1), protein kinase B (AKT), and glycogen synthase kinase 3 beta (GSK-3β). Moreover, liraglutide reduced the activity of beta secretase 1 (BACE-1) enzyme, which then decreased the formation of beta-amyloid in insulin-resistant cells. This indicated that liraglutide can reverse the defect of phosphorylation status of insulin signal transduction but also inhibit the formation of pathogenic Alzheimer’s proteins like Aβ in neuronal cells. We herein provided the possibility that the liraglutide-based therapy may be able to reduce such deleterious effects caused by insulin resistance. In view of the beneficial effects of liraglutide administration, these findings suggest that the use of liraglutide may be a promising therapy for AD with insulin-resistant condition.

Hyperinsulinism, Insulin Resistance and Insulin Receptors in Obese Patients

2015 ◽  
pp. 231-234
Author(s):  
A. Carducci Artenisio ◽  
F. Ragonese ◽  
F. Forte ◽  
G. Saitta ◽  
G. Perrone ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptors ◽  
Obese Patients
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