Assessment of red blood cell glutathione status in insulin resistance

2012 ◽  
Vol 37 (5) ◽  
pp. 997-1002
Author(s):  
Jose E. Galgani ◽  
Karla Vasquez ◽  
Giannella Leonelli ◽  
Alejandra Espinosa ◽  
Hector Araya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Postprandial Glucose ◽  
Serum Glucose ◽  
Oral Glucose ◽  
Glucose Response ◽  
Insulin Resistant ◽  
Glucose Ingestion ◽  
Before And After

The aim of this study was to assess red blood cell glutathione from insulin-sensitive and insulin-resistant individuals before and after an oral glucose dose. Fifteen healthy, young (24 ± 5 years), nonobese (23 ± 2 kg·m–2), insulin-sensitive (ISI composite = 6.0 ± 1.2) individuals and 14 healthy, young (22 ± 2 years), nonobese (24 ± 2 kg·m–2), insulin-resistant (ISI composite = 2.7 ± 1.1) individuals received a 75 g oral glucose dose. Blood samples were drawn before and for 2 h after glucose ingestion for red blood cell glutathione and serum glucose and insulin concentrations. Glycemia before and after glucose ingestion was similar between groups (p = 0.17), which suggest that hyperinsulinemia compensated impaired insulin sensitivity. Red blood cell total (p = 0.81), reduced (p = 0.79), and oxidized (p = 0.88) glutathione concentrations were similar between groups under fasting and postprandial conditions. However, in response to glucose, increases in total and reduced glutathione concentrations were found at the end of the 2 h assessment period in both groups (p < 0.05). Direct associations between postprandial glucose response and red blood cell total (r = 0.52; p < 0.05) and oxidized (r = 0.61; p = 0.02) glutathione concentrations were observed only in insulin-sensitive subjects. In conclusion, healthy individuals differing in their degree of insulin resistance showed similar red blood cell glutathione concentrations under non-glucose- and glucose-stimulated conditions.

scholarly journals Effects of Polyphenols on Insulin Resistance

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3135
Author(s):  
Gary Williamson ◽  
Katherine Sheedy
Keyword(s):  
Insulin Resistance ◽  
Intervention Studies ◽  
Insulin Signalling ◽  
Fasting Blood Glucose ◽  
Postprandial Glucose ◽  
Oral Glucose ◽  
Β Cells ◽  
Insulin Resistant ◽  
Improve Insulin Resistance ◽  
Glucose Challenge

Insulin resistance (IR) is apparent when tissues responsible for clearing glucose from the blood, such as adipose and muscle, do not respond properly to appropriate signals. IR is estimated based on fasting blood glucose and insulin, but some measures also incorporate an oral glucose challenge. Certain (poly)phenols, as supplements or in foods, can improve insulin resistance by several mechanisms including lowering postprandial glucose, modulating glucose transport, affecting insulin signalling pathways, and by protecting against damage to insulin-secreting pancreatic β-cells. As shown by intervention studies on volunteers, the most promising candidates for improving insulin resistance are (−)-epicatechin, (−)-epicatechin-containing foods and anthocyanins. It is possible that quercetin and phenolic acids may also be active, but data from intervention studies are mixed. Longer term and especially dose-response studies on mildly insulin resistant participants are required to establish the extent to which (poly)phenols and (poly)phenol-rich foods may improve insulin resistance in compromised groups.

Tissue- and isoform-specific effects of aging in rats on protein kinase C in insulin-sensitive tissues

1999 ◽  
Vol 97 (3) ◽  
pp. 355-361 ◽  
Author(s):  
Xianqin QU ◽  
J. Paul SEALE ◽  
Richard DONNELLY
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Serum Glucose ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Insulin Resistant ◽  
Kinase C ◽  
Age Related

