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.

Key Factors for Overcoming Psychological Insulin Resistance—An Examination of a Large International Sample through Content Analysis

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 221-OR ◽  
Author(s):  
HEATHER L. STUCKEY ◽  
WILLIAM POLONSKY ◽  
LAWRENCE FISHER ◽  
DANIELLE M. HESSLER ◽  
FRANK J. SNOEK ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Content Analysis ◽  
Key Factors

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 Association of hormonal dysregulation with metabolic syndrome in older women: data from the InCHIANTI study

2007 ◽  
Vol 292 (1) ◽  
pp. E353-E358 ◽  
Author(s):  
Marcello Maggio ◽  
Fulvio Lauretani ◽  
Gian Paolo Ceda ◽  
Stefania Bandinelli ◽  
Shehzad Basaria ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Older Women ◽  
Inflammatory Markers ◽  
Hormone Replacement ◽  
Sex Hormone Binding Globulin ◽  
Bilateral Oophorectomy ◽  
Age Related ◽  
Increased Risk ◽  
Igf I

Metabolic syndrome (MetS) is a strong risk factor for type 2 diabetes and cardiovascular disease. Conditions associated with hyperandrogenism are often associated with glucose intolerance and other features of MetS in young women. As the prevalence of MetS increases with age and is probably multifactorial, it is reasonable to hypothesize that age-related changes in androgens and other hormones might contribute to the development of MetS in older persons. However, this hypothesis has never been tested in older women. We hypothesized that high levels of testosterone, dehydroepiandrosterone sulfate (DHEA-S), and cortisol and low levels of sex hormone-binding globulin (SHBG) and IGF-I would be associated with MetS in a representative cohort of older Italian women independently of confounders (including inflammatory markers). After exclusion of participants on hormone replacement therapy and those with a history of bilateral oophorectomy, 512 women (≥65 yr) had complete data on testosterone, cortisol, DHEA-S, SHBG, fasting insulin, total and free IGF-I, IL-6, and C-reactive protein (CRP). MetS was defined according to ATP-III criteria. Insulin resistance was calculated according to HOMA. MetS was found in 145 women (28.3%). Participants with vs. those without MetS had higher age-adjusted levels of bioavailable testosterone ( P < 0.001), IL-6 ( P < 0.001), CRP ( P < 0.001), and HOMA ( P < 0.001) and lower levels of SHBG ( P < 0.001). After adjustment for potential confounders, participants with decreased SHBG had an increased risk of MetS ( P < 0.0001) vs. those with low SHBG. In a further model including all hormones and confounders, log SHBG was the only independent factor associated with MetS (OR: 0.44, 95% CI 0.21–0.91, P = 0.027). In older women, SHBG is negatively associated with MetS independently of confounders, including inflammatory markers and insulin resistance. Further studies are needed to support the notion that raising SHBG is a potential therapeutic target for prevention and treatment of MetS.

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.

A Copeptin as a Predictor Marker for Insulin Resistance Among Women with Polycystic Ovary Syndrome

2021 ◽  
Vol 17 ◽  
Author(s):  
Alaa Ibrahim Ali ◽  
Wassan Nori Mohammed Hassan ◽  
Sumaya Alrawi
Keyword(s):  
Insulin Resistance ◽  
Polycystic Ovary ◽  
Transvaginal Ultrasound ◽  
Predictive Marker ◽  
University Hospital ◽  
Sex Hormone Binding Globulin ◽  
Total Testosterone ◽  
Model Assessment ◽  
Homeostasis Model Assessment ◽  
Wide Range

Background: A polycystic ovarian syndrome (PCOS) is a common endocrine syndrome in which women have a wide range of clinical presentations; insulin resistance was linked to its pathogenesis. Objective: We aimed to investigate the copeptin role as a predictive marker of insulin resistance among PCOS women. Material and Methods: In University Hospital, we included 280 women, with 140 of them being healthy controls. 140 out of 280 cases of PCOS subdivided into two groups depending on the insulin resistance; group 1 with homeostasis model assessment for the insulin resistance < 2.5. Group 2 with homeostasis model assessment for the insulin resistance >2.5. The evaluation of body mass index and blood pressure for all besides the blood sampling for estimation of a follicular stimulating hormone, luteinizing hormone, prolactin, estradiol, sex hormone-binding globulin, total testosterone, fasting insulin dehydroepiandrosterone sulfate, C-reactive protein, plasma glucose, free androgen index, and plasma copeptin using the Copeptin-Human EIA Kit besides the transvaginal ultrasound for ovarian assessment. Results: When compared to other groups, PCOS women with positive insulin resistance >2.5 had a significantly higher plasma copeptin level. The ROC curve calculated a 1.94 pmol/L; plasma copeptin cutoff value for detecting the insulin resistance in PCOS with 88% sensitivity value and 36% specificity, AUC was 0.88. Conclusion: The significant positive relationship between serum copeptin and insulin resistance with high sensitivity implies its usefulness as a marker of insulin resistance among PCOS patients with a high prediction of its complication.

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.

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.

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