The mechanisms responsible for the age-related decline in insulin sensitivity have not been clearly identified, but activation of the diacylglycerol/protein kinase C (PKC) signalling pathway (often confined to individual isoforms of PKC) has recently been implicated in the pathogenesis of other insulin-resistant states in both humans and animal models. Fasting serum glucose, insulin and triacylglycerol (triglyceride) concentrations, and results of oral glucose tolerance tests, were compared in groups of 6-week-old (n = 8) and 6-month-old (n = 8) Sprague–Dawley rats. Insulin-responsive tissues (liver, soleus muscle and epididymal fat pad) were collected to compare levels of diacylglycerol, PKC enzyme activity and protein expression of individual PKC isoforms in cytosol and membrane fractions. The older group were heavier (556±14 g, compared with 188±7 g) and relatively insulin-resistant and hyperinsulinaemic (477±73 pM compared with 293±51 pM; P < 0.05) compared with young rats; they also had greater areas under the serum glucose (old, 20.3±1.1; young, 17.3±0.7 mmol·h-1·l-1) and insulin (old, 1254±76; young, 721±113 mmol·h-1·l-1) profiles following an oral glucose tolerance test, and significantly higher fasting triacylglycerol levels (old, 1.24±0.06 mM; young, 0.92±0.07 mM; P < 0.01). There were no age-related differences in diacylglycerol levels or PKC activity in muscle and liver, but membrane-associated PKC activity was 2.5-fold higher in the adipose tissue of older rats (101±19 compared with 40±5 pmol·min-1·mg-1 protein; P < 0.05) due to increased translocation of PKC-βI, -βII and -ε. Thus insulin resistance due to normal aging is associated with tissue- and isoform-specific changes in diacylglycerol/PKC signalling. In contrast with diabetes and dietary-induced insulin resistance, there were no changes in diacylglycerol/PKC signalling in skeletal muscle and liver, but isoform-specific translocation and higher PKC activity in adipose tissue may blunt the insulin-mediated inhibition of lipolysis and contribute to the increased triacylglycerol levels observed in older animals.

Insulin resistance and blood pressure in Dahl rats and in one-kidney, one-clip hypertensive rats

1991 ◽  
Vol 261 (6) ◽  
pp. E692-E697 ◽  
Author(s):  
T. A. Kotchen ◽  
H. Y. Zhang ◽  
M. Covelli ◽  
N. Blehschmidt
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Genetic Model ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Oral Glucose ◽  
Hypertensive Rats ◽  
Insulin Resistant ◽  
Sucrose Feeding ◽  
The One

In normal rats, sucrose feeding results in insulin resistance and an elevation of arterial pressure. The purpose of this study was twofold: 1) to evaluate the effect of sucrose feeding on blood pressure in a genetic model and in an acquired model of hypertension and 2) to determine whether these models of hypertension are associated with insulin resistance. In Dahl salt-resistant (Dahl-R) rats on both a 0.45 and a 3% NaCl intake, systolic blood pressures were higher (P less than 0.01) in sucrose-drinking than in water-drinking animals. In contrast, blood pressure was not affected by dietary sucrose in Dahl salt-sensitive (Dahl-S) rats. Blood pressure was also not affected by sucrose in the one-kidney, one-clip (1K,1C) hypertensive rat. In response to an oral glucose load, serum glucose was similar in Dahl-R and Dahl-S rats, although serum insulin was higher (P less than 0.05) in Dahl-S rats, suggesting that Dahl-S rats are insulin resistant. In contrast, glucose and insulin responses were similar in hypertensive 1K,1C animals and normotensive controls. In conclusion, sucrose feeding increased blood pressure in Dahl-R but not in Dahl-S or 1K,1C hypertensive rats. Additionally, Dahl-S rats, but not hypertensive 1K,1C rats, are insulin resistant.

Altering Physical Activity Influences Insulin Responses to Glucose Ingestion in Healthy Adults

2018 ◽  
Vol 39 (13) ◽  
pp. 972-977 ◽  
Author(s):  
Kyle Timmerman ◽  
Kevin Ballard ◽  
Gabrielle Volk ◽  
Michael Deal ◽  
Adam Meisler ◽  
...  
Keyword(s):  
Physical Activity ◽  
Blood Glucose ◽  
Repeated Measures ◽  
Serum Insulin ◽  
Fasting Blood Glucose ◽  
Area Under The Curve ◽  
Postprandial Glucose ◽  
Oral Glucose ◽  
Glucose Response ◽  
Glucose Ingestion

AbstractThis study determined if varying physical activity (PA) the day prior to an oral glucose tolerance test (OGTT) differentially influenced postprandial glucose and insulin kinetics. Fifteen healthy, young adults participated in three OGTT trials the morning after performing 50% (LOW), 100% (HABITUAL), or 150% (HIGH) of their habitual PA (determined by 7-day pedometry). Trials were randomized and separated by at least 1-wk. For each OGTT trial, blood glucose and insulin were measured after an overnight fast and at 30-min intervals for 2 h following ingestion of the glucose beverage. Between-trial differences were analyzed using a general linear model with repeated measures. Subjects successfully achieved the desired percentage of habitual steps prior to each trial: LOW: 51±5%, HABITUAL: 99±6%, and HIGH: 149±9%. Fasting blood glucose and glucose total area under the curve (AUC) did not differ between trials. Serum insulin AUC was lower (p<0.05) following the HIGH (34,158±8,786 pmol·min·L−1) compared to the LOW (40,738±9,276 pmol·min·L−1) trial. No differences were observed when the LOW and HIGH trials were compared to HABITUAL. These data suggest that varying the PA level (from 50 to 150% of habitual PA) the day prior to an OGTT influences the insulin (but not blood glucose) response to an OGTT.

Relationship between Insulin Release, Antinatriuresis and Hypokalaemia after Glucose Ingestion in Normal and Hypertensive Man

1993 ◽  
Vol 85 (3) ◽  
pp. 327-335 ◽  
Author(s):  
Andrea Natali ◽  
Alfredo Quiñones Galvan ◽  
Donatella Santoro ◽  
Neda Pecori ◽  
Stefano Taddei ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Potassium Concentration ◽  
Plasma Potassium ◽  
Oral Glucose ◽  
Plasma Insulin Concentration ◽  
Hypertensive Patients ◽  
Insulin Resistant ◽  
Glucose Ingestion ◽  
Before And After ◽  
Tightly Coupled

1. Insulin simultaneously causes hypokalaemia and antinatriuresis, and it has been suggested that the two effects are tightly coupled. Whether these actions are preserved in patients with essential hypertension is not known. 2. Eight hypertensive patients and eight normotensive control subjects were studied before and after the ingestion of 75 g of glucose. Despite similar glycaemic profiles, the patients showed a hyperinsulinaemic response incremental area 49 ±8 versus 27 ± 6 nmoll−1 3h, P <0.04) but a blunted hypokalemic response (−7±1 versus −16±1%, P <0.001). Both absolute and fractional urinary excretion of sodium and potassium were significantly decreased during glucose-induced hyperinsulinaemia in hypertensive patients as well as in normotensive subjects (P <0.05 for all changes). 3. To test whether hypokalaemia is required for insulin-induced antinatriuresis, each hypertensive patient received another oral glucose load during which enough potassium chloride was given to clamp the plasma potassium concentration at baseline. Under these conditions, significant insulin-induced antinatriuresis still occurred. In addition, whereas the glycaemic profile was superimposable, the response of the plasma insulin concentration was significantly greater with than without maintenance of the plasma potassium concentration (total area 79 ± 14 versus 63 ± 8 nmoll−1 3h, P <0.04). 4. We conclude that (a) insulin causes antinatriuresis, antikaliuresis and hypokalaemia under physiological conditions; (b) in hyperinsulinaemic (insulin-resistant) patients with essential hypertension, the anti-natriuretic action of insulin is quantitatively preserved; and (c) clamping plasma potassium levels prevents insulin-induced antikaliuresis but not anti-natriuresis, and potentiates the insulin secretory response to glucose.

scholarly journals Changes of Hematocrit, Hemoglobin, Serum Protein Levels and Red Blood Cell Counts Before and After Stroke

1976 ◽  
Vol 13 (4) ◽  
pp. 207-214
Author(s):  
Hiroshi Yamanouchi ◽  
Hideo Tohgi ◽  
Masakuni Kameyama ◽  
Mototaka Murakami ◽  
Tamotsu Matsuda
Keyword(s):  
Blood Cell ◽  
Serum Protein ◽  
Red Blood Cell ◽  
Protein Levels ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Before And After

scholarly journals Scutellaria baicalensis Alleviates Insulin Resistance in Diet-Induced Obese Mice by Modulating Inflammation

2019 ◽  
Vol 20 (3) ◽  
pp. 727 ◽  
Author(s):  
Hyun-Young Na ◽  
Byung-Cheol Lee
Keyword(s):  
Insulin Resistance ◽  
Inflammatory Responses ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Postprandial Glucose ◽  
Scutellaria Baicalensis ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Epididymal Fat

Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.

scholarly journals Endothelial dysfunction precedes hypertension in diet-induced insulin resistance

1998 ◽  
Vol 275 (3) ◽  
pp. R788-R792 ◽  
Author(s):  
Prasad V. G. Katakam ◽  
Michael R. Ujhelyi ◽  
Margarethe E. Hoenig ◽  
Allison Winecoff Miller
Keyword(s):  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Serum Insulin ◽  
Serum Glucose ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Sprague Dawley ◽  
Insulin Resistant ◽  
Glucose Levels

The insulin-resistant (IR) syndrome may be an impetus for the development of hypertension (HTN). Unfortunately, the mechanism by which this could occur is unclear. Our laboratory and others have described impaired endothelium-mediated relaxation in IR, mildly hypertensive rats. The purpose of the current study is to determine if HTN is most likely a cause or result of impaired endothelial function. Sprague-Dawley rats were randomized to receive a fructose-rich diet for 3, 7, 10, 14, 18, or 28 days or were placed in a control group. The control group received rat chow. After diet treatment, animals were instrumented with arterial cannulas, and while awake and unrestrained, their blood pressure (BP) was measured. Subsequently, endothelium-mediated relaxation to acetylcholine was determined (in vitro) by measuring intraluminal diameter of phenylephrine-preconstricted mesenteric arteries (∼250 μM). Serum insulin levels were significantly elevated in all groups receiving fructose feeding compared with control, whereas there were no differences in serum glucose levels between groups. Impairment of endothelium-mediated relaxation starts by day 14 [mean percent maximal relaxation (Emax): 69 ± 10% of baseline] and becomes significant by day 18 (Emax: 52 ± 11% of baseline; P < 0.01). However, the mean BP (mmHg) does not become significantly elevated until day 28 [BP: 132 ± 1 ( day 28) vs. 116 ± 3 (control); P < 0.05]. These findings demonstrate that both IR and endothelial dysfunction occur before HTN in this model and suggest that endothelial dysfunction may be a mechanism linking insulin resistance and essential HTN.

scholarly journals Evaluation of Peripheral Blood Neutrophil Functions after an Oral Carbohydrate Overload in Obese and Insulin Resistant Horses

2020 ◽  
Author(s):  
Constanza Salinas ◽  
Gabriel Espinosa ◽  
Natalia Morales ◽  
Claudio Henriquez ◽  
Gabriel Moran ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Oxidative Burst ◽  
Peripheral Blood ◽  
Oral Glucose ◽  
Close Monitoring ◽  
Metabolic Dysfunction ◽  
Phagocytic Capacity ◽  
Insulin Resistant ◽  
Peripheral Blood Neutrophil ◽  
Stimulation Of

Abstract Background: Obesity and insulin resistance (IR) are conditions of increasing prevalence in populations of equids worldwide. The immune impairment described in metabolic dysfunction status in humans has been extensively reported with minimal data regarding horses. The objective of the study was to evaluate the effect of obesity as an isolated factor and in association with insulin resistance on apoptosis, phagocytosis and oxidative burst activity of neutrophils isolated from peripheral blood of lean and obese adult horses with or without insulin resistance, basally and after induction of hyperglycemia through an oral glucose test. Results: No differences in apoptosis were observed between experimental groups at any time point. Phagocytic capacity was significantly diminished at baseline in the obese-IR group (P<0.05) but increased after stimulation of hyperglycemia (P=0.007). Basal reactive oxygen species production differed significantly (P=0.0001) between the obese-insulin sensitive (IS) and lean-IS or obese-IR groups, and decreased significantly after stimulation of hyperglycemia in the lean-IS and obese-IS groups (P<0.05).Conclusions: Results from this study showed that both metabolic status itself, and acute hyperglycemia, are factors that influence PMNs functionality in horses, specifically phagocytosis and oxidative burst. This indicates the need for close monitoring of immune function in horses with inflammatory disease and concurrent obesity and insulin resistance.

